#psychedelicresearch — Public Fediverse posts
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DATE: July 18, 2026 at 06:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Brain scans reveal how LSD desynchronizes local neural activity to alter consciousness
A new analysis of brain imaging data reveals that lysergic acid diethylamide, commonly known as LSD, reduces the synchronization of local brain activity to produce its mind-altering effects. Published in the European Journal of Neuroscience, the research suggests the hallucinogenic drug interacts with a wider array of brain receptors than previously assumed. These insights help map the biological mechanisms underlying altered states of consciousness and could inform future therapeutic uses of psychedelics.
Over the past decade, medical researchers have renewed their focus on classic psychedelic drugs as potential treatments for psychiatric conditions. Compounds like LSD and psilocybin produce profound changes in perception, mood, and thought. Researchers largely attribute these effects to how the chemical binds to a specific type of serotonin receptor in the brain. But the drug structurally mimics several other chemical messengers, including dopamine and different subtypes of serotonin.
Paolo La-Torraca-Vittori, a researcher at the University of Pavia, and Livio Tarchi of the University of Florence led the current investigation. They aimed to fill a gap in current neuroimaging literature. Most brain scans of people on psychedelics look at large-scale, long-distance communication between widespread brain networks. Few studies have examined what happens to the tiny, localized clusters of brain cells when someone is under the influence of LSD.
The research team focused on two specific metrics that measure the resting state of the brain. The first metric captures the amplitude of low-frequency fluctuations. This assesses the power of slow, spontaneous brain waves in a very localized area. When a person is resting, their brain usually produces stable, low-frequency rhythms. A drop in this amplitude means the brain activity is becoming noisier, faster, and more desynchronized.
The second metric evaluates regional homogeneity. This assesses how well a tiny patch of brain tissue synchronizes its electrical activity with its immediate neighboring cells. High regional homogeneity indicates that a small cluster of neurons is firing together in unison. A drop in regional homogeneity suggests that local neurons are operating independently of one another.
To explain why this matters, scientists point to the entropic brain hypothesis. Entropy is a physics concept related to disorder and randomness. In neuroscience, higher entropy means a richer, less predictable pattern of brain states. The entropic brain hypothesis proposes that psychedelics push the brain into a state of higher entropy, increasing disorder in a way that allows for more flexible and dynamic thought processes.
The investigators utilized an open-access database containing the brain scans of 15 healthy adults. Because it involved fewer than 50 participants, this was a small study. During the original data collection, each participant underwent two brain scanning sessions held at least two weeks apart. On one day, they received an intravenous saline placebo. On the other day, they received a moderate, hallucinogenic dose of LSD.
The scanning took place roughly an hour after the drug was administered, capturing the peak of the psychedelic experience. The participants rested inside the scanner with their eyes closed. The scanning device tracked changes in blood flow to map neural activity. La-Torraca-Vittori, Tarchi, and their colleagues computed the two localized metrics for both the placebo and the LSD states. The researchers then overlaid these results onto established brain maps showing the typical distribution of various chemical receptors.
The analysis revealed widespread reductions in both the amplitude of low-frequency fluctuations and regional homogeneity when participants were under the influence of LSD. These drops were particularly pronounced in the visual and somatosensory cortices, the brain areas that process sight and incoming touch. The researchers noted that this local fragmentation forces the brain to abandon its normal hierarchical processing setup.
Normally, the human brain operates in a strict functional hierarchy. Sensory regions process basic inputs and then send that data up the chain to associative regions, which interpret the information. Under LSD, this structured hierarchy flattens. Instead of local clusters processing sensory information in specialized silos, the brain integrates information broadly across the entire cortex, blending visual and physical sensations.
The two metrics also highlighted distinct changes in other brain regions. The low-frequency fluctuation metric dropped heavily in areas associated with the default mode network. This network is a group of brain areas active during passive rest, daydreaming, and self-reflection. Disruptions in this network are strongly associated with the breakdown of the conscious self commonly reported by users of psychedelics.
At the same time, regional homogeneity decreased notably in deep subcortical regions like the thalamus and amygdala. These structures act as central hubs for sensory relay and emotional processing. When local synchronization drops in these relay centers, it likely changes how sensory information gets routed to the rest of the brain.
When linking these functional changes to brain chemistry, the team found robust correlations that expanded beyond the primary target of LSD. As expected, some localization related to the primary 5-HT2A serotonin receptor. Yet the drops in both brain metrics consistently mirrored the distribution patterns of dopamine D2 receptors and an alternative serotonin receptor known as 5-HT1A.
A receptor is a protein structure on the surface of a cell that receives chemical signals. When a chemical locks into a receptor, it triggers a biological response inside the cell. Brain areas with fewer of these specific dopamine and serotonin receptors experienced the greatest decreases in local synchronization and low-frequency rhythms under LSD.
This alignment dictates that LSD initiates a cascade of neurochemical events spanning multiple messenger systems. The authors suggest that regions enriched with certain dopamine and serotonin receptors might actually be shielded from the desynchronizing effects of the drug. Alternatively, the drug might indirectly activate these adjacent pathways, leading to the varied sensory and emotional shifts that characterize the experience.
While the data offers new perspectives on the physical mechanics of psychedelics, the researchers acknowledged several limitations. The analysis relied on a small sample size, requiring replication in broader populations to ensure the ultimate reliability of the findings. The team also used standardized maps of receptor density from a general population rather than maps of the actual participants’ brains, which limits the precision of the chemical correlations.
In addition, the resting scans analyzed in this project took place after a music-listening session. The researchers caution that the lingering emotional or neurological effects of listening to music could have shaped the resting state data independently of the chemical infusion. A slight difference in head motion between the placebo and LSD groups remained even after data filtering, leaving open the possibility of minor scanning artifacts.
Future investigations will likely compare these localized measures with other brain monitoring technologies. By mapping both the physical location and the precise timing of these neural changes, scientists hope to fully decode how altered brain chemistry reshapes the human mind. The exploration of localized dynamics offers a key stepping stone toward developing safe, targeted psychedelic therapies in the future.
The study, “Knocking at the Doors of Perception: Relating LSD Effects on Low-Frequency Fluctuations and Regional Homogeneity to Receptor Densities in fMRI,” was authored by Paolo La-Torraca-Vittori, Livio Tarchi, Elisa Arrigo, Stefano Lanterna, Eleonora Tosi, Arne Doose, Fulvia Palesi, Doris Pischedda, Valdo Ricca, Paolo Fusar-Poli, and Stefano Damiani.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #LSD BrainImaging #PsychedelicResearch #Neuroscience #BrainConnectivity #LowFrequencyFluctuations #RegionalHomogeneity #5HT2A #DopamineD2 #ConsciousnessAlteration #PsychedelicTherapy
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DATE: July 18, 2026 at 06:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Brain scans reveal how LSD desynchronizes local neural activity to alter consciousness
A new analysis of brain imaging data reveals that lysergic acid diethylamide, commonly known as LSD, reduces the synchronization of local brain activity to produce its mind-altering effects. Published in the European Journal of Neuroscience, the research suggests the hallucinogenic drug interacts with a wider array of brain receptors than previously assumed. These insights help map the biological mechanisms underlying altered states of consciousness and could inform future therapeutic uses of psychedelics.
Over the past decade, medical researchers have renewed their focus on classic psychedelic drugs as potential treatments for psychiatric conditions. Compounds like LSD and psilocybin produce profound changes in perception, mood, and thought. Researchers largely attribute these effects to how the chemical binds to a specific type of serotonin receptor in the brain. But the drug structurally mimics several other chemical messengers, including dopamine and different subtypes of serotonin.
Paolo La-Torraca-Vittori, a researcher at the University of Pavia, and Livio Tarchi of the University of Florence led the current investigation. They aimed to fill a gap in current neuroimaging literature. Most brain scans of people on psychedelics look at large-scale, long-distance communication between widespread brain networks. Few studies have examined what happens to the tiny, localized clusters of brain cells when someone is under the influence of LSD.
The research team focused on two specific metrics that measure the resting state of the brain. The first metric captures the amplitude of low-frequency fluctuations. This assesses the power of slow, spontaneous brain waves in a very localized area. When a person is resting, their brain usually produces stable, low-frequency rhythms. A drop in this amplitude means the brain activity is becoming noisier, faster, and more desynchronized.
The second metric evaluates regional homogeneity. This assesses how well a tiny patch of brain tissue synchronizes its electrical activity with its immediate neighboring cells. High regional homogeneity indicates that a small cluster of neurons is firing together in unison. A drop in regional homogeneity suggests that local neurons are operating independently of one another.
To explain why this matters, scientists point to the entropic brain hypothesis. Entropy is a physics concept related to disorder and randomness. In neuroscience, higher entropy means a richer, less predictable pattern of brain states. The entropic brain hypothesis proposes that psychedelics push the brain into a state of higher entropy, increasing disorder in a way that allows for more flexible and dynamic thought processes.
The investigators utilized an open-access database containing the brain scans of 15 healthy adults. Because it involved fewer than 50 participants, this was a small study. During the original data collection, each participant underwent two brain scanning sessions held at least two weeks apart. On one day, they received an intravenous saline placebo. On the other day, they received a moderate, hallucinogenic dose of LSD.
The scanning took place roughly an hour after the drug was administered, capturing the peak of the psychedelic experience. The participants rested inside the scanner with their eyes closed. The scanning device tracked changes in blood flow to map neural activity. La-Torraca-Vittori, Tarchi, and their colleagues computed the two localized metrics for both the placebo and the LSD states. The researchers then overlaid these results onto established brain maps showing the typical distribution of various chemical receptors.
The analysis revealed widespread reductions in both the amplitude of low-frequency fluctuations and regional homogeneity when participants were under the influence of LSD. These drops were particularly pronounced in the visual and somatosensory cortices, the brain areas that process sight and incoming touch. The researchers noted that this local fragmentation forces the brain to abandon its normal hierarchical processing setup.
Normally, the human brain operates in a strict functional hierarchy. Sensory regions process basic inputs and then send that data up the chain to associative regions, which interpret the information. Under LSD, this structured hierarchy flattens. Instead of local clusters processing sensory information in specialized silos, the brain integrates information broadly across the entire cortex, blending visual and physical sensations.
The two metrics also highlighted distinct changes in other brain regions. The low-frequency fluctuation metric dropped heavily in areas associated with the default mode network. This network is a group of brain areas active during passive rest, daydreaming, and self-reflection. Disruptions in this network are strongly associated with the breakdown of the conscious self commonly reported by users of psychedelics.
At the same time, regional homogeneity decreased notably in deep subcortical regions like the thalamus and amygdala. These structures act as central hubs for sensory relay and emotional processing. When local synchronization drops in these relay centers, it likely changes how sensory information gets routed to the rest of the brain.
When linking these functional changes to brain chemistry, the team found robust correlations that expanded beyond the primary target of LSD. As expected, some localization related to the primary 5-HT2A serotonin receptor. Yet the drops in both brain metrics consistently mirrored the distribution patterns of dopamine D2 receptors and an alternative serotonin receptor known as 5-HT1A.
A receptor is a protein structure on the surface of a cell that receives chemical signals. When a chemical locks into a receptor, it triggers a biological response inside the cell. Brain areas with fewer of these specific dopamine and serotonin receptors experienced the greatest decreases in local synchronization and low-frequency rhythms under LSD.
This alignment dictates that LSD initiates a cascade of neurochemical events spanning multiple messenger systems. The authors suggest that regions enriched with certain dopamine and serotonin receptors might actually be shielded from the desynchronizing effects of the drug. Alternatively, the drug might indirectly activate these adjacent pathways, leading to the varied sensory and emotional shifts that characterize the experience.
While the data offers new perspectives on the physical mechanics of psychedelics, the researchers acknowledged several limitations. The analysis relied on a small sample size, requiring replication in broader populations to ensure the ultimate reliability of the findings. The team also used standardized maps of receptor density from a general population rather than maps of the actual participants’ brains, which limits the precision of the chemical correlations.
In addition, the resting scans analyzed in this project took place after a music-listening session. The researchers caution that the lingering emotional or neurological effects of listening to music could have shaped the resting state data independently of the chemical infusion. A slight difference in head motion between the placebo and LSD groups remained even after data filtering, leaving open the possibility of minor scanning artifacts.
