#neuroinflammation — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #neuroinflammation, aggregated by home.social.
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DATE: August 31, 2026 at 07:00AM
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: Researchers discover preventative immune benefits of a little-known psychedelic compound
URL: https://www.psypost.org/a-psychedelic-compound-primes-the-mouse-brain-to-resist-severe-inflammation/
A small study in mice suggests that administering a psychedelic compound before an immune system challenge can prevent brain inflammation and associated behavioral changes. The findings, published in the journal BMC Neuroscience, hint that these drugs might prime the nervous system to resist future damage.
Neuroinflammation is a biological response where the body’s immune system activates within the brain or spinal cord. While short-term inflammation helps eliminate infections, long-term or excessive immune activity can damage brain tissue. The brain is usually protected from the body’s general immune responses by a specialized cellular boundary. When severe physical stress or infection occurs, signaling molecules can breach this boundary, causing specialized brain cells to initiate a localized immune response.
When the immune system activates, cells release signaling proteins called cytokines. Some cytokines promote inflammation to attack pathogens, while others suppress inflammation to help the body heal. An imbalance leaning toward pro-inflammatory cytokines can disrupt brain circuits and alter an animal’s mood or behavior. This excessive response is a common biological feature in many brain conditions, from Alzheimer’s disease to severe depression.
Psychedelic drugs have gained attention for their ability to treat certain psychiatric conditions, but researchers are also investigating their physical effects on the brain. Many classical psychedelics bind to a specific protein on the surface of brain cells called the serotonin 5-HT2A receptor. Activating this receptor alters perception, but it also appears to influence how immune cells respond to stress. Researchers Michael Fiorillo and Javier González-Maeso of the Virginia Commonwealth University School of Medicine wanted to see if these immune-altering effects could work preventatively.
The researchers began by mapping how the mouse immune system reacts to a specific chemical trigger. They injected a small group of mice with lipopolysaccharide, a molecule found on the outer shell of bacteria. This molecule reliably provokes a strong immune reaction without causing an actual bacterial infection. Following the injection, the team measured chemical markers in the hippocampus, a brain region involved in memory and emotion.
They found that levels of pro-inflammatory cytokines peaked four hours after the injection. Specifically, the proteins interleukin-6 and tumor necrosis factor alpha reached their highest concentrations at this time. This four-hour mark became the target window for evaluating the effects of the psychedelic drug.
In a separate test, the team gave healthy mice varying doses of a psychedelic compound known as DOI. This laboratory chemical activates the same serotonin receptors as drugs like LSD and psilocybin. When they measured brain tissue 24 hours later, they found that DOI alone did not change baseline cytokine levels. The drug did not cause an immune reaction on its own.
Next, the researchers designed an experiment to test DOI as a preventative measure. They injected wild-type mice with either a low or high dose of the psychedelic compound. After waiting 24 hours, they administered the bacterial molecule to trigger systemic inflammation. Four hours after that, they measured cytokine levels in the hippocampus.
Mice that received the low dose of DOI before the immune challenge showed lower levels of interleukin-6 and tumor necrosis factor alpha. Their immune response was notably muted compared to mice that did not receive the psychedelic. The higher dose of the drug did not effectively reduce the inflammatory response, a phenomenon that sometimes occurs when cellular receptors become overwhelmed and shut down.
The team then wanted to know if this protective effect relied entirely on the serotonin 5-HT2A receptor. They repeated the prevention experiment using genetically modified mice that were bred without this specific receptor. In these modified animals, the low dose of DOI failed to prevent the spike in interleukin-6. This outcome indicates that the drug requires the 5-HT2A receptor to suppress this specific inflammatory protein.
However, the drug still successfully reduced levels of tumor necrosis factor alpha in the genetically modified mice. This suggests the psychedelic also interacts with other physiological pathways or different serotonin receptors to manage separate parts of the immune response. The researchers also observed that the modified mice experienced a much stronger overall inflammatory response to the bacterial molecule than unmodified mice. Natural serotonin activity at this receptor normally acts as a biological brake to keep the immune system from overreacting.
To see if the chemical changes in the brain translated to physical actions, the team ran a series of behavioral tests. They placed the mice in an open enclosure monitored by infrared beams to measure general movement and exploration. The bacterial molecule normally causes mice to move less, mimicking the physical lethargy people feel when they are sick.
