#neuroimaging — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #neuroimaging, aggregated by home.social.
-
DATE: September 11, 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: Brain scans reveal how recurrent depression leaves a lasting mark on the amygdala
Brain scans reveal that elevated activity in the emotion-processing center is tied to a person’s history of recurrent depression, rather than their current mood. The large study, published in Psychological Medicine, suggests that each major depressive episode may leave a lasting biological mark that increases future vulnerability to the disease.
Major depressive disorder is a common psychiatric condition that affects millions of people worldwide. Currently, psychiatrists diagnose the condition based on clinical interviews and patient history. There are no biological markers, like a blood test or a brain scan, to guide treatment choices.
Functional magnetic resonance imaging, or fMRI, allows researchers to observe the brain in action by tracking blood-oxygen levels. When a brain region becomes active, it requires more oxygen, leading to localized changes in blood flow. The scanner detects these magnetic differences to map out neural activity.
Scientists often use this technology to study the amygdala, an almond-shaped structure deep inside the brain that processes fear and negative emotions. Early brain imaging research suggested that people with clinical depression have hyperactive amygdalae when looking at negative images. But a recent analysis of a massive dataset called the UK Biobank found no association between amygdala activity and current depression symptoms.
Jerke J. van den Berg, a biomedical researcher at the University of Amsterdam, and his colleagues designed a new study to better understand this discrepancy. They suspected that previous research might have missed the broader picture by only looking at a patient’s current mood. The researchers focused on a concept called the kindling theory.
The kindling theory proposes that an initial depressive episode makes the brain more sensitive to stress. After the brain has been sensitized by that first experience, it takes progressively less trauma to trigger a relapse. To test if the amygdala reflects this effect, the research team decided to look at a person’s lifetime history of depression, known as a trait, rather than their current symptoms, known as a state.
The researchers utilized data from the UK Biobank, a long-term population health study. They analyzed functional MRI scans from a subset of participants, totaling more than 11,000 individuals. While inside the scanner, participants completed a visual exercise called the Hariri task.
During the task, participants were shown a target image of an angry or fearful face at the top of a screen. They were then asked to select the matching face from two options at the bottom. This specific visual matching exercise is known to reliably stimulate the amygdala.
Brain activity can vary widely from person to person based on age, gender, and head movement during a scan. To account for this natural variation, the research team used a statistical technique called normative modeling. They analyzed scans from over 6,400 healthy participants to establish a baseline of expected amygdala activity. This works much like a pediatric growth chart, which maps out normal ranges for a child’s height and weight.
Next, the researchers evaluated how much the brain activity of nearly 5,000 other participants deviated from this baseline model. They categorized these individuals based on their self-reported mental health histories. The groups included healthy controls, people who had experienced a single depressive episode, those with moderate recurrence involving two to five episodes, and those with a high recurrence of six or more episodes.
For this initial cross-sectional analysis, the team focused strictly on participants who were currently in remission from their depression. The initial results were not statistically significant when the team analyzed the unaltered brain scans. However, once they applied the normative modeling technique to account for age and gender variations, a distinct pattern emerged.
The analysis revealed a measurable association between an individual’s history of depression and their amygdala response. Participants with a high recurrence of depressive episodes showed a heightened amygdala reaction to negative faces compared to healthy controls.
When the researchers looked at individuals actively experiencing a depressive episode, they found no distinct increase in brain activity compared to controls. This suggested that amygdala reactivity represents a long-term biological trait, rather than a temporary state reflecting current mood.
The researchers also wanted to know how medication might influence these brain signals. They noticed that a higher percentage of people in the severe recurrence group were taking antidepressants compared to those with a single past episode. They repeated their cross-sectional analysis, this time removing any participants who were actively taking antidepressant medications.
Excluding medicated individuals strengthened the observed differences between the healthy controls and the recurrent depression groups. The findings indicated that antidepressants might dampen the hyperactive amygdala signal associated with a history of recurrent depression. Because the medication reduced amygdala reactivity, including these participants in the initial data pool slightly masked the true extent of the brain changes.