Future investigations will likely compare these localized measures with other brain monitoring technologies. By mapping both the physical location and the precise timing of these neural changes, scientists hope to fully decode how altered brain chemistry reshapes the human mind. The exploration of localized dynamics offers a key stepping stone toward developing safe, targeted psychedelic therapies in the future.
The study, “Knocking at the Doors of Perception: Relating LSD Effects on Low-Frequency Fluctuations and Regional Homogeneity to Receptor Densities in fMRI,” was authored by Paolo La-Torraca-Vittori, Livio Tarchi, Elisa Arrigo, Stefano Lanterna, Eleonora Tosi, Arne Doose, Fulvia Palesi, Doris Pischedda, Valdo Ricca, Paolo Fusar-Poli, and Stefano Damiani.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #LSD BrainImaging #PsychedelicResearch #Neuroscience #BrainConnectivity #LowFrequencyFluctuations #RegionalHomogeneity #5HT2A #DopamineD2 #ConsciousnessAlteration #PsychedelicTherapy
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DATE: July 18, 2026 at 06:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Brain scans reveal how LSD desynchronizes local neural activity to alter consciousness
A new analysis of brain imaging data reveals that lysergic acid diethylamide, commonly known as LSD, reduces the synchronization of local brain activity to produce its mind-altering effects. Published in the European Journal of Neuroscience, the research suggests the hallucinogenic drug interacts with a wider array of brain receptors than previously assumed. These insights help map the biological mechanisms underlying altered states of consciousness and could inform future therapeutic uses of psychedelics.
Over the past decade, medical researchers have renewed their focus on classic psychedelic drugs as potential treatments for psychiatric conditions. Compounds like LSD and psilocybin produce profound changes in perception, mood, and thought. Researchers largely attribute these effects to how the chemical binds to a specific type of serotonin receptor in the brain. But the drug structurally mimics several other chemical messengers, including dopamine and different subtypes of serotonin.
Paolo La-Torraca-Vittori, a researcher at the University of Pavia, and Livio Tarchi of the University of Florence led the current investigation. They aimed to fill a gap in current neuroimaging literature. Most brain scans of people on psychedelics look at large-scale, long-distance communication between widespread brain networks. Few studies have examined what happens to the tiny, localized clusters of brain cells when someone is under the influence of LSD.
The research team focused on two specific metrics that measure the resting state of the brain. The first metric captures the amplitude of low-frequency fluctuations. This assesses the power of slow, spontaneous brain waves in a very localized area. When a person is resting, their brain usually produces stable, low-frequency rhythms. A drop in this amplitude means the brain activity is becoming noisier, faster, and more desynchronized.
The second metric evaluates regional homogeneity. This assesses how well a tiny patch of brain tissue synchronizes its electrical activity with its immediate neighboring cells. High regional homogeneity indicates that a small cluster of neurons is firing together in unison. A drop in regional homogeneity suggests that local neurons are operating independently of one another.
To explain why this matters, scientists point to the entropic brain hypothesis. Entropy is a physics concept related to disorder and randomness. In neuroscience, higher entropy means a richer, less predictable pattern of brain states. The entropic brain hypothesis proposes that psychedelics push the brain into a state of higher entropy, increasing disorder in a way that allows for more flexible and dynamic thought processes.
The investigators utilized an open-access database containing the brain scans of 15 healthy adults. Because it involved fewer than 50 participants, this was a small study. During the original data collection, each participant underwent two brain scanning sessions held at least two weeks apart. On one day, they received an intravenous saline placebo. On the other day, they received a moderate, hallucinogenic dose of LSD.
The scanning took place roughly an hour after the drug was administered, capturing the peak of the psychedelic experience. The participants rested inside the scanner with their eyes closed. The scanning device tracked changes in blood flow to map neural activity. La-Torraca-Vittori, Tarchi, and their colleagues computed the two localized metrics for both the placebo and the LSD states. The researchers then overlaid these results onto established brain maps showing the typical distribution of various chemical receptors.
The analysis revealed widespread reductions in both the amplitude of low-frequency fluctuations and regional homogeneity when participants were under the influence of LSD. These drops were particularly pronounced in the visual and somatosensory cortices, the brain areas that process sight and incoming touch. The researchers noted that this local fragmentation forces the brain to abandon its normal hierarchical processing setup.
Normally, the human brain operates in a strict functional hierarchy. Sensory regions process basic inputs and then send that data up the chain to associative regions, which interpret the information. Under LSD, this structured hierarchy flattens. Instead of local clusters processing sensory information in specialized silos, the brain integrates information broadly across the entire cortex, blending visual and physical sensations.
The two metrics also highlighted distinct changes in other brain regions. The low-frequency fluctuation metric dropped heavily in areas associated with the default mode network. This network is a group of brain areas active during passive rest, daydreaming, and self-reflection. Disruptions in this network are strongly associated with the breakdown of the conscious self commonly reported by users of psychedelics.
At the same time, regional homogeneity decreased notably in deep subcortical regions like the thalamus and amygdala. These structures act as central hubs for sensory relay and emotional processing. When local synchronization drops in these relay centers, it likely changes how sensory information gets routed to the rest of the brain.
When linking these functional changes to brain chemistry, the team found robust correlations that expanded beyond the primary target of LSD. As expected, some localization related to the primary 5-HT2A serotonin receptor. Yet the drops in both brain metrics consistently mirrored the distribution patterns of dopamine D2 receptors and an alternative serotonin receptor known as 5-HT1A.
A receptor is a protein structure on the surface of a cell that receives chemical signals. When a chemical locks into a receptor, it triggers a biological response inside the cell. Brain areas with fewer of these specific dopamine and serotonin receptors experienced the greatest decreases in local synchronization and low-frequency rhythms under LSD.
This alignment dictates that LSD initiates a cascade of neurochemical events spanning multiple messenger systems. The authors suggest that regions enriched with certain dopamine and serotonin receptors might actually be shielded from the desynchronizing effects of the drug. Alternatively, the drug might indirectly activate these adjacent pathways, leading to the varied sensory and emotional shifts that characterize the experience.
While the data offers new perspectives on the physical mechanics of psychedelics, the researchers acknowledged several limitations. The analysis relied on a small sample size, requiring replication in broader populations to ensure the ultimate reliability of the findings. The team also used standardized maps of receptor density from a general population rather than maps of the actual participants’ brains, which limits the precision of the chemical correlations.
In addition, the resting scans analyzed in this project took place after a music-listening session. The researchers caution that the lingering emotional or neurological effects of listening to music could have shaped the resting state data independently of the chemical infusion. A slight difference in head motion between the placebo and LSD groups remained even after data filtering, leaving open the possibility of minor scanning artifacts.
Future investigations will likely compare these localized measures with other brain monitoring technologies. By mapping both the physical location and the precise timing of these neural changes, scientists hope to fully decode how altered brain chemistry reshapes the human mind. The exploration of localized dynamics offers a key stepping stone toward developing safe, targeted psychedelic therapies in the future.
The study, “Knocking at the Doors of Perception: Relating LSD Effects on Low-Frequency Fluctuations and Regional Homogeneity to Receptor Densities in fMRI,” was authored by Paolo La-Torraca-Vittori, Livio Tarchi, Elisa Arrigo, Stefano Lanterna, Eleonora Tosi, Arne Doose, Fulvia Palesi, Doris Pischedda, Valdo Ricca, Paolo Fusar-Poli, and Stefano Damiani.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #LSD BrainImaging #PsychedelicResearch #Neuroscience #BrainConnectivity #LowFrequencyFluctuations #RegionalHomogeneity #5HT2A #DopamineD2 #ConsciousnessAlteration #PsychedelicTherapy
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DATE: June 26, 2026 at 06:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: An 80-year-old woman with advanced Alzheimer’s regained speech and mobility after taking psilocybin
A recently published case report in Frontiers in Neuroscience details how a high dose of psilocybin mushrooms appeared to temporarily restore specific daily functions and communication abilities in an individual with advanced Alzheimer’s disease. The findings suggest that certain brain networks might retain dormant capacities even in the late stages of neurodegeneration.
This discovery opens new avenues for symptom management and provides a foundation for future clinical trials. The report was published in the medical literature alongside growing scientific interest in the therapeutic potential of psychedelic compounds.
Alzheimer’s disease is a progressive brain condition that gradually impairs memory, thinking, and the ability to carry out daily tasks. In advanced stages, the condition tends to result in a severe loss of autonomy, limited communication, and a high reliance on caregivers. Current medical approaches for advanced Alzheimer’s disease focus largely on supportive care, as significant recovery of lost function is generally considered unlikely.
Alzheimer’s disease involves a breakdown in neuroplasticity, which is the capacity of the brain to form new connections and adapt to internal and external changes. Patients experience a loss of synapses, the microscopic junctions where neurons communicate, alongside an accumulation of specific proteins and increased brain inflammation.
Patients with Alzheimer’s disease also frequently experience depression and anxiety, which can accelerate their cognitive decline. To explore alternative ways to manage these profound symptoms, a team of researchers explored the use of psilocybin. Psilocybin is a naturally occurring psychedelic compound found in certain species of so-called “magic” mushrooms.
Marcos Lago, a psychiatrist and independent clinical researcher at his private practice in São Paulo, Brazil, led the observation. He noted that the case emerged organically during routine patient care.
“My clinical work with psilocybin, together with my interest in consciousness, neuroplasticity, and preserved functional capacity in severe neurological illness, led me to consider whether some abilities might remain present but inaccessible in advanced Alzheimer’s disease,” Lago said. “This case arose in an individual clinical context, and we decided to document it scientifically because the changes observed after the session were unexpected and involved several functional domains.”
The researchers cited a 2024 review article, which noted that when ingested, psilocybin is metabolized into an active compound called psilocin. This active compound crosses the blood-brain barrier and binds to a specific type of serotonin receptor known as the 5-HT2A receptor. Activation of this receptor suggests a potential to stimulate neuroplasticity and temporarily alter large-scale brain networks. One such network is the default mode network, a group of connected brain regions associated with mind-wandering, self-reflection, and depression.
Preclinical models provide evidence that psilocin can promote the growth of new dendritic spines, which are the branching structures on neurons that help transmit signals. This process involves the release of glutamate and the activation of specific proteins, including brain-derived neurotrophic factor. This neurotrophic factor then triggers signaling pathways in the brain that support neuronal survival, growth, and the remodeling of synapses.
Additionally, research suggests that psilocybin may help reduce neuroinflammation by modulating the activity of microglial cells, which act as the primary immune cells in the central nervous system. In Alzheimer’s disease, these immune cells often become overactive in response to protein deposits, worsening the damage to brain tissue. Psilocybin tends to suppress the production of pro-inflammatory cytokines, potentially easing this damaging immune response.
This capacity to induce structural and functional brain changes motivated the authors to observe how a high dose of psilocybin might impact a patient with severe dementia. Currently, clinical investigation of psilocybin has focused mostly on psychiatric disorders like severe depression. Very little clinical data exists regarding the use of psychedelic compounds in cases of advanced dementia.
The research team observed a single patient, an 80-year-old Japanese-American woman, to document the physiological and behavioral effects of the intervention. She had experienced progressive cognitive and functional decline over a ten-year period, eventually leading to a clinical diagnosis of advanced Alzheimer’s disease. For the five years leading up to the study, she experienced marked physical and cognitive limitations that required constant management.
Her baseline condition included chronic urinary incontinence, difficulty swallowing, an inability to walk independently, and a flat emotional affect. Her communication had become severely reduced, mostly consisting of monosyllabic speech and a profound lack of spontaneous social interaction. She required continuous family supervision and caregiver support for all her basic activities of daily living, including dressing and eating.
The researchers administered a single oral dose of five grams of psilocybin-containing mushrooms, specifically using a cultivated strain known as Enigma. The intervention was observational and exploratory in nature, as there is currently no established dosing framework for psilocybin in advanced dementia. The authors selected a relatively high dose based on previous observations of how psychedelic effects impact neurobehavioral states and the duration of those effects.