Pretreating the mice with the low dose of DOI prevented this lethargy. The pretreated animals maintained normal movement levels despite the immune challenge. The team also evaluated the mice using a swimming test that measures passive coping, a behavior often compared to human depression. Mice that received the bacterial molecule spent more time floating passively instead of actively swimming.
Animals given the low dose of DOI beforehand remained active and spent less time floating. The researchers also tracked the animals’ body weight over a single week. The immune challenge typically causes severe weight loss, but the psychedelic treatment lessened this physical toll. The pretreated mice recovered their normal weight faster than the untreated control group.
Finally, the researchers looked for links between the chemical markers in the brain and the animals’ physical behavior. They found that higher levels of the inflammatory cytokine interleukin-6 matched up with increased passive behavior in the swimming test. Conversely, higher levels of two other cytokines associated with cellular healing aligned with more active swimming. This chemical shift points toward a more resilient biological state.
While these results offer a look at how psychedelics might shield the brain, the research relied on a single strong immune trigger. This acute response does not fully capture the persistent, low-grade inflammation seen in human neurodegenerative and psychiatric diseases. Additionally, the study evaluated whole sections of the hippocampus rather than looking at individual cell types. It remains unknown exactly which immune or nervous system cells are actually suppressing the inflammation.
The bacterial molecule and the drug were injected into the animals’ bodies rather than directly into the brain. It is possible that the psychedelic suppressed the immune response in the bloodstream first, which then reduced the secondary inflammation in the brain. The genetically modified mice used in the study lacked the serotonin receptor for their entire lives, which might have caused developmental changes that independently altered their baseline immune system.
All the experiments were conducted using male mice. Future research will need to include female animals to determine if these preventative immune effects apply equally across sexes. Scientists also need to test other psychedelic compounds to see if they offer similar protective benefits.
The study, “Pretreatment with the psychedelic DOI mitigates LPS-induced hippocampal inflammation and behavioral impairments in mice,” was authored by Michael Fiorillo and Javier González-Maeso.
URL: https://www.psypost.org/a-psychedelic-compound-primes-the-mouse-brain-to-resist-severe-inflammation/
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PsychedelicsAndImmuneHealth #DOIPrevention #5HT2AReceptor #Neuroinflammation #HippocampusProtection #LPSInflammation #Cytokines #NeuropsychiatricResearch #MiceStudy #BrainImmuneInteraction
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DATE: August 31, 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: Blood markers reveal two separate inflammatory pathways driving Alzheimer’s disease
Alzheimer’s disease is traditionally characterized by the buildup of amyloid plaques and tau protein tangles, but brain inflammation appears to play an early role in this process. A new study provides evidence that two separate inflammatory proteins in the blood signal two distinct paths of brain damage, both of which eventually lead to memory problems. The findings were published in Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring.
Alzheimer’s disease involves a complex interplay of biological events that begin long before memory loss becomes noticeable. Researchers suspect that brain inflammation acts as an early trigger in this disease process, rather than just a reaction to it. A study covered by PsyPost in 2025 indicated that markers of brain inflammation increase years before symptoms appear, right alongside the initial formation of amyloid plaques.
Building on this timeline, a 2021 cross-sectional study found that measuring an inflammatory protein called GFAP in the blood can reliably detect early amyloid accumulation in the brain before cognitive issues arise. Similarly, a 2021 study of cognitively unimpaired and impaired adults found that blood levels of GFAP specifically reflect amyloid plaque buildup rather than tau protein tangles.
The new study builds on this progression by exploring how GFAP and a second inflammatory marker, YKL-40, fit into a larger sequence of biological events.
“There is growing evidence that inflammation and the brain’s immune response play an important role in Alzheimer’s disease, potentially well before symptoms emerge. But the literature has been somewhat inconsistent,” said study co-authors Michael A. Yassa and Batool Rizvi. Yassa is a professor of neurobiology and behavior, the James L. McGaugh Endowed Chair, and director of the Center for the Neurobiology of Learning and Memory at the University of California, Irvine; Rizvi is a postdoctoral scholar in the Department of Public Health Sciences at the University of California, Davis.
“That made us wonder whether we were trying to fit several different biological processes into a single pathway,” the researchers added. “We hypothesized that different forms of neuroinflammatory activity might be associated with different aspects of disease.”