To see how the brain changes over time, the team conducted a longitudinal analysis. They focused on a smaller group of participants who returned for a second brain scan roughly two and a half years after their initial visit. The researchers categorized these individuals based on whether they had suffered new depressive episodes between the two scans.
For this longitudinal evaluation, the team specifically analyzed people who were in remission during both of their imaging sessions. Participants who began the study with a history of just one depressive episode, but then experienced multiple new episodes before their second scan, exhibited an increase in amygdala reactivity over time.
This brain change supported the kindling theory. It suggests that new depressive episodes incrementally alter how the brain processes negative emotional information, leaving a biological mark even after symptoms fade.
The study relied on a large dataset, but the researchers noted that the effect sizes were relatively small. These findings do not mean that a functional MRI scan can be used to diagnose depression in a clinical setting right now. The results are not robust enough to predict an individual’s exact risk of a relapse based on a single brain scan.
The data collection methods also presented certain limitations. The study depended on participants accurately recalling their own mental health histories, which can introduce memory biases. People might misremember exactly how many distinct depressive episodes they experienced over the course of their lives.
The mental health questionnaires also combined treatments for nerves, anxiety, and depression into a single metric. Because of this, the researchers could not strictly isolate the effects of anxiety disorders from the effects of clinical depression. Future studies will need to track larger groups of symptomatic individuals over extended periods of time to untangle these variables.
Scientists hope that advancing neuroimaging techniques will eventually reduce the normal fluctuations seen in brain scans. Over time, mapping the biology of recurrent depression could help psychiatrists tailor treatments to a patient’s individual history, moving away from the current trial-and-error approach to prescribing medication.
The study, “Normative amygdala fMRI response during emotional processing as a trait of depressive symptoms in the UK Biobank,” was authored by Jerke J. van den Berg, Henricus G. Ruhé, Henk A. Marquering, Liesbeth Reneman, and Matthan W. A. Caan.
-------------------------------------------------
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 #DepressionResearch #Amygdala #fMRI #Neuroimaging #KindlingTheory #UKBiobank #MentalHealthAwareness #BiomarkersInDepression #LongitudinalStudy #NeuroscienceAdvances
-
DATE: September 11, 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: Brain scans reveal how recurrent depression leaves a lasting mark on the amygdala
Brain scans reveal that elevated activity in the emotion-processing center is tied to a person’s history of recurrent depression, rather than their current mood. The large study, published in Psychological Medicine, suggests that each major depressive episode may leave a lasting biological mark that increases future vulnerability to the disease.
Major depressive disorder is a common psychiatric condition that affects millions of people worldwide. Currently, psychiatrists diagnose the condition based on clinical interviews and patient history. There are no biological markers, like a blood test or a brain scan, to guide treatment choices.
Functional magnetic resonance imaging, or fMRI, allows researchers to observe the brain in action by tracking blood-oxygen levels. When a brain region becomes active, it requires more oxygen, leading to localized changes in blood flow. The scanner detects these magnetic differences to map out neural activity.
Scientists often use this technology to study the amygdala, an almond-shaped structure deep inside the brain that processes fear and negative emotions. Early brain imaging research suggested that people with clinical depression have hyperactive amygdalae when looking at negative images. But a recent analysis of a massive dataset called the UK Biobank found no association between amygdala activity and current depression symptoms.
Jerke J. van den Berg, a biomedical researcher at the University of Amsterdam, and his colleagues designed a new study to better understand this discrepancy. They suspected that previous research might have missed the broader picture by only looking at a patient’s current mood. The researchers focused on a concept called the kindling theory.
The kindling theory proposes that an initial depressive episode makes the brain more sensitive to stress. After the brain has been sensitized by that first experience, it takes progressively less trauma to trigger a relapse. To test if the amygdala reflects this effect, the research team decided to look at a person’s lifetime history of depression, known as a trait, rather than their current symptoms, known as a state.