During the acute phase of the intervention, the patient experienced several strong physical and autonomic reactions. These reactions included profuse sweating, suspected elevated body temperature, and a prolonged state resembling deep sleep. Approximately 19 hours after the administration of the mushrooms, a notable change occurred when the patient spontaneously woke up and initiated an autobiographical conversation that lasted for several hours.
Over the following days and weeks, the researchers documented multiple functional improvements across several cognitive and physical domains. The patient regained urinary continence, a function she had lacked for five years, and she began to walk independently. She also demonstrated the ability to dress herself autonomously and showed increased emotional responsiveness, including making sustained eye contact and smiling at her family members.
“What surprised us most was the multidomain nature of the changes,” Lago told PsyPost. “The patient showed spontaneous autobiographical conversation, improved social interaction and recognition, better mobility, and improvement in urinary continence after having been severely impaired for several years.”
“Any one of these changes might have been interpreted as a fluctuation, but their convergence across several domains made the observation particularly striking,” Lago added. “Nevertheless, these outcomes were primarily clinical and observational rather than measured using standardized neuropsychological instruments.”
The patient also exhibited improvements in working memory and episodic memory. For example, she successfully recognized vehicles and asked contextual questions about where specific individuals had gone. Because the improvements, particularly her urinary continence, persisted for a month, the team conducted a second supervised session using a lower dose of three grams of the mushrooms.
During this second experience, the patient remained significantly more verbally expressive. She described positive emotional imagery, such as surfing with her son on a peaceful island. She also displayed spontaneous humor, improved facial expressions, increased walking agility, and explicitly stated that the experience was pleasant.
“The story is remarkable because the patient reportedly had advanced Alzheimer’s with years of severe impairment, then showed transient gains. That is extraordinary. However, as a neuroscientist who studies serotonin 5-HT2A signaling, I am not surprised that a powerful serotonergic psychedelic could acutely reorganize brain network activity and temporarily reveal capacities that seemed lost,” Dustin Hines, an associate professor of psychology at the University of Nevada, Las Vegas, who was not involved in the study, told Medical News Today.
While these observations document an unusual functional recovery, the authors note several limitations inherent to the design of the report. A case report involves only a single individual, meaning the findings cannot be automatically generalized to all patients with Alzheimer’s disease. The study also lacked formal clinical monitoring tools, such as brain imaging, quantitative sleep tracking, or standardized cognitive tests.
“There are several major limitations,” Lago said. “This was a single case without a control group or placebo condition, so causality cannot be established and the findings cannot be generalized to other patients. The outcomes were based largely on clinical observation and caregiver reports, and we did not have neuroimaging, biomarkers, or standardized cognitive testing capable of demonstrating the underlying mechanism.”
The natural course of neurodegenerative diseases can sometimes include spontaneous fluctuations in a patient’s cognitive and physical state. These natural variations cannot be entirely ruled out as a factor in her temporary improvement. Additionally, the type of substance used introduces variability. “In addition, mushroom preparations do not provide the same precise dose standardization as pharmaceutical-grade psilocybin,” Lago said.
The researchers advise against misinterpreting these observations as a cure or a reversal of Alzheimer’s pathology. The underlying physical damage to the brain, such as the buildup of amyloid and tau proteins, was not measured and is not assumed to have been resolved. The case mainly provides evidence that latent functional capacities might still exist in the brain even during late-stage neurodegeneration.
“The main takeaway is not that psilocybin has been proven to treat Alzheimer’s disease,” Lago said. “Rather, this single case raises the possibility that some functional abilities may remain temporarily accessible even in advanced disease, suggesting that severe dementia may not always represent the complete and irreversible loss of every previously acquired capacity.”
“At the same time, this is only one case and should be understood as a hypothesis-generating observation, not as evidence of an established treatment,” Lago added. “This was not a clinical trial, and the report should not be interpreted as evidence that psilocybin is effective or safe for people with Alzheimer’s disease.”
Case reports are highly useful in the medical field for generating new hypotheses and pointing scientists toward unexplored areas of study. The transient improvements seen in this patient suggest that dormant capacities can become temporarily accessible under specific conditions that alter brain network dynamics. The authors advise that systematic, controlled clinical trials are now needed to better understand the safety, efficacy, and mechanisms of psilocybin for individuals with advanced dementia.
“The appropriate next step would be formal, prospective research conducted under ethical and regulatory oversight,” Lago said. “Initial studies should focus primarily on safety and feasibility, using carefully selected participants, standardized preparations, objective cognitive and functional measures, longer follow-up, and, when possible, neuroimaging and biological markers.”
The scientists hope to identify the physiological factors driving this phenomenon. “The broader scientific question is whether residual functional networks can be temporarily re-engaged in advanced neurodegenerative disease and, if so, under what conditions,” Lago added.
The authors caution that this report is strictly observational and carries potential risks. “Families and patients should not interpret this report as a recommendation for unsupervised use,” Lago said. “Older adults with advanced neurodegenerative disease may have substantial medical vulnerability, and the safety profile of psilocybin in this population remains largely unknown.”
“The value of this case is that it identifies a phenomenon worthy of careful investigation,” Lago added. “It does not provide a clinical protocol or establish a treatment.”
Similarly, writing for The Conversation, Rahul Sidhu of the University of Sheffield said that there “are important reasons for caution.”
“Psilocybin is not risk-free. Psychedelic experiences can be frightening and disorienting, particularly for vulnerable people. Older adults may face increased risks of falls, heart and circulation problems and interactions with medications.”
“The woman experienced heavy sweating, suspected high body temperature and a prolonged sleep-like state. The absence of lasting complications does not establish that the approach is safe. It would be dangerous to interpret the report as a reason to experiment with psychedelic mushrooms outside a closely supervised research or clinical setting.”
In a related effort to understand how psychedelics affect the aging brain, researchers at the UC Berkeley Center for the Science of Psychedelics recently launched the PLASTICITY study, the first psychedelic neuroimaging trial specifically focused on healthy older adults. Because older populations have been largely excluded from modern psychedelic research, this study will investigate whether synthetic psilocybin can enhance neuroplasticity and counteract the structural brain changes associated with aging.
Participants between the ages of 60 and 85 will receive 1 to 30 milligrams of psilocybin, with researchers using advanced MRI and cognitive testing before and after the intervention to track changes in memory, perception, and emotional regulation. The interdisciplinary team hopes to determine if the positive brain changes observed in animal models translate to humans, potentially offering new strategies to promote successful aging, improve mental well-being, and mitigate cognitive decline.
The study, “Transient multidomain functional improvement in advanced Alzheimer’s disease following high-dose psilocybin-containing mushroom administration: a case report,” was authored by Marcos Lago, Mariana Cerveira, and Joe Xavier Simonet.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PsilocybinInAlzheimers #Neuroplasticity #BrainNetworkReorganization #AdvancedDementiaCase #PsychedelicResearch #OldAgeNeuroscience #5HT2AReceptor #NeuroinflammationModulation #FunctionalRecovery #ClinicalCaseReport
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DATE: June 26, 2026 at 06:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: An 80-year-old woman with advanced Alzheimer’s regained speech and mobility after taking psilocybin
A recently published case report in Frontiers in Neuroscience details how a high dose of psilocybin mushrooms appeared to temporarily restore specific daily functions and communication abilities in an individual with advanced Alzheimer’s disease. The findings suggest that certain brain networks might retain dormant capacities even in the late stages of neurodegeneration.
This discovery opens new avenues for symptom management and provides a foundation for future clinical trials. The report was published in the medical literature alongside growing scientific interest in the therapeutic potential of psychedelic compounds.
Alzheimer’s disease is a progressive brain condition that gradually impairs memory, thinking, and the ability to carry out daily tasks. In advanced stages, the condition tends to result in a severe loss of autonomy, limited communication, and a high reliance on caregivers. Current medical approaches for advanced Alzheimer’s disease focus largely on supportive care, as significant recovery of lost function is generally considered unlikely.
Alzheimer’s disease involves a breakdown in neuroplasticity, which is the capacity of the brain to form new connections and adapt to internal and external changes. Patients experience a loss of synapses, the microscopic junctions where neurons communicate, alongside an accumulation of specific proteins and increased brain inflammation.
Patients with Alzheimer’s disease also frequently experience depression and anxiety, which can accelerate their cognitive decline. To explore alternative ways to manage these profound symptoms, a team of researchers explored the use of psilocybin. Psilocybin is a naturally occurring psychedelic compound found in certain species of so-called “magic” mushrooms.
Marcos Lago, a psychiatrist and independent clinical researcher at his private practice in São Paulo, Brazil, led the observation. He noted that the case emerged organically during routine patient care.
“My clinical work with psilocybin, together with my interest in consciousness, neuroplasticity, and preserved functional capacity in severe neurological illness, led me to consider whether some abilities might remain present but inaccessible in advanced Alzheimer’s disease,” Lago said. “This case arose in an individual clinical context, and we decided to document it scientifically because the changes observed after the session were unexpected and involved several functional domains.”
The researchers cited a 2024 review article, which noted that when ingested, psilocybin is metabolized into an active compound called psilocin. This active compound crosses the blood-brain barrier and binds to a specific type of serotonin receptor known as the 5-HT2A receptor. Activation of this receptor suggests a potential to stimulate neuroplasticity and temporarily alter large-scale brain networks. One such network is the default mode network, a group of connected brain regions associated with mind-wandering, self-reflection, and depression.
Preclinical models provide evidence that psilocin can promote the growth of new dendritic spines, which are the branching structures on neurons that help transmit signals. This process involves the release of glutamate and the activation of specific proteins, including brain-derived neurotrophic factor. This neurotrophic factor then triggers signaling pathways in the brain that support neuronal survival, growth, and the remodeling of synapses.
Additionally, research suggests that psilocybin may help reduce neuroinflammation by modulating the activity of microglial cells, which act as the primary immune cells in the central nervous system. In Alzheimer’s disease, these immune cells often become overactive in response to protein deposits, worsening the damage to brain tissue. Psilocybin tends to suppress the production of pro-inflammatory cytokines, potentially easing this damaging immune response.
This capacity to induce structural and functional brain changes motivated the authors to observe how a high dose of psilocybin might impact a patient with severe dementia. Currently, clinical investigation of psilocybin has focused mostly on psychiatric disorders like severe depression. Very little clinical data exists regarding the use of psychedelic compounds in cases of advanced dementia.
The research team observed a single patient, an 80-year-old Japanese-American woman, to document the physiological and behavioral effects of the intervention. She had experienced progressive cognitive and functional decline over a ten-year period, eventually leading to a clinical diagnosis of advanced Alzheimer’s disease. For the five years leading up to the study, she experienced marked physical and cognitive limitations that required constant management.
Her baseline condition included chronic urinary incontinence, difficulty swallowing, an inability to walk independently, and a flat emotional affect. Her communication had become severely reduced, mostly consisting of monosyllabic speech and a profound lack of spontaneous social interaction. She required continuous family supervision and caregiver support for all her basic activities of daily living, including dressing and eating.
The researchers administered a single oral dose of five grams of psilocybin-containing mushrooms, specifically using a cultivated strain known as Enigma. The intervention was observational and exploratory in nature, as there is currently no established dosing framework for psilocybin in advanced dementia. The authors selected a relatively high dose based on previous observations of how psychedelic effects impact neurobehavioral states and the duration of those effects.
During the acute phase of the intervention, the patient experienced several strong physical and autonomic reactions. These reactions included profuse sweating, suspected elevated body temperature, and a prolonged state resembling deep sleep. Approximately 19 hours after the administration of the mushrooms, a notable change occurred when the patient spontaneously woke up and initiated an autobiographical conversation that lasted for several hours.
Over the following days and weeks, the researchers documented multiple functional improvements across several cognitive and physical domains. The patient regained urinary continence, a function she had lacked for five years, and she began to walk independently. She also demonstrated the ability to dress herself autonomously and showed increased emotional responsiveness, including making sustained eye contact and smiling at her family members.
“What surprised us most was the multidomain nature of the changes,” Lago told PsyPost. “The patient showed spontaneous autobiographical conversation, improved social interaction and recognition, better mobility, and improvement in urinary continence after having been severely impaired for several years.”