To map these intersecting biological pathways, the team—whose work is detailed on the Yassa Lab website—recruited 126 older adults from the local community. The participants had an average age of 70 and were cognitively unimpaired, meaning they showed no signs of dementia or mild cognitive impairment and performed normally on standard memory tests.
To assess the participants’ brain health, the scientists collected a variety of medical data. They drew blood to measure the levels of three specific proteins: YKL-40 and GFAP, which are markers of nervous system inflammation, and p-tau217, a marker of tau protein tangles. The participants also underwent two types of brain scans. Magnetic resonance imaging (MRI) was used to measure the volume of the hippocampus and the thickness of the medial temporal lobe, brain regions essential for memory.
The MRI scans also allowed the team to quantify white matter hyperintensities. These are bright spots on a brain scan that indicate small blood vessel disease and structural damage in the brain’s white matter. Additionally, positron emission tomography (PET) scans were used to measure the accumulation of amyloid beta plaques in the brain.
Finally, the participants completed a series of neuropsychological assessments, including the Rey Auditory Verbal Learning Test. This test measures a person’s ability to learn a list of words and remember them after a delay or after being exposed to distracting information. The researchers specifically focused on a measure of memory called retroactive interference, which shows how well a person can retain original information when new information is introduced.
To make sense of all these measurements, the team used a statistical technique called structural equation modeling. This approach allows scientists to test proposed chains of cause and effect by examining how multiple variables interact simultaneously.
The modeling revealed two separate pathways linking inflammation to brain damage. First, higher levels of the inflammatory protein YKL-40 in the blood were associated with more white matter damage in the brain. However, YKL-40 levels did not relate to amyloid plaque buildup.
Second, higher levels of the inflammatory protein GFAP were associated with increased amyloid plaque buildup. But unlike YKL-40, GFAP levels did not relate to white matter damage. This provides evidence that YKL-40 and GFAP represent two parallel, independent tracks of neuroinflammation, one tied to blood vessel damage and the other tied to Alzheimer’s-related plaque.
“What surprised us was how clearly the two inflammatory markers separated,” the researchers noted. “That suggests that calling something simply ‘neuroinflammation’ may obscure important biological differences. Different inflammatory or glial responses may be associated with different aspects of Alzheimer’s disease and brain aging.” This refers to reactions from glial cells, which are non-neuronal cells that support and protect the brain.
Despite their separate tracks, both white matter damage and amyloid plaque accumulation independently linked to higher blood levels of p-tau217. In other words, both vascular damage and amyloid pathology appear to converge, promoting the accumulation of toxic tau tangles.
Following this point of convergence, the pathway led directly to structural brain changes and cognitive deficits. Higher levels of p-tau217 were associated with a thinner medial temporal lobe cortex and a smaller hippocampal volume. In turn, a smaller hippocampus was associated with worse memory performance on the word-recall test.
“So rather than seeing Alzheimer’s disease as a single chain of events, our findings suggest that several biological processes may be occurring in parallel and ultimately contributing to the same downstream brain changes,” the authors said.
The results align with research covered by PsyPost in 2026, which indicated that elevated blood levels of tau and hippocampal shrinkage are tied to memory impairment in older adults without dementia. One difference in measurement is that the earlier study tracked memory decline trajectories over several years, whereas the new study modeled a single cross-sectional snapshot in time that included markers of brain inflammation.
The new findings are also consistent with a study covered by PsyPost in 2024, which found that tau accumulation and hippocampal shrinkage relate to cognitive decline even in individuals with low levels of amyloid plaque. Together, these studies suggest that tau and brain shrinkage are predictors of memory issues, regardless of which initial pathway triggered the damage.
As with all research, there are some caveats. The study relied on observational data collected at a single point in time, which restricts the ability to confirm a strict cause-and-effect sequence among the biological markers. “The most important limitation is that this was a cross-sectional study, meaning that the biomarkers were measured at approximately the same stage rather than tracked over many years,” the researchers explained. “Our statistical model allowed us to test a biologically motivated sequence of relationships, but it cannot establish that one biomarker caused the next or prove the order in which these changes occur.”
Another limitation is that blood-based markers of brain inflammation can sometimes reflect systemic inflammation from other parts of the body. Furthermore, the researchers noted that the participant sample lacked diversity. “The study also involved a relatively modest sample of cognitively unimpaired older adults recruited from a single research cohort, and the participants were predominantly White,” they said. “That limits how broadly we can generalize the findings.”