The researchers utilized data from the UK Biobank, a long-term population health study. They analyzed functional MRI scans from a subset of participants, totaling more than 11,000 individuals. While inside the scanner, participants completed a visual exercise called the Hariri task.
During the task, participants were shown a target image of an angry or fearful face at the top of a screen. They were then asked to select the matching face from two options at the bottom. This specific visual matching exercise is known to reliably stimulate the amygdala.
Brain activity can vary widely from person to person based on age, gender, and head movement during a scan. To account for this natural variation, the research team used a statistical technique called normative modeling. They analyzed scans from over 6,400 healthy participants to establish a baseline of expected amygdala activity. This works much like a pediatric growth chart, which maps out normal ranges for a child’s height and weight.
Next, the researchers evaluated how much the brain activity of nearly 5,000 other participants deviated from this baseline model. They categorized these individuals based on their self-reported mental health histories. The groups included healthy controls, people who had experienced a single depressive episode, those with moderate recurrence involving two to five episodes, and those with a high recurrence of six or more episodes.
For this initial cross-sectional analysis, the team focused strictly on participants who were currently in remission from their depression. The initial results were not statistically significant when the team analyzed the unaltered brain scans. However, once they applied the normative modeling technique to account for age and gender variations, a distinct pattern emerged.
The analysis revealed a measurable association between an individual’s history of depression and their amygdala response. Participants with a high recurrence of depressive episodes showed a heightened amygdala reaction to negative faces compared to healthy controls.
When the researchers looked at individuals actively experiencing a depressive episode, they found no distinct increase in brain activity compared to controls. This suggested that amygdala reactivity represents a long-term biological trait, rather than a temporary state reflecting current mood.
The researchers also wanted to know how medication might influence these brain signals. They noticed that a higher percentage of people in the severe recurrence group were taking antidepressants compared to those with a single past episode. They repeated their cross-sectional analysis, this time removing any participants who were actively taking antidepressant medications.
Excluding medicated individuals strengthened the observed differences between the healthy controls and the recurrent depression groups. The findings indicated that antidepressants might dampen the hyperactive amygdala signal associated with a history of recurrent depression. Because the medication reduced amygdala reactivity, including these participants in the initial data pool slightly masked the true extent of the brain changes.
To see how the brain changes over time, the team conducted a longitudinal analysis. They focused on a smaller group of participants who returned for a second brain scan roughly two and a half years after their initial visit. The researchers categorized these individuals based on whether they had suffered new depressive episodes between the two scans.
For this longitudinal evaluation, the team specifically analyzed people who were in remission during both of their imaging sessions. Participants who began the study with a history of just one depressive episode, but then experienced multiple new episodes before their second scan, exhibited an increase in amygdala reactivity over time.
This brain change supported the kindling theory. It suggests that new depressive episodes incrementally alter how the brain processes negative emotional information, leaving a biological mark even after symptoms fade.
The study relied on a large dataset, but the researchers noted that the effect sizes were relatively small. These findings do not mean that a functional MRI scan can be used to diagnose depression in a clinical setting right now. The results are not robust enough to predict an individual’s exact risk of a relapse based on a single brain scan.
The data collection methods also presented certain limitations. The study depended on participants accurately recalling their own mental health histories, which can introduce memory biases. People might misremember exactly how many distinct depressive episodes they experienced over the course of their lives.
The mental health questionnaires also combined treatments for nerves, anxiety, and depression into a single metric. Because of this, the researchers could not strictly isolate the effects of anxiety disorders from the effects of clinical depression. Future studies will need to track larger groups of symptomatic individuals over extended periods of time to untangle these variables.
Scientists hope that advancing neuroimaging techniques will eventually reduce the normal fluctuations seen in brain scans. Over time, mapping the biology of recurrent depression could help psychiatrists tailor treatments to a patient’s individual history, moving away from the current trial-and-error approach to prescribing medication.
The study, “Normative amygdala fMRI response during emotional processing as a trait of depressive symptoms in the UK Biobank,” was authored by Jerke J. van den