“Any one of these changes might have been interpreted as a fluctuation, but their convergence across several domains made the observation particularly striking,” Lago added. “Nevertheless, these outcomes were primarily clinical and observational rather than measured using standardized neuropsychological instruments.”
The patient also exhibited improvements in working memory and episodic memory. For example, she successfully recognized vehicles and asked contextual questions about where specific individuals had gone. Because the improvements, particularly her urinary continence, persisted for a month, the team conducted a second supervised session using a lower dose of three grams of the mushrooms.
During this second experience, the patient remained significantly more verbally expressive. She described positive emotional imagery, such as surfing with her son on a peaceful island. She also displayed spontaneous humor, improved facial expressions, increased walking agility, and explicitly stated that the experience was pleasant.
“The story is remarkable because the patient reportedly had advanced Alzheimer’s with years of severe impairment, then showed transient gains. That is extraordinary. However, as a neuroscientist who studies serotonin 5-HT2A signaling, I am not surprised that a powerful serotonergic psychedelic could acutely reorganize brain network activity and temporarily reveal capacities that seemed lost,” Dustin Hines, an associate professor of psychology at the University of Nevada, Las Vegas, who was not involved in the study, told Medical News Today.
While these observations document an unusual functional recovery, the authors note several limitations inherent to the design of the report. A case report involves only a single individual, meaning the findings cannot be automatically generalized to all patients with Alzheimer’s disease. The study also lacked formal clinical monitoring tools, such as brain imaging, quantitative sleep tracking, or standardized cognitive tests.
“There are several major limitations,” Lago said. “This was a single case without a control group or placebo condition, so causality cannot be established and the findings cannot be generalized to other patients. The outcomes were based largely on clinical observation and caregiver reports, and we did not have neuroimaging, biomarkers, or standardized cognitive testing capable of demonstrating the underlying mechanism.”
The natural course of neurodegenerative diseases can sometimes include spontaneous fluctuations in a patient’s cognitive and physical state. These natural variations cannot be entirely ruled out as a factor in her temporary improvement. Additionally, the type of substance used introduces variability. “In addition, mushroom preparations do not provide the same precise dose standardization as pharmaceutical-grade psilocybin,” Lago said.
The researchers advise against misinterpreting these observations as a cure or a reversal of Alzheimer’s pathology. The underlying physical damage to the brain, such as the buildup of amyloid and tau proteins, was not measured and is not assumed to have been resolved. The case mainly provides evidence that latent functional capacities might still exist in the brain even during late-stage neurodegeneration.
“The main takeaway is not that psilocybin has been proven to treat Alzheimer’s disease,” Lago said. “Rather, this single case raises the possibility that some functional abilities may remain temporarily accessible even in advanced disease, suggesting that severe dementia may not always represent the complete and irreversible loss of every previously acquired capacity.”
“At the same time, this is only one case and should be understood as a hypothesis-generating observation, not as evidence of an established treatment,” Lago added. “This was not a clinical trial, and the report should not be interpreted as evidence that psilocybin is effective or safe for people with Alzheimer’s disease.”
Case reports are highly useful in the medical field for generating new hypotheses and pointing scientists toward unexplored areas of study. The transient improvements seen in this patient suggest that dormant capacities can become temporarily accessible under specific conditions that alter brain network dynamics. The authors advise that systematic, controlled clinical trials are now needed to better understand the safety, efficacy, and mechanisms of psilocybin for individuals with advanced dementia.
“The appropriate next step would be formal, prospective research conducted under ethical and regulatory oversight,” Lago said. “Initial studies should focus primarily on safety and feasibility, using carefully selected participants, standardized preparations, objective cognitive and functional measures, longer follow-up, and, when possible, neuroimaging and biological markers.”
The scientists hope to identify the physiological factors driving this phenomenon. “The broader scientific question is whether residual functional networks can be temporarily re-engaged in advanced neurodegenerative disease and, if so, under what conditions,” Lago added.
The authors caution that this report is strictly observational and carries potential risks. “Families and patients should not interpret this report as a recommendation for unsupervised use,” Lago said. “Older adults with advanced neurodegenerative disease may have substantial medical vulnerability, and the safety profile of psilocybin in this population remains largely unknown.”
“The value of this case is that it identifies a phenomenon worthy of careful investigation,” Lago added. “It does not provide a clinical protocol or establish a treatment.”
Similarly, writing for The Conversation, Rahul Sidhu of the University of Sheffield said that there “are important reasons for caution.”
“Psilocybin is not risk-free. Psychedelic experiences can be frightening and disorienting, particularly for vulnerable people. Older adults may face increased risks of falls, heart and circulation problems and interactions with medications.”
“The woman experienced heavy sweating, suspected high body temperature and a prolonged sleep-like state. The absence of lasting complications does not establish that the approach is safe. It would be dangerous to interpret the report as a reason to experiment with psychedelic mushrooms outside a closely supervised research or clinical setting.”
In a related effort to understand how psychedelics affect the aging brain, researchers at the UC Berkeley Center for the Science of Psychedelics recently launched the PLASTICITY study, the first psychedelic neuroimaging trial specifically focused on healthy older adults. Because older populations have been largely excluded from modern psychedelic research, this study will investigate whether synthetic psilocybin can enhance neuroplasticity and counteract the structural brain changes associated with aging.
Participants between the ages of 60 and 85 will receive 1 to 30 milligrams of psilocybin, with researchers using advanced MRI and cognitive testing before and after the intervention to track changes in memory, perception, and emotional regulation. The interdisciplinary team hopes to determine if the positive brain changes observed in animal models translate to humans, potentially offering new strategies to promote successful aging, improve mental well-being, and mitigate cognitive decline.
The study, “Transient multidomain functional improvement in advanced Alzheimer’s disease following high-dose psilocybin-containing mushroom administration: a case report,” was authored by Marcos Lago, Mariana Cerveira, and Joe Xavier Simonet.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PsilocybinInAlzheimers #Neuroplasticity #BrainNetworkReorganization #AdvancedDementiaCase #PsychedelicResearch #OldAgeNeuroscience #5HT2AReceptor #NeuroinflammationModulation #FunctionalRecovery #ClinicalCaseReport
-
DATE: June 26, 2026 at 06:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: An 80-year-old woman with advanced Alzheimer’s regained speech and mobility after taking psilocybin
A recently published case report in Frontiers in Neuroscience details how a high dose of psilocybin mushrooms appeared to temporarily restore specific daily functions and communication abilities in an individual with advanced Alzheimer’s disease. The findings suggest that certain brain networks might retain dormant capacities even in the late stages of neurodegeneration.
This discovery opens new avenues for symptom management and provides a foundation for future clinical trials. The report was published in the medical literature alongside growing scientific interest in the therapeutic potential of psychedelic compounds.
Alzheimer’s disease is a progressive brain condition that gradually impairs memory, thinking, and the ability to carry out daily tasks. In advanced stages, the condition tends to result in a severe loss of autonomy, limited communication, and a high reliance on caregivers. Current medical approaches for advanced Alzheimer’s disease focus largely on supportive care, as significant recovery of lost function is generally considered unlikely.
Alzheimer’s disease involves a breakdown in neuroplasticity, which is the capacity of the brain to form new connections and adapt to internal and external changes. Patients experience a loss of synapses, the microscopic junctions where neurons communicate, alongside an accumulation of specific proteins and increased brain inflammation.
Patients with Alzheimer’s disease also frequently experience depression and anxiety, which can accelerate their cognitive decline. To explore alternative ways to manage these profound symptoms, a team of researchers explored the use of psilocybin. Psilocybin is a naturally occurring psychedelic compound found in certain species of so-called “magic” mushrooms.
Marcos Lago, a psychiatrist and independent clinical researcher at his private practice in São Paulo, Brazil, led the observation. He noted that the case emerged organically during routine patient care.
“My clinical work with psilocybin, together with my interest in consciousness, neuroplasticity, and preserved functional capacity in severe neurological illness, led me to consider whether some abilities might remain present but inaccessible in advanced Alzheimer’s disease,” Lago said. “This case arose in an individual clinical context, and we decided to document it scientifically because the changes observed after the session were unexpected and involved several functional domains.”
The researchers cited a 2024 review article, which noted that when ingested, psilocybin is metabolized into an active compound called psilocin. This active compound crosses the blood-brain barrier and binds to a specific type of serotonin receptor known as the 5-HT2A receptor. Activation of this receptor suggests a potential to stimulate neuroplasticity and temporarily alter large-scale brain networks. One such network is the default mode network, a group of connected brain regions associated with mind-wandering, self-reflection, and depression.
Preclinical models provide evidence that psilocin can promote the growth of new dendritic spines, which are the branching structures on neurons that help transmit signals. This process involves the release of glutamate and the activation of specific proteins, including brain-derived neurotrophic factor. This neurotrophic factor then triggers signaling pathways in the brain that support neuronal survival, growth, and the remodeling of synapses.
Additionally, research suggests that psilocybin may help reduce neuroinflammation by modulating the activity of microglial cells, which act as the primary immune cells in the central nervous system. In Alzheimer’s disease, these immune cells often become overactive in response to protein deposits, worsening the damage to brain tissue. Psilocybin tends to suppress the production of pro-inflammatory cytokines, potentially easing this damaging immune response.
This capacity to induce structural and functional brain changes motivated the authors to observe how a high dose of psilocybin might impact a patient with severe dementia. Currently, clinical investigation of psilocybin has focused mostly on psychiatric disorders like severe depression. Very little clinical data exists regarding the use of psychedelic compounds in cases of advanced dementia.
The research team observed a single patient, an 80-year-old Japanese-American woman, to document the physiological and behavioral effects of the intervention. She had experienced progressive cognitive and functional decline over a ten-year period, eventually leading to a clinical diagnosis of advanced Alzheimer’s disease. For the five years leading up to the study, she experienced marked physical and cognitive limitations that required constant management.
Her baseline condition included chronic urinary incontinence, difficulty swallowing, an inability to walk independently, and a flat emotional affect. Her communication had become severely reduced, mostly consisting of monosyllabic speech and a profound lack of spontaneous social interaction. She required continuous family supervision and caregiver support for all her basic activities of daily living, including dressing and eating.
The researchers administered a single oral dose of five grams of psilocybin-containing mushrooms, specifically using a cultivated strain known as Enigma. The intervention was observational and exploratory in nature, as there is currently no established dosing framework for psilocybin in advanced dementia. The authors selected a relatively high dose based on previous observations of how psychedelic effects impact neurobehavioral states and the duration of those effects.
During the acute phase of the intervention, the patient experienced several strong physical and autonomic reactions. These reactions included profuse sweating, suspected elevated body temperature, and a prolonged state resembling deep sleep. Approximately 19 hours after the administration of the mushrooms, a notable change occurred when the patient spontaneously woke up and initiated an autobiographical conversation that lasted for several hours.
Over the following days and weeks, the researchers documented multiple functional improvements across several cognitive and physical domains. The patient regained urinary continence, a function she had lacked for five years, and she began to walk independently. She also demonstrated the ability to dress herself autonomously and showed increased emotional responsiveness, including making sustained eye contact and smiling at her family members.
“What surprised us most was the multidomain nature of the changes,” Lago told PsyPost. “The patient showed spontaneous autobiographical conversation, improved social interaction and recognition, better mobility, and improvement in urinary continence after having been severely impaired for several years.”
“Any one of these changes might have been interpreted as a fluctuation, but their convergence across several domains made the observation particularly striking,” Lago added. “Nevertheless, these outcomes were primarily clinical and observational rather than measured using standardized neuropsychological instruments.”
The patient also exhibited improvements in working memory and episodic memory. For example, she successfully recognized vehicles and asked contextual questions about where specific individuals had gone. Because the improvements, particularly her urinary continence, persisted for a month, the team conducted a second supervised session using a lower dose of three grams of the mushrooms.
During this second experience, the patient remained significantly more verbally expressive. She described positive emotional imagery, such as surfing with her son on a peaceful island. She also displayed spontaneous humor, improved facial expressions, increased walking agility, and explicitly stated that the experience was pleasant.