Future research will need to track individuals over many years to verify the temporal sequence of these two inflammatory pathways. “If YKL-40 and GFAP are identifying different biological processes, we want to know when each process begins, how it changes as Alzheimer’s pathology develops, and whether it predicts who is most likely to experience subsequent neurodegeneration or cognitive decline,” the authors explained.
The researchers hope to eventually use combinations of blood biomarkers and brain scans to identify distinct biological profiles of Alzheimer’s risk. “The broader point is that Alzheimer’s disease is biologically heterogeneous,” they noted. “Our findings suggest that two people could potentially arrive at similar downstream signs of Alzheimer’s disease through somewhat different combinations of biological processes.”
Because different pathways may be active in different individuals, a single intervention might not work for everyone. “Identifying distinct biological pathways is an important step toward eventually developing a more individualized approach to prevention and treatment,” the researchers concluded.
The study, “Parallel neuroinflammatory pathways to cerebrovascular burden and amyloid beta in Alzheimer’s disease,” was authored by Batool Rizvi, Jenna N. Adams, Alison Bamford, Soyun Kim, Mithra Sathishkumar, Nicholas J. Tustison, Lisa Taylor, Nandita Tuteja, Liv McMillan, Bin Nan, Hengrui Cai, Yuritza Y. Escalante, Novelle J. Meza, Alyssa L. Harris, Rond Malhas, Adam M. Brickman, Mark Mapstone, Elizabeth A. Thomas, and Michael A. Yassa.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AlzheimersDisease #neuroinflammation #GFAP #YKL40 #pTau217 #blood biomarkers #white matter damage #amyloid plaques #cognitivedecline # brainhealth
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DATE: August 21, 2026 at 12:00PM
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: Caffeine might ease anxiety and depression by calming brain inflammation
Caffeine appears to alleviate symptoms of anxiety and depression in rodents by reducing inflammation in the brain. A recent systematic review of 17 animal studies found that the widely consumed stimulant consistently diminished behavioral signs of distress and lowered levels of inflammatory molecules. The findings were published in Translational Psychiatry.
Mental health conditions like anxiety and depression involve physical changes in the nervous system. Over the past few decades, researchers have identified neuroinflammation as a major contributor to these mood disorders. When the body experiences chronic psychological stress or illness, the immune system often responds by releasing proteins called cytokines.
These cytokines travel to the brain and activate specialized immune cells known as microglia and astrocytes. Once activated, these glial cells can disrupt the normal balance of neurotransmitters like dopamine and serotonin. This inflammatory process can trigger behaviors associated with mood disorders, such as a loss of motivation or heightened fear responses.
Caffeine is a psychoactive substance that primarily works by blocking adenosine receptors in the brain. Adenosine is a chemical that naturally accumulates during the day, binding to specific receptors to promote sleepiness. By blocking these receptors, caffeine keeps the brain alert.
Adenosine receptors are not just involved in wakefulness. A specific subtype, called the A2A receptor, is prominently featured on the surface of microglia and astrocytes. Prolonged stress can cause an overabundance of these A2A receptors, which makes the brain’s immune cells highly sensitive and prone to causing inflammation.
Because caffeine blocks these A2A receptors, scientists suspect it might act as a brake on the brain’s inflammatory response. Neurobiologists Laís da Silva Neves and Paula Campello-Costa at the Fluminense Federal University in Brazil wanted to synthesize the existing data on this topic. Along with their colleagues, they set out to analyze how caffeine influences both brain inflammation and behavior in animal models.
The research team conducted a systematic review, a process that involves collecting and evaluating all the published scientific literature on a specific research question. They combed through online databases and identified 17 rodent studies that met their strict inclusion criteria. Every selected study featured a control group to allow for objective comparisons.
The team first looked at six studies focusing on anxiety. In these experiments, researchers induced anxiety in adult rats through various stressful scenarios. These included acute stressors, like a brief period of sleep deprivation or exposure to the scent of a predator, as well as chronic stressors, such as repeated physical restraint.
During or after these stressful events, the rodents received caffeine. The method of administration varied by study. Some animals received the substance through their drinking water, while others were given direct injections or fed through a gastric tube.
Scientists then measured the animals’ anxiety levels using established behavioral tests. A common method involves placing the rodent in an elevated, cross-shaped maze with both open and enclosed arms. Anxious animals will generally hide in the dark, enclosed arms, while less anxious animals will spend more time exploring the exposed sections.