“The story is remarkable because the patient reportedly had advanced Alzheimer’s with years of severe impairment, then showed transient gains. That is extraordinary. However, as a neuroscientist who studies serotonin 5-HT2A signaling, I am not surprised that a powerful serotonergic psychedelic could acutely reorganize brain network activity and temporarily reveal capacities that seemed lost,” Dustin Hines, an associate professor of psychology at the University of Nevada, Las Vegas, who was not involved in the study, told Medical News Today.
While these observations document an unusual functional recovery, the authors note several limitations inherent to the design of the report. A case report involves only a single individual, meaning the findings cannot be automatically generalized to all patients with Alzheimer’s disease. The study also lacked formal clinical monitoring tools, such as brain imaging, quantitative sleep tracking, or standardized cognitive tests.
“There are several major limitations,” Lago said. “This was a single case without a control group or placebo condition, so causality cannot be established and the findings cannot be generalized to other patients. The outcomes were based largely on clinical observation and caregiver reports, and we did not have neuroimaging, biomarkers, or standardized cognitive testing capable of demonstrating the underlying mechanism.”
The natural course of neurodegenerative diseases can sometimes include spontaneous fluctuations in a patient’s cognitive and physical state. These natural variations cannot be entirely ruled out as a factor in her temporary improvement. Additionally, the type of substance used introduces variability. “In addition, mushroom preparations do not provide the same precise dose standardization as pharmaceutical-grade psilocybin,” Lago said.
The researchers advise against misinterpreting these observations as a cure or a reversal of Alzheimer’s pathology. The underlying physical damage to the brain, such as the buildup of amyloid and tau proteins, was not measured and is not assumed to have been resolved. The case mainly provides evidence that latent functional capacities might still exist in the brain even during late-stage neurodegeneration.
“The main takeaway is not that psilocybin has been proven to treat Alzheimer’s disease,” Lago said. “Rather, this single case raises the possibility that some functional abilities may remain temporarily accessible even in advanced disease, suggesting that severe dementia may not always represent the complete and irreversible loss of every previously acquired capacity.”
“At the same time, this is only one case and should be understood as a hypothesis-generating observation, not as evidence of an established treatment,” Lago added. “This was not a clinical trial, and the report should not be interpreted as evidence that psilocybin is effective or safe for people with Alzheimer’s disease.”
Case reports are highly useful in the medical field for generating new hypotheses and pointing scientists toward unexplored areas of study. The transient improvements seen in this patient suggest that dormant capacities can become temporarily accessible under specific conditions that alter brain network dynamics. The authors advise that systematic, controlled clinical trials are now needed to better understand the safety, efficacy, and mechanisms of psilocybin for individuals with advanced dementia.
“The appropriate next step would be formal, prospective research conducted under ethical and regulatory oversight,” Lago said. “Initial studies should focus primarily on safety and feasibility, using carefully selected participants, standardized preparations, objective cognitive and functional measures, longer follow-up, and, when possible, neuroimaging and biological markers.”
The scientists hope to identify the physiological factors driving this phenomenon. “The broader scientific question is whether residual functional networks can be temporarily re-engaged in advanced neurodegenerative disease and, if so, under what conditions,” Lago added.
The authors caution that this report is strictly observational and carries potential risks. “Families and patients should not interpret this report as a recommendation for unsupervised use,” Lago said. “Older adults with advanced neurodegenerative disease may have substantial medical vulnerability, and the safety profile of psilocybin in this population remains largely unknown.”
“The value of this case is that it identifies a phenomenon worthy of careful investigation,” Lago added. “It does not provide a clinical protocol or establish a treatment.”
Similarly, writing for The Conversation, Rahul Sidhu of the University of Sheffield said that there “are important reasons for caution.”
“Psilocybin is not risk-free. Psychedelic experiences can be frightening and disorienting, particularly for vulnerable people. Older adults may face increased risks of falls, heart and circulation problems and interactions with medications.”
“The woman experienced heavy sweating, suspected high body temperature and a prolonged sleep-like state. The absence of lasting complications does not establish that the approach is safe. It would be dangerous to interpret the report as a reason to experiment with psychedelic mushrooms outside a closely supervised research or clinical setting.”
In a related effort to understand how psychedelics affect the aging brain, researchers at the UC Berkeley Center for the Science of Psychedelics recently launched the PLASTICITY study, the first psychedelic neuroimaging trial specifically focused on healthy older adults. Because older populations have been largely excluded from modern psychedelic research, this study will investigate whether synthetic psilocybin can enhance neuroplasticity and counteract the structural brain changes associated with aging.
Participants between the ages of 60 and 85 will receive 1 to 30 milligrams of psilocybin, with researchers using advanced MRI and cognitive testing before and after the intervention to track changes in memory, perception, and emotional regulation. The interdisciplinary team hopes to determine if the positive brain changes observed in animal models translate to humans, potentially offering new strategies to promote successful aging, improve mental well-being, and mitigate cognitive decline.
The study, “Transient multidomain functional improvement in advanced Alzheimer’s disease following high-dose psilocybin-containing mushroom administration: a case report,” was authored by Marcos Lago, Mariana Cerveira, and Joe Xavier Simonet.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PsilocybinInAlzheimers #Neuroplasticity #BrainNetworkReorganization #AdvancedDementiaCase #PsychedelicResearch #OldAgeNeuroscience #5HT2AReceptor #NeuroinflammationModulation #FunctionalRecovery #ClinicalCaseReport
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DATE: June 19, 2026 at 06:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Psychedelic compound reduces cocaine motivation and cravings in animal models
Recent laboratory research reveals that a chemical compound known for inducing psychedelic effects reduces the motivation to consume cocaine in animal models. The findings suggest that targeting specific serotonin receptors in the brain could offer a novel biological approach to treating stimulant use disorders. The study detailing these outcomes was published in the journal Psychopharmacology.
Cocaine use continues to present a massive public health challenge across the globe. Millions of individuals struggle with stimulant addiction every year, and overdose fatalities involving the drug have trended steadily upward over the past decade. Traditional medical interventions and behavioral therapies have largely struggled to help individuals maintain long-term abstinence. Cocaine produces its highly addictive profile by infiltrating and altering communication within the brain’s reward centers. It physically blocks the normal recycling process of dopamine, a chemical messenger heavily involved in anticipating and experiencing pleasure.
Normally, brain cells release dopamine to signal that something good has happened, and then quickly vacuum it back up to reset the system. By jamming this biological vacuum system, cocaine creates an unnatural flood of dopamine. This flooding occurs specifically within the meso-corticolimbic circuitry, a network of brain regions that governs how living creatures learn to seek out rewards and find the motivation to survive. Over time, this intense chemical stimulation fundamentally rewires the brain, making it increasingly difficult for a person to feel motivated by anything other than the drug.
While dopamine receives the vast majority of attention in addiction literature, cocaine also substantially increases the brain’s levels of serotonin. Serotonin is a separate chemical messenger best known for regulating mood, sleep, and sensory perception. Investigators at the University of Texas Medical Branch suspected that a specific cellular landing pad for serotonin, known as the serotonin 2A receptor, might help dictate the brain’s overriding addiction mechanics. Leah Salinsky and Christina Merritt led a research team to investigate whether activating this exact receptor could alter how much cocaine animals would willingly self-administer.
To test this hypothesis, the researchers used a laboratory compound named (-)-DOI. While not regularly encountered outside of research settings, (-)-DOI belongs to a broad class of drugs known as hallucinogens or psychedelics. Like classical psychedelics such as LSD and psilocybin, the compound produces its main behavioral effects by strongly binding to and activating the serotonin 2A receptor in the brain. Unlike those classical drugs, (-)-DOI is highly selective. It primarily interacts with this single receptor subtype without strongly stimulating the numerous other serotonin receptors scattered throughout the nervous system.
This extreme chemical precision makes the compound an ideal tool for scientists trying to isolate biological mechanisms. If a highly selective compound changes a specific behavior, researchers can be relatively confident that the target receptor is directly responsible for the shift. To ensure the validity of their tests, the team also utilized a second specialized chemical that acts as an antagonist. This second chemical acts like a cellular shield, sitting on the serotonin 2A receptor and preventing any other drugs from activating it.
The team began the experimental phase by training adult male rats to self-administer cocaine over several weeks. The animals were placed in specialized soundproof enclosures equipped with a small metal lever. When the rats pressed the lever a set number of times, a mechanized pump delivered a highly controlled amount of cocaine directly into their bloodstream. Once the rats learned this relationship and began pressing the lever at a highly consistent rate, the researchers introduced the psychedelic compound into the daily routine. They injected the rats with varying, controlled doses of (-)-DOI shortly before placing them back into the testing chambers.
The experimental results showed a steep decline in cocaine consumption after the rats received the psychedelic compound. Across all the tested doses, the animals pressed the active lever far fewer times and subsequently delivered much less cocaine to themselves compared to when they received a neutral saline solution. To ensure the rats were not simply too sedated to move, the researchers tracked how often the animals pressed a secondary dummy lever that provided no drug. The rate at which the rats pressed the inactive dummy lever remained completely unchanged. The animals also approached the active lever just as quickly as usual initially, indicating that their basic physical coordination and alertness were intact.
The researchers then completely verified the biological pathway. They conducted another round of testing where they treated the animals with the receptor-blocking agent prior to administering the highest dose of the psychedelic. When the rats received this blocking agent first, their rate of cocaine consumption rebounded. The blocking agent largely muted the suppressive effect of the psychedelic, establishing that the serotonin 2A receptor is the primary gateway through which the drug curtails immediate reward-seeking behavior.
For their next experiment, the researchers utilized a testing framework drawn from the principles of behavioral economics. This analytical approach measures a subject’s absolute motivation to obtain a reward by steadily increasing the physical effort required to get it. Humans experience this concept intuitively: someone might buy a cup of coffee every day if it costs two dollars, but they will likely stop buying it entirely if the price jumps to twenty dollars. In this rodent trial, the rats initially earned a large, satisfying dose of cocaine for just a few lever presses.
As the session progressed, the volume of cocaine delivered with each successful lever press steadily shrank at scheduled intervals. To maintain the same level of intoxication, the animals had to press the lever at intensely high, escalating rates. By the final block of the testing session, the rats had to expend an immense amount of physical effort to receive barely a fraction of the starting drug dosage. This procedure effectively estimates the absolute maximum price an animal is willing to pay before giving up completely.
This economic analysis tracks a metric known as demand elasticity, which describes just how sensitive a subject behaves when facing price hikes. The researchers found that the highest administered dose of the psychedelic compound left the rats dramatically more sensitive to the rising cost of the stimulant. When treated with the highest dose of (-)-DOI, the animals gave up much sooner as the required lever presses rapidly multiplied. Their overarching motivation to work for the stimulant eroded. The total overall amount of cocaine they managed to consume during the demanding session also dropped immensely compared to their untreated baseline behavior.
Just as in the simplest trials, administering the receptor-blocking agent before the psychedelic reversed these sweeping behavioral changes. The rats treated with the blocker returned to working incredibly hard for shrinking amounts of cocaine. This data confirmed again that turning on the serotonin 2A receptor specifically devalues the perceived, essential reward of the stimulant. The psychedelic essentially caused the cocaine to lose its overpowering appeal once the physical price of obtaining it became excessively high.
The investigators highlighted several basic boundaries to their current findings. The study exclusively observed male rats, creating a gap in understanding how female biology might alter or amplify these outcomes. Fluctuations in ovarian hormones are widely reported to influence how the brain responds to cocaine. Future laboratory trials must include female animal models to provide the complete biological picture required for medical science.
The research team also pointed out that their complex economic demand tests required delivering very high initial bursts of cocaine at the start of the session. The sheer volume of this early drug exposure might temporarily change how the entire serotonin system physically functions compared to continuous low-dose use. Future research efforts will need to test these psychedelic compounds against different ingestion patterns and observe if the effects hold steady. Scientists must also determine if activating these receptors specifically alters basic sensory perception during drug taking.
These laboratory findings arrive precisely as massive medical institutions are conducting early human trials using classical psychedelics for substance use issues. By pinpointing the exact cellular receptors that reduce drug consumption, researchers hope to guide the creation of highly specialized new medications. Ongoing medicinal chemistry projects are currently attempting to design novel drugs that can activate the serotonin 2A receptor to squelch cravings without causing the intense hallucinogenic side effects normally associated with psychedelics.
The study, “The psychedelic (−)‑2,5‑dimethoxy‑4‑iodoamphetamine [(−)‑DOI] demonstrates efficacy in reducing cocaine reward and motivation in male rats,” was authored by Leah M. Salinsky, Christina R. Merritt, Erik J. Garcia, Robert G. Fox, Joshua C. Zamora, Noelle C. Anastasio, and Kathryn A. Cunningham.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PsychedelicResearch #CocaineCravings #Serotonin2A #DOI # addictionscience #drugrewards #neuroscience #behavioraleconomics #ratstudies #substanceabusetherapy
-
DATE: June 19, 2026 at 06:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Psychedelic compound reduces cocaine motivation and cravings in animal models
Recent laboratory research reveals that a chemical compound known for inducing psychedelic effects reduces the motivation to consume cocaine in animal models. The findings suggest that targeting specific serotonin receptors in the brain could offer a novel biological approach to treating stimulant use disorders. The study detailing these outcomes was published in the journal Psychopharmacology.
Cocaine use continues to present a massive public health challenge across the globe. Millions of individuals struggle with stimulant addiction every year, and overdose fatalities involving the drug have trended steadily upward over the past decade. Traditional medical interventions and behavioral therapies have largely struggled to help individuals maintain long-term abstinence. Cocaine produces its highly addictive profile by infiltrating and altering communication within the brain’s reward centers. It physically blocks the normal recycling process of dopamine, a chemical messenger heavily involved in anticipating and experiencing pleasure.
Normally, brain cells release dopamine to signal that something good has happened, and then quickly vacuum it back up to reset the system. By jamming this biological vacuum system, cocaine creates an unnatural flood of dopamine. This flooding occurs specifically within the meso-corticolimbic circuitry, a network of brain regions that governs how living creatures learn to seek out rewards and find the motivation to survive. Over time, this intense chemical stimulation fundamentally rewires the brain, making it increasingly difficult for a person to feel motivated by anything other than the drug.
While dopamine receives the vast majority of attention in addiction literature, cocaine also substantially increases the brain’s levels of serotonin. Serotonin is a separate chemical messenger best known for regulating mood, sleep, and sensory perception. Investigators at the University of Texas Medical Branch suspected that a specific cellular landing pad for serotonin, known as the serotonin 2A receptor, might help dictate the brain’s overriding addiction mechanics. Leah Salinsky and Christina Merritt led a research team to investigate whether activating this exact receptor could alter how much cocaine animals would willingly self-administer.
To test this hypothesis, the researchers used a laboratory compound named (-)-DOI. While not regularly encountered outside of research settings, (-)-DOI belongs to a broad class of drugs known as hallucinogens or psychedelics. Like classical psychedelics such as LSD and psilocybin, the compound produces its main behavioral effects by strongly binding to and activating the serotonin 2A receptor in the brain. Unlike those classical drugs, (-)-DOI is highly selective. It primarily interacts with this single receptor subtype without strongly stimulating the numerous other serotonin receptors scattered throughout the nervous system.
This extreme chemical precision makes the compound an ideal tool for scientists trying to isolate biological mechanisms. If a highly selective compound changes a specific behavior, researchers can be relatively confident that the target receptor is directly responsible for the shift. To ensure the validity of their tests, the team also utilized a second specialized chemical that acts as an antagonist. This second chemical acts like a cellular shield, sitting on the serotonin 2A receptor and preventing any other drugs from activating it.
The team began the experimental phase by training adult male rats to self-administer cocaine over several weeks. The animals were placed in specialized soundproof enclosures equipped with a small metal lever. When the rats pressed the lever a set number of times, a mechanized pump delivered a highly controlled amount of cocaine directly into their bloodstream. Once the rats learned this relationship and began pressing the lever at a highly consistent rate, the researchers introduced the psychedelic compound into the daily routine. They injected the rats with varying, controlled doses of (-)-DOI shortly before placing them back into the testing chambers.
The experimental results showed a steep decline in cocaine consumption after the rats received the psychedelic compound. Across all the tested doses, the animals pressed the active lever far fewer times and subsequently delivered much less cocaine to themselves compared to when they received a neutral saline solution. To ensure the rats were not simply too sedated to move, the researchers tracked how often the animals pressed a secondary dummy lever that provided no drug. The rate at which the rats pressed the inactive dummy lever remained completely unchanged. The animals also approached the active lever just as quickly as usual initially, indicating that their basic physical coordination and alertness were intact.
The researchers then completely verified the biological pathway. They conducted another round of testing where they treated the animals with the receptor-blocking agent prior to administering the highest dose of the psychedelic. When the rats received this blocking agent first, their rate of cocaine consumption rebounded. The blocking agent largely muted the suppressive effect of the psychedelic, establishing that the serotonin 2A receptor is the primary gateway through which the drug curtails immediate reward-seeking behavior.
For their next experiment, the researchers utilized a testing framework drawn from the principles of behavioral economics. This analytical approach measures a subject’s absolute motivation to obtain a reward by steadily increasing the physical effort required to get it. Humans experience this concept intuitively: someone might buy a cup of coffee every day if it costs two dollars, but they will likely stop buying it entirely if the price jumps to twenty dollars. In this rodent trial, the rats initially earned a large, satisfying dose of cocaine for just a few lever presses.
As the session progressed, the volume of cocaine delivered with each successful lever press steadily shrank at scheduled intervals. To maintain the same level of intoxication, the animals had to press the lever at intensely high, escalating rates. By the final block of the testing session, the rats had to expend an immense amount of physical effort to receive barely a fraction of the starting drug dosage. This procedure effectively estimates the absolute maximum price an animal is willing to pay before giving up completely.
This economic analysis tracks a metric known as demand elasticity, which describes just how sensitive a subject behaves when facing price hikes. The researchers found that the highest administered dose of the psychedelic compound left the rats dramatically more sensitive to the rising cost of the stimulant. When treated with the highest dose of (-)-DOI, the animals gave up much sooner as the required lever presses rapidly multiplied. Their overarching motivation to work for the stimulant eroded. The total overall amount of cocaine they managed to consume during the demanding session also dropped immensely compared to their untreated baseline behavior.
Just as in the simplest trials, administering the receptor-blocking agent before the psychedelic reversed these sweeping behavioral changes. The rats treated with the blocker returned to working incredibly hard for shrinking amounts of cocaine. This data confirmed again that turning on the serotonin 2A receptor specifically devalues the perceived, essential reward of the stimulant. The psychedelic essentially caused the cocaine to lose its overpowering appeal once the physical price of obtaining it became excessively high.
The investigators highlighted several basic boundaries to their current findings. The study exclusively observed male rats, creating a gap in understanding how female biology might alter or amplify these outcomes. Fluctuations in ovarian hormones are widely reported to influence how the brain responds to cocaine. Future laboratory trials must include female animal models to provide the complete biological picture required for medical science.
The research team also pointed out that their complex economic demand tests required delivering very high initial bursts of cocaine at the start of the session. The sheer volume of this early drug exposure might temporarily change how the entire serotonin system physically functions compared to continuous low-dose use. Future research efforts will need to test these psychedelic compounds against different ingestion patterns and observe if the effects hold steady. Scientists must also determine if activating these receptors specifically alters basic sensory perception during drug taking.
These laboratory findings arrive precisely as massive medical institutions are conducting early human trials using classical psychedelics for substance use issues. By pinpointing the exact cellular receptors that reduce drug consumption, researchers hope to guide the creation of highly specialized new medications. Ongoing medicinal chemistry projects are currently attempting to design novel drugs that can activate the serotonin 2A receptor to squelch cravings without causing the intense hallucinogenic side effects normally associated with psychedelics.
The study, “The psychedelic (−)‑2,5‑dimethoxy‑4‑iodoamphetamine [(−)‑DOI] demonstrates efficacy in reducing cocaine reward and motivation in male rats,” was authored by Leah M. Salinsky, Christina R. Merritt, Erik J. Garcia, Robert G. Fox, Joshua C. Zamora, Noelle C. Anastasio, and Kathryn A. Cunningham.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PsychedelicResearch #CocaineCravings #Serotonin2A #DOI # addictionscience #drugrewards #neuroscience #behavioraleconomics #ratstudies #substanceabusetherapy
-
DATE: June 19, 2026 at 06:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Psychedelic compound reduces cocaine motivation and cravings in animal models
Recent laboratory research reveals that a chemical compound known for inducing psychedelic effects reduces the motivation to consume cocaine in animal models. The findings suggest that targeting specific serotonin receptors in the brain could offer a novel biological approach to treating stimulant use disorders. The study detailing these outcomes was published in the journal Psychopharmacology.
Cocaine use continues to present a massive public health challenge across the globe. Millions of individuals struggle with stimulant addiction every year, and overdose fatalities involving the drug have trended steadily upward over the past decade. Traditional medical interventions and behavioral therapies have largely struggled to help individuals maintain long-term abstinence. Cocaine produces its highly addictive profile by infiltrating and altering communication within the brain’s reward centers. It physically blocks the normal recycling process of dopamine, a chemical messenger heavily involved in anticipating and experiencing pleasure.
Normally, brain cells release dopamine to signal that something good has happened, and then quickly vacuum it back up to reset the system. By jamming this biological vacuum system, cocaine creates an unnatural flood of dopamine. This flooding occurs specifically within the meso-corticolimbic circuitry, a network of brain regions that governs how living creatures learn to seek out rewards and find the motivation to survive. Over time, this intense chemical stimulation fundamentally rewires the brain, making it increasingly difficult for a person to feel motivated by anything other than the drug.
While dopamine receives the vast majority of attention in addiction literature, cocaine also substantially increases the brain’s levels of serotonin. Serotonin is a separate chemical messenger best known for regulating mood, sleep, and sensory perception. Investigators at the University of Texas Medical Branch suspected that a specific cellular landing pad for serotonin, known as the serotonin 2A receptor, might help dictate the brain’s overriding addiction mechanics. Leah Salinsky and Christina Merritt led a research team to investigate whether activating this exact receptor could alter how much cocaine animals would willingly self-administer.
To test this hypothesis, the researchers used a laboratory compound named (-)-DOI. While not regularly encountered outside of research settings, (-)-DOI belongs to a broad class of drugs known as hallucinogens or psychedelics. Like classical psychedelics such as LSD and psilocybin, the compound produces its main behavioral effects by strongly binding to and activating the serotonin 2A receptor in the brain. Unlike those classical drugs, (-)-DOI is highly selective. It primarily interacts with this single receptor subtype without strongly stimulating the numerous other serotonin receptors scattered throughout the nervous system.
This extreme chemical precision makes the compound an ideal tool for scientists trying to isolate biological mechanisms. If a highly selective compound changes a specific behavior, researchers can be relatively confident that the target receptor is directly responsible for the shift. To ensure the validity of their tests, the team also utilized a second specialized chemical that acts as an antagonist. This second chemical acts like a cellular shield, sitting on the serotonin 2A receptor and preventing any other drugs from activating it.
The team began the experimental phase by training adult male rats to self-administer cocaine over several weeks. The animals were placed in specialized soundproof enclosures equipped with a small metal lever. When the rats pressed the lever a set number of times, a mechanized pump delivered a highly controlled amount of cocaine directly into their bloodstream. Once the rats learned this relationship and began pressing the lever at a highly consistent rate, the researchers introduced the psychedelic compound into the daily routine. They injected the rats with varying, controlled doses of (-)-DOI shortly before placing them back into the testing chambers.
The experimental results showed a steep decline in cocaine consumption after the rats received the psychedelic compound. Across all the tested doses, the animals pressed the active lever far fewer times and subsequently delivered much less cocaine to themselves compared to when they received a neutral saline solution. To ensure the rats were not simply too sedated to move, the researchers tracked how often the animals pressed a secondary dummy lever that provided no drug. The rate at which the rats pressed the inactive dummy lever remained completely unchanged. The animals also approached the active lever just as quickly as usual initially, indicating that their basic physical coordination and alertness were intact.