Neves, Campello-Costa, and their team noted that caffeine consistently promoted exploratory behaviors, indicating a reduction in anxiety. This behavioral shift was accompanied by distinct physical changes in the animals’ brains. The rodents treated with caffeine exhibited lower levels of oxidative stress, a type of cellular damage associated with psychological strain.
Brain tissue analysis also revealed a drop in several pro-inflammatory cytokines, including interleukin-6 and tumor necrosis factor-alpha. At the same time, the caffeine-treated animals showed increased levels of anti-inflammatory molecules. The substance effectively prevented the microglia and astrocytes from entering a highly reactive, damaging state.
The remaining eleven studies in the review focused on animal models of depression. To mimic the biological mechanisms of depression, researchers in several of these studies injected the mice or rats with lipopolysaccharide. This molecule is a structural component of bacterial cell walls, and injecting it tricks the animal’s immune system into launching a massive, body-wide inflammatory response.
Other depression models utilized chronic unpredictable mild stress or long-term sleep deprivation. To assess whether the animals had entered a depressive-like state, researchers used tests that measure motivation and the capacity to experience pleasure. For example, they tracked whether the rodents lost interest in drinking sweetened water, a behavior that mirrors the loss of pleasure seen in human depression.
Across the different models, caffeine administration protected the rodents from developing these depressive-like behaviors. The animals maintained their motivation in physical tests and continued to seek out rewards like sugar water. In some of the studies, caffeine performed just as well as standard antidepressant medications like imipramine.
When examining the biological data from these depression models, the reviewers found a similar pattern to the anxiety studies. Caffeine reversed the chemical changes induced by the bacterial components or the chronic stress. The treated rodents displayed higher levels of protective antioxidant enzymes and fewer inflammatory markers in regions of the brain associated with memory and emotion.
A few of the evaluated studies also tested substances closely related to caffeine, such as caffeic acid and green tea extract. These compounds provided similar mood-boosting and anti-inflammatory benefits. Some research even suggested that standard caffeinated coffee and decaffeinated coffee both lowered inflammation, though the behavioral benefits were sometimes tied strictly to the caffeine.
While the review points to a robust anti-inflammatory effect, translating these findings to humans requires caution. Animal models can replicate specific neurochemical mechanisms, but they cannot capture the subjective, conscious experience of human anxiety or depression. The behavioral tests only act as proxies for actual mood disorders.
Almost all the studies in this review used adult male rodents. This uniformity makes the data easier to pool and compare, but it leaves a major gap in the scientific literature. It remains unknown if caffeine produces the exact same neuroinflammatory responses in female rodents or in animals at different developmental stages, such as adolescents or the elderly.
The amount of caffeine administered in these experiments also varied widely. Some doses were relatively low, mimicking the concentration a human might get from a standard cup of coffee. Other studies used extremely high doses that would be toxic to humans.
One study in the review actually demonstrated that a massive dose of caffeine worsened anxiety and increased brain inflammation in sleep-deprived rats. High doses of stimulants are known to trigger panic and hyperactivity in both humans and animals. Future research will need to determine the exact doses and consumption habits required to safely harness caffeine’s anti-inflammatory properties for mental health treatments.
The study, “Effects of caffeine on neuroinflammation in anxiety and depression: a systematic review of rodent studies,” was authored by Laís da Silva Neves, Giovanna Várzea Roberti Monteiro de Mattos, Yasmin Oliveira-Nazareth, Rosane Souza da Silva, and Paula Campello-Costa.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #CaffeineForMentalHealth #Neuroinflammation #AnxietyAndDepression #MicrogliaAstrocytes #A2AR #InflammationAndMood #RodentStudyInsights #CaffeineBenefits #MentalHealthResearch #TranslationalPsychiatry
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DATE: August 14, 2026 at 09:28AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Immune cells flood into the aging brain, Stanford scientists discover
URL: https://www.sciencedaily.com/releases/2026/08/260814011033.htm
Scientists have discovered that the aging human brain may be far less isolated from the rest of the body than once believed. Stanford researchers found that large numbers of immune cells from the blood begin entering the brain as early as middle age, where they can transform into microglia, the brain’s specialized immune cells. The finding overturns a long-standing assumption that these cells remain largely separate from the body’s immune system throughout life.