The researchers then completely verified the biological pathway. They conducted another round of testing where they treated the animals with the receptor-blocking agent prior to administering the highest dose of the psychedelic. When the rats received this blocking agent first, their rate of cocaine consumption rebounded. The blocking agent largely muted the suppressive effect of the psychedelic, establishing that the serotonin 2A receptor is the primary gateway through which the drug curtails immediate reward-seeking behavior.
For their next experiment, the researchers utilized a testing framework drawn from the principles of behavioral economics. This analytical approach measures a subject’s absolute motivation to obtain a reward by steadily increasing the physical effort required to get it. Humans experience this concept intuitively: someone might buy a cup of coffee every day if it costs two dollars, but they will likely stop buying it entirely if the price jumps to twenty dollars. In this rodent trial, the rats initially earned a large, satisfying dose of cocaine for just a few lever presses.
As the session progressed, the volume of cocaine delivered with each successful lever press steadily shrank at scheduled intervals. To maintain the same level of intoxication, the animals had to press the lever at intensely high, escalating rates. By the final block of the testing session, the rats had to expend an immense amount of physical effort to receive barely a fraction of the starting drug dosage. This procedure effectively estimates the absolute maximum price an animal is willing to pay before giving up completely.
This economic analysis tracks a metric known as demand elasticity, which describes just how sensitive a subject behaves when facing price hikes. The researchers found that the highest administered dose of the psychedelic compound left the rats dramatically more sensitive to the rising cost of the stimulant. When treated with the highest dose of (-)-DOI, the animals gave up much sooner as the required lever presses rapidly multiplied. Their overarching motivation to work for the stimulant eroded. The total overall amount of cocaine they managed to consume during the demanding session also dropped immensely compared to their untreated baseline behavior.
Just as in the simplest trials, administering the receptor-blocking agent before the psychedelic reversed these sweeping behavioral changes. The rats treated with the blocker returned to working incredibly hard for shrinking amounts of cocaine. This data confirmed again that turning on the serotonin 2A receptor specifically devalues the perceived, essential reward of the stimulant. The psychedelic essentially caused the cocaine to lose its overpowering appeal once the physical price of obtaining it became excessively high.
The investigators highlighted several basic boundaries to their current findings. The study exclusively observed male rats, creating a gap in understanding how female biology might alter or amplify these outcomes. Fluctuations in ovarian hormones are widely reported to influence how the brain responds to cocaine. Future laboratory trials must include female animal models to provide the complete biological picture required for medical science.
The research team also pointed out that their complex economic demand tests required delivering very high initial bursts of cocaine at the start of the session. The sheer volume of this early drug exposure might temporarily change how the entire serotonin system physically functions compared to continuous low-dose use. Future research efforts will need to test these psychedelic compounds against different ingestion patterns and observe if the effects hold steady. Scientists must also determine if activating these receptors specifically alters basic sensory perception during drug taking.
These laboratory findings arrive precisely as massive medical institutions are conducting early human trials using classical psychedelics for substance use issues. By pinpointing the exact cellular receptors that reduce drug consumption, researchers hope to guide the creation of highly specialized new medications. Ongoing medicinal chemistry projects are currently attempting to design novel drugs that can activate the serotonin 2A receptor to squelch cravings without causing the intense hallucinogenic side effects normally associated with psychedelics.
The study, “The psychedelic (−)‑2,5‑dimethoxy‑4‑iodoamphetamine [(−)‑DOI] demonstrates efficacy in reducing cocaine reward and motivation in male rats,” was authored by Leah M. Salinsky, Christina R. Merritt, Erik J. Garcia, Robert G. Fox, Joshua C. Zamora, Noelle C. Anastasio, and Kathryn A. Cunningham.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PsychedelicResearch #CocaineCravings #Serotonin2A #DOI # addictionscience #drugrewards #neuroscience #behavioraleconomics #ratstudies #substanceabusetherapy
-
DATE: June 19, 2026 at 06:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Psychedelic compound reduces cocaine motivation and cravings in animal models
Recent laboratory research reveals that a chemical compound known for inducing psychedelic effects reduces the motivation to consume cocaine in animal models. The findings suggest that targeting specific serotonin receptors in the brain could offer a novel biological approach to treating stimulant use disorders. The study detailing these outcomes was published in the journal Psychopharmacology.
Cocaine use continues to present a massive public health challenge across the globe. Millions of individuals struggle with stimulant addiction every year, and overdose fatalities involving the drug have trended steadily upward over the past decade. Traditional medical interventions and behavioral therapies have largely struggled to help individuals maintain long-term abstinence. Cocaine produces its highly addictive profile by infiltrating and altering communication within the brain’s reward centers. It physically blocks the normal recycling process of dopamine, a chemical messenger heavily involved in anticipating and experiencing pleasure.
Normally, brain cells release dopamine to signal that something good has happened, and then quickly vacuum it back up to reset the system. By jamming this biological vacuum system, cocaine creates an unnatural flood of dopamine. This flooding occurs specifically within the meso-corticolimbic circuitry, a network of brain regions that governs how living creatures learn to seek out rewards and find the motivation to survive. Over time, this intense chemical stimulation fundamentally rewires the brain, making it increasingly difficult for a person to feel motivated by anything other than the drug.
While dopamine receives the vast majority of attention in addiction literature, cocaine also substantially increases the brain’s levels of serotonin. Serotonin is a separate chemical messenger best known for regulating mood, sleep, and sensory perception. Investigators at the University of Texas Medical Branch suspected that a specific cellular landing pad for serotonin, known as the serotonin 2A receptor, might help dictate the brain’s overriding addiction mechanics. Leah Salinsky and Christina Merritt led a research team to investigate whether activating this exact receptor could alter how much cocaine animals would willingly self-administer.
To test this hypothesis, the researchers used a laboratory compound named (-)-DOI. While not regularly encountered outside of research settings, (-)-DOI belongs to a broad class of drugs known as hallucinogens or psychedelics. Like classical psychedelics such as LSD and psilocybin, the compound produces its main behavioral effects by strongly binding to and activating the serotonin 2A receptor in the brain. Unlike those classical drugs, (-)-DOI is highly selective. It primarily interacts with this single receptor subtype without strongly stimulating the numerous other serotonin receptors scattered throughout the nervous system.
This extreme chemical precision makes the compound an ideal tool for scientists trying to isolate biological mechanisms. If a highly selective compound changes a specific behavior, researchers can be relatively confident that the target receptor is directly responsible for the shift. To ensure the validity of their tests, the team also utilized a second specialized chemical that acts as an antagonist. This second chemical acts like a cellular shield, sitting on the serotonin 2A receptor and preventing any other drugs from activating it.
The team began the experimental phase by training adult male rats to self-administer cocaine over several weeks. The animals were placed in specialized soundproof enclosures equipped with a small metal lever. When the rats pressed the lever a set number of times, a mechanized pump delivered a highly controlled amount of cocaine directly into their bloodstream. Once the rats learned this relationship and began pressing the lever at a highly consistent rate, the researchers introduced the psychedelic compound into the daily routine. They injected the rats with varying, controlled doses of (-)-DOI shortly before placing them back into the testing chambers.
The experimental results showed a steep decline in cocaine consumption after the rats received the psychedelic compound. Across all the tested doses, the animals pressed the active lever far fewer times and subsequently delivered much less cocaine to themselves compared to when they received a neutral saline solution. To ensure the rats were not simply too sedated to move, the researchers tracked how often the animals pressed a secondary dummy lever that provided no drug. The rate at which the rats pressed the inactive dummy lever remained completely unchanged. The animals also approached the active lever just as quickly as usual initially, indicating that their basic physical coordination and alertness were intact.
The researchers then completely verified the biological pathway. They conducted another round of testing where they treated the animals with the receptor-blocking agent prior to administering the highest dose of the psychedelic. When the rats received this blocking agent first, their rate of cocaine consumption rebounded. The blocking agent largely muted the suppressive effect of the psychedelic, establishing that the serotonin 2A receptor is the primary gateway through which the drug curtails immediate reward-seeking behavior.
For their next experiment, the researchers utilized a testing framework drawn from the principles of behavioral economics. This analytical approach measures a subject’s absolute motivation to obtain a reward by steadily increasing the physical effort required to get it. Humans experience this concept intuitively: someone might buy a cup of coffee every day if it costs two dollars, but they will likely stop buying it entirely if the price jumps to twenty dollars. In this rodent trial, the rats initially earned a large, satisfying dose of cocaine for just a few lever presses.
As the session progressed, the volume of cocaine delivered with each successful lever press steadily shrank at scheduled intervals. To maintain the same level of intoxication, the animals had to press the lever at intensely high, escalating rates. By the final block of the testing session, the rats had to expend an immense amount of physical effort to receive barely a fraction of the starting drug dosage. This procedure effectively estimates the absolute maximum price an animal is willing to pay before giving up completely.
This economic analysis tracks a metric known as demand elasticity, which describes just how sensitive a subject behaves when facing price hikes. The researchers found that the highest administered dose of the psychedelic compound left the rats dramatically more sensitive to the rising cost of the stimulant. When treated with the highest dose of (-)-DOI, the animals gave up much sooner as the required lever presses rapidly multiplied. Their overarching motivation to work for the stimulant eroded. The total overall amount of cocaine they managed to consume during the demanding session also dropped immensely compared to their untreated baseline behavior.
Just as in the simplest trials, administering the receptor-blocking agent before the psychedelic reversed these sweeping behavioral changes. The rats treated with the blocker returned to working incredibly hard for shrinking amounts of cocaine. This data confirmed again that turning on the serotonin 2A receptor specifically devalues the perceived, essential reward of the stimulant. The psychedelic essentially caused the cocaine to lose its overpowering appeal once the physical price of obtaining it became excessively high.
The investigators highlighted several basic boundaries to their current findings. The study exclusively observed male rats, creating a gap in understanding how female biology might alter or amplify these outcomes. Fluctuations in ovarian hormones are widely reported to influence how the brain responds to cocaine. Future laboratory trials must include female animal models to provide the complete biological picture required for medical science.
The research team also pointed out that their complex economic demand tests required delivering very high initial bursts of cocaine at the start of the session. The sheer volume of this early drug exposure might temporarily change how the entire serotonin system physically functions compared to continuous low-dose use. Future research efforts will need to test these psychedelic compounds against different ingestion patterns and observe if the effects hold steady. Scientists must also determine if activating these receptors specifically alters basic sensory perception during drug taking.
These laboratory findings arrive precisely as massive medical institutions are conducting early human trials using classical psychedelics for substance use issues. By pinpointing the exact cellular receptors that reduce drug consumption, researchers hope to guide the creation of highly specialized new medications. Ongoing medicinal chemistry projects are currently attempting to design novel drugs that can activate the serotonin 2A receptor to squelch cravings without causing the intense hallucinogenic side effects normally associated with psychedelics.
The study, “The psychedelic (−)‑2,5‑dimethoxy‑4‑iodoamphetamine [(−)‑DOI] demonstrates efficacy in reducing cocaine reward and motivation in male rats,” was authored by Leah M. Salinsky, Christina R. Merritt, Erik J. Garcia, Robert G. Fox, Joshua C. Zamora, Noelle C. Anastasio, and Kathryn A. Cunningham.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PsychedelicResearch #CocaineCravings #Serotonin2A #DOI # addictionscience #drugrewards #neuroscience #behavioraleconomics #ratstudies #substanceabusetherapy
-
Andrew Huberman has repeatedly emphasized that psychedelics interact with neuroplasticity and learning states.
We are aligned with this direction.
→ Heightened plasticity increases the importance of post-experience infrastructure, monitoring, and continuity systems.
#Psychedelics #Neuroscience #MentalHealth #PsychedelicResearch #Neuroplasticity #PublicHealth
-
Andrew Huberman has repeatedly emphasized that psychedelics interact with neuroplasticity and learning states.
We are aligned with this direction.
→ Heightened plasticity increases the importance of post-experience infrastructure, monitoring, and continuity systems.
#Psychedelics #Neuroscience #MentalHealth #PsychedelicResearch #Neuroplasticity #PublicHealth
-
Andrew Huberman has repeatedly emphasized that psychedelics interact with neuroplasticity and learning states.
We are aligned with this direction.
→ Heightened plasticity increases the importance of post-experience infrastructure, monitoring, and continuity systems.
#Psychedelics #Neuroscience #MentalHealth #PsychedelicResearch #Neuroplasticity #PublicHealth
-
Andrew Huberman has repeatedly emphasized that psychedelics interact with neuroplasticity and learning states.
We are aligned with this direction.
→ Heightened plasticity increases the importance of post-experience infrastructure, monitoring, and continuity systems.
#Psychedelics #Neuroscience #MentalHealth #PsychedelicResearch #Neuroplasticity #PublicHealth
-
Andrew Huberman has repeatedly emphasized that psychedelics interact with neuroplasticity and learning states.
We are aligned with this direction.
→ Heightened plasticity increases the importance of post-experience infrastructure, monitoring, and continuity systems.
#Psychedelics #Neuroscience #MentalHealth #PsychedelicResearch #Neuroplasticity #PublicHealth
-
#Psychedelic therapy assumed the hallucination was part of the mechanism.
UC Davis researchers created compounds that fully activate the same brain receptor as psychedelics - with zero hallucinogenic effects in animal tests.
Therapeutic benefit and the trip may operate through different pathways.A rare new molecular scaffold with implications for #depression, PTSD, and addiction treatment.
#Neuroscience #MentalHealth #PsychedelicResearch #Science
https://www.sciencedaily.com/releases/2026/05/260512202325.htm
-
#Psychedelic therapy assumed the hallucination was part of the mechanism.
UC Davis researchers created compounds that fully activate the same brain receptor as psychedelics - with zero hallucinogenic effects in animal tests.
Therapeutic benefit and the trip may operate through different pathways.A rare new molecular scaffold with implications for #depression, PTSD, and addiction treatment.
#Neuroscience #MentalHealth #PsychedelicResearch #Science
https://www.sciencedaily.com/releases/2026/05/260512202325.htm
-
#Psychedelic therapy assumed the hallucination was part of the mechanism.
UC Davis researchers created compounds that fully activate the same brain receptor as psychedelics - with zero hallucinogenic effects in animal tests.
Therapeutic benefit and the trip may operate through different pathways.A rare new molecular scaffold with implications for #depression, PTSD, and addiction treatment.
#Neuroscience #MentalHealth #PsychedelicResearch #Science
https://www.sciencedaily.com/releases/2026/05/260512202325.htm
-
#Psychedelic therapy assumed the hallucination was part of the mechanism.
UC Davis researchers created compounds that fully activate the same brain receptor as psychedelics - with zero hallucinogenic effects in animal tests.
Therapeutic benefit and the trip may operate through different pathways.A rare new molecular scaffold with implications for #depression, PTSD, and addiction treatment.
#Neuroscience #MentalHealth #PsychedelicResearch #Science
https://www.sciencedaily.com/releases/2026/05/260512202325.htm
-
#Psychedelic therapy assumed the hallucination was part of the mechanism.
UC Davis researchers created compounds that fully activate the same brain receptor as psychedelics - with zero hallucinogenic effects in animal tests.
Therapeutic benefit and the trip may operate through different pathways.A rare new molecular scaffold with implications for #depression, PTSD, and addiction treatment.
#Neuroscience #MentalHealth #PsychedelicResearch #Science
https://www.sciencedaily.com/releases/2026/05/260512202325.htm
-
Psychedelic Research Edges Toward Nuance, Moving Beyond Broad Strokes
New research shows low sensory changes from psychedelics like psilocybin may improve therapy for depression and PTSD. Learn how.
#PsychedelicResearch, #PsilocybinTherapy, #MentalHealth, #PTSD, #Depression
https://newsletter.tf/psychedelics-low-sensory-changes-therapy-outcomes/
-
Psychedelic Research Edges Toward Nuance, Moving Beyond Broad Strokes
New research shows low sensory changes from psychedelics like psilocybin may improve therapy for depression and PTSD. Learn how.
#PsychedelicResearch, #PsilocybinTherapy, #MentalHealth, #PTSD, #Depression
https://newsletter.tf/psychedelics-low-sensory-changes-therapy-outcomes/
-
Psychedelic Research Edges Toward Nuance, Moving Beyond Broad Strokes
New research shows low sensory changes from psychedelics like psilocybin may improve therapy for depression and PTSD. Learn how.
#PsychedelicResearch, #PsilocybinTherapy, #MentalHealth, #PTSD, #Depression
https://newsletter.tf/psychedelics-low-sensory-changes-therapy-outcomes/
-
Psychedelic Research Edges Toward Nuance, Moving Beyond Broad Strokes
New research shows low sensory changes from psychedelics like psilocybin may improve therapy for depression and PTSD. Learn how.
#PsychedelicResearch, #PsilocybinTherapy, #MentalHealth, #PTSD, #Depression
https://newsletter.tf/psychedelics-low-sensory-changes-therapy-outcomes/
-
Scientists now believe small sensory changes from psychedelics are key to therapy, not just side effects. This is a big shift from older ideas.
#PsychedelicResearch, #PsilocybinTherapy, #MentalHealth, #PTSD, #Depression
https://newsletter.tf/psychedelics-low-sensory-changes-therapy-outcomes/ -
Scientists now believe small sensory changes from psychedelics are key to therapy, not just side effects. This is a big shift from older ideas.
#PsychedelicResearch, #PsilocybinTherapy, #MentalHealth, #PTSD, #Depression
https://newsletter.tf/psychedelics-low-sensory-changes-therapy-outcomes/ -
Scientists now believe small sensory changes from psychedelics are key to therapy, not just side effects. This is a big shift from older ideas.
#PsychedelicResearch, #PsilocybinTherapy, #MentalHealth, #PTSD, #Depression
https://newsletter.tf/psychedelics-low-sensory-changes-therapy-outcomes/ -
Scientists now believe small sensory changes from psychedelics are key to therapy, not just side effects. This is a big shift from older ideas.
#PsychedelicResearch, #PsilocybinTherapy, #MentalHealth, #PTSD, #Depression
https://newsletter.tf/psychedelics-low-sensory-changes-therapy-outcomes/ -
TEXT MESSAGE SHAKES UP DRUG POLICY LANDSCAPE
President Trump signed an order to speed up research on psychedelic drugs after a text from Joe Rogan. Find out how this affects medical trials.
#PsychedelicResearch, #JoeRogan, #DonaldTrump, #DrugPolicy, #Ibogaine
https://newsletter.tf/rogan-text-trump-psychedelic-drug-research-order/
-
President Trump signed an executive order to speed up research on psychedelic drugs. This is a major policy change following a text message from Joe Rogan.
#PsychedelicResearch, #JoeRogan, #DonaldTrump, #DrugPolicy, #Ibogaine
https://newsletter.tf/rogan-text-trump-psychedelic-drug-research-order/ -
They served us. Now we serve them. Veterans and first responders deserve every tool available for mental health— including safe, research-backed psychedelic therapy. It’s time to move from stigma to solutions. 🇺🇸 #Veterans #FirstResponders #MentalHealth #PsychedelicResearch #PTSD #EndTheStigma
-
They served us. Now we serve them. Veterans and first responders deserve every tool available for mental health— including safe, research-backed psychedelic therapy. It’s time to move from stigma to solutions. 🇺🇸 #Veterans #FirstResponders #MentalHealth #PsychedelicResearch #PTSD #EndTheStigma
-
"A rigorous new study finds that a single dose of LSD can ease anxiety and depression for months.... #mentalhealth #anxiety #PsychedelicSunday #neuroskyence #saludmental #paychopharmacology #neuropsychiatry #psychedelictherapy #anxietyrelief #psychedelicresearch
'One and done' dose of LSD kee... -
"A rigorous new study finds that a single dose of LSD can ease anxiety and depression for months.... #mentalhealth #anxiety #PsychedelicSunday #neuroskyence #saludmental #paychopharmacology #neuropsychiatry #psychedelictherapy #anxietyrelief #psychedelicresearch
'One and done' dose of LSD kee... -
https://psychiatryonline.org/doi/10.1176/appi.ajp.20230785 Healing, Harms, and Humility: Expanding the Scope of Psychedelic-Assisted Psychotherapy Research (O’Donnell, et al 2025) #psychedelic #psychedelics #psychedelicassistedpsychotherapy #psychedelicassistedtherapy #psychedelicresearch #mentalhealth #psychedelicmentalhealth
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https://pubmed.ncbi.nlm.nih.gov/39720814/ General Anesthesia Occludes Ketamine's Antidepressant Response in a Rodent Model of Chronic Stress (Markman, et al, 2024) #ketamine #psychedelic #neuroscience #psychedelics #depression #mentalhealth #psychedelicresearch #psychedelicmentalhealth
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https://www.sciencedirect.com/science/article/abs/pii/S0165178124005584?via%3Dihub Association of intravenous ketamine with change in depressive symptoms in a large integrated health care system (Li, et al, 2025) #ketamine #mentalhealth #depression #ketaminetherapy #psychedelic #psychedelics #psychedelicmentalhealth #psychedelicresearch
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https://pubmed.ncbi.nlm.nih.gov/39688236/ Is there a risk of addiction to ketamine during the treatment of depression? A systematic review of available literature (Ingrosso, et al, 2024) #ketamine #addiction #psychedelic #psychedelics #mentalhealth #recovery #psychedelicresearch #depression #psychedelicmentalhealth #ketaminetherapy #ketamineassistedpsychotherapy
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https://psychedelicmentalhealth.net/spotlight-smart-recovery-psychedelic-assisted-psychotherapy/ #psychedelics #ketamine #mentalhealth #psychedelicmentalhealth #recovery #cognitivebehavioraltherapy #neuroscience #psychedelictherapy #psychedelicassistedtherapy #psychedelicassistedpsychotherapy #ketaminetherapy #ketamineassistedpsychotherapy #psychedelicresearch #smartrecovery
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https://www.eurekalert.org/news-releases/1066594 Scientists map how ayahuasca affects fear circuits in comprehensive review #ayahausca #plantmedicine #psychedelics #psychedelic #psychedelicresearch #psychedelicmentalhealth
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https://pubmed.ncbi.nlm.nih.gov/39608192/ Association of intravenous ketamine with change in depressive symptoms in a large integrated health care system (Li, et al, 2024) #ketamine #psychedelic #psychedelics #mentalhealth #psychedelicresearch #psychedelicmentalhealth #ketaminetherapy
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Ketamine treats depression better than other meds. Researchers finally know why https://www.msn.com/en-us/health/other/ketamine-treats-depression-better-than-other-meds-researchers-finally-know-why/ar-AA1utfOx #ketamine #mentalhealth #depression #psychedelicmentalhealth #psychedelic #psychedelics #neuroscience #psychedelicresearch
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Changes in dysfunctional attitudes linked to improved wellbeing after psychedelic use https://flip.it/q1HWlY #ketamine #psychedelic #psychedelics #mentalhealth #psychedelicresearch #psychedelicmentalhealth #neuroscience #thepsychedelicexperience
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https://www.nature.com/articles/s41380-024-02729-9 Allosteric inhibition of NMDA receptors by low dose ketamine (Abbot, et al, 2024) #ketamine #depression #psychedelic #psychedelics #neuroscience #psychedelicmentalhealth #psychedelicresearch
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https://www.nature.com/articles/s41380-024-02419-6 (R)-ketamine restores anterior insular cortex activity and cognitive deficits in social isolation-reared mice (Yokohama, et al, 2024) Arketamine is part of racemic ketamine along with esketamine. Spravato is esketamine only, one half of the racemic ketamine molecule. #arketamine #ketamine #psychedelic #psychedelics #psychedelicresearch #socialisolation #neuroscience #mentalhealth #cognition
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https://pubmed.ncbi.nlm.nih.gov/38981574/ Shared effects of electroconvulsive shocks and ketamine on neuroplasticity: A Systematic Review of Animal Models of Depression (De Jager, et al, 2024) #ketamine #neuroplasticity #brains #electroshock #depression #neurogenesis #bdnf #brains #neuroscience #psychedelic #psychedelics #psychedelicresearch #fda #ketaminetherapy #psychedelictherapy