URL: https://www.sciencedaily.com/releases/2026/08/260814011033.htm
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AgingBrain #ImmuneCells #Microglia #StanfordResearch #Neuroscience #BrainHealth #Immunology #MiddleAge #Neuroinflammation # BrainBodyConnection
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A Courier Service for the Brain: Nanovesicles Silence METTL3 to Cool Neuroinflammation
Stay curious — follow @1ban_news.
https://1ban.news/mettl3-nanovesicles-neuroinflammation/
#1ban #mettl3 #nanovesicles #neuroinflammation #science #research
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Tiziana Life Sciences reports reductions in brain inflammation in third MSA patient | Yahoo!Finance
31 July 2026
https://finance.yahoo.com/healthcare/articles/tiziana-life-sciences-reports-reductions-125500680.html"Intranasal foralumab is a fully human anti-CD3 monoclonal antibody designed to modulate the immune system through mucosal tolerance mechanisms while aiming to reduce inflammation without the systemic toxicities associated with traditional anti-CD3 therapies."
#MultipleSystemAtrophy #neuroinflammation #immunology #neurology #neuroscience
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Study in mice suggests CBD may reduce brain inflammation linked to Alzheimer’s disease
📰 Original title: CBD may slow Alzheimer’s by calming the brain’s immune system
🤖 IA: It's not clickbait ✅
👥 Users: It's not clickbait ✅ -
However: The paper/comment does not point to one magic compound, but to a mixture of #caffeine, #catechins, #flavonoids, #theaflavins, #GABA and #tea #polysaccharides. The proposed links are lower oxidative stress and #inflammation, improved endothelial and glucose/insulin function, gut microbiome effects, and possibly reduced #neuroinflammation. …
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🧠 Alzheimer Microglia — Jan 2026
• Distinct microglial states emerge with disease-specific gene programs
• TREM2 and metabolic wiring shape microglial function in AD
• Environmental and infectious signals modulate neuroinflammation
• Exosomes, miRNAs, and Aβ disaggregation explored as therapeutic angles -
Aspirin and N-acetylcysteine co-administration markedly inhibit chronic ethanol intake and block relapse binge drinking: Role of neuroinflammation-oxidative stress self-perpetuation [2019]
https://pubmed.ncbi.nlm.nih.gov/31733014/link to full text:
https://repositorio.udd.cl/server/api/core/bitstreams/19b18abc-323a-4be6-9fa9-b084fa5ec1ab/content~
Female only study ('Adult female rats, Wistar-derived, bred for over 90 generations as alcohol consumers').#neuroinflammation #glutamate #AlcoholUseDisorder #NAC #aspirin
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Repetitive transcranial magnetic stimulation alleviates glial activation through suppressing HMGB1/TLR4 pathway in a rat model of Parkinson’s disease [2023]
https://doi.org/10.1007/s11033-023-08561-8"This study showed that rTMS might be a promising method for alleviating neuroinflammation in PD rat models, and the effects might be mediated through the downregulation of the HMGB1/TLR4 pathway."
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.. promise in modulating numerous processes associated with #neurodegenerativediseases, #cancer, #epilepsy, and #traumaticbraininjury [Table 1]. In addition, the #ECS is known to influence #neuroplasticity, #apoptosis, #excitotoxicity, #neuroinflammation, and #cerebrovascularbreakdown associated with #stroke and #trauma.[105]
https://pmc.ncbi.nlm.nih.gov/articles/PMC5938896/
#WEEDMoB #Hanfgeschichten #hanf #hemp #marijuana
#Streeck 🙏 #NinaWarken 🙏
Herr #Merz #Söder #Klingbeil 😀 #Cannabis -
Myeloid cells drive #neuroinflammation in #MultipleSclerosis by promoting immune activation in the #CentralNervousSystem. This study identifies SLAMF5 as a key myeloid receptor that regulates this process, showing that its blockade reduces disease progression @PLOSBiology https://plos.io/3Vb7xhx
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#COVID19-associated #neuroinflammation and #astrocyte death in the #brain linked to ORF3a-induced activation of Sur1-mediated ion channels, https://etidiohnew.blogspot.com/2025/08/covid19-associated-neuroinflammation.html
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Neuroinflammation and Oxidative Stress: How Science is Helping Your Brain
#BrainHealth #Neuroscience #HydrogenTherapy #OxidativeStress #Neuroinflammation #BrainRecovery #NeuroScience #MentalHealth #InnovativeMedicine #Neuroprotection
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Inflammation, Mitochondria, and Mood: The Biological Roots of Mental Health
#MentalHealth #Neuroscience #BrainScience #Neurotransmitters #Mitochondria #Neuroinflammation #MentalWellness #BiologyOfTheMind #Psychology #HealthScience
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The Brain’s Response to Injury: Proteins, Immune Cells, and Structural Changes
#BrainHealth #ConcussionRecovery #NeuroScience #TraumaticBrainInjury #TauProteins #Neuroinflammation #BrainAnatomy #AutoimmuneBrain #BrainResearch #MentalHealthMatters
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Understanding Brain Trauma: Cellular Responses and Molecular Cascades
#BrainInjury #Neuroinflammation #TraumaticBrainInjury #Microglia #Astrocytes #BloodBrainBarrier #Neuroregeneration #BrainHealth #Neuroscience #BrainRecovery
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From Trauma to Treatment: Navigating Brain Injury and Inflammation
#BrainInjury #Neuroinflammation #Concussion #BrainHealth #Microglia #NeuroScience #BrainRecovery #Neurodegeneration #MentalHealth #NeuroscienceResearch
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When Brain Balance Tips: Understanding Neuroinflammation After Head Injuries
#BrainHealth #Microglia #Neuroinflammation #Neurodegeneration #Alzheimers #Parkinsons #BrainScience #Neuroscience #BrainAging #Neurobiology #ProteinAggregates #BrainRepair #Neuroimmunology #BrainCells #CognitiveHealth
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Sleep, Stress, and Brain Health: The Intricate Balance of Your Mind's Support Systems
#BrainScience #Neuroscience #GlymphaticSystem #BrainHealth #Neurobiology #SleepAndMemory #Neuroinflammation #BrainSupportSystems #MindAndBody #BrainResearch
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Tryptophan and the Kynurenine Pathway: Metabolic Routes Impacting Mood and Neurodegeneration
#BrainChemistry #Neuroimmune #KynureninePathway #GutBrainAxis #Neuroinflammation #Microglia #Astrocytes #Neurodegeneration #OxidativeStress #MentalHealth #BrainHealth #Metabolism #NervousSystem #DietAndBrain #Neuroscience
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The Chemistry of Mood: Serotonin, Tryptamine, and Neurotransmitter Regulation
#Neurochemistry #BrainHealth #GutBrainAxis #Tryptophan #Serotonin #Microbiome #Neuroinflammation #Toxins #BloodBrainBarrier #BrainRecovery #Neuroscience #MentalHealth #CellularBiology #BrainProtection #MolecularScience
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Inside the Brain: Exploring Neurotransmitters, Pathways, and Neuroimmune Interactions
#BrainChemistry #Neuroscience #Neurotransmitters #NeuralCircuits #Dopamine #Serotonin #Neuroinflammation #Neurodegeneration #BrainHealth #Neuroplasticity
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Neurons, Glia, and Blood Vessels: The Complex City of the Brain
#BrainHealth #Neuroscience #AlzheimersDisease #Neuroinflammation #Microglia #CognitiveHealth #Neurodegeneration #BrainResearch #NeurotrophicFactors #HealthyBrain #MindAndMemory #BrainScience #NeuralNetworks #BrainCare #Neuroprotection
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The Brain’s Tiny Guardians: Microglia and Neuroinflammation Explained
#Microglia #Neurodegeneration #BrainHealth #Alzheimers #Parkinsons #Neuroinflammation #CognitiveHealth #BrainScience #Neuroscience #Neurotherapy
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The Brain's Metropolis: How Microglia, Gut Microbes, and Stress Shape Your Mind
#BrainHealth #Neuroinflammation #GutBrainAxis #Microglia #MentalHealth #Neuroplasticity #GutMicrobiome #StressAndBrain #NeuroScience #BrainTour
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The Brain’s Immune System: Microglia and Inflammation Explained
#BrainScience #Neuroscience #GlialCells #Microglia #Astrocytes #Neuroinflammation #BrainHealth #Neurodegeneration #Demyelination #Cytokines #Neurons #BrainResearch #Neurobiology #BrainInjury #BrainRecovery
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Neurobiologist Bente Winkler @b-wink.bsky.social investigates how the brain reacts to #neuroinflammation. For this, she is using genetically modified #Drosophila flies that enable an artificial activation of the immune system. Read more: uni.ms/48q7k
Inflammation in the brain: My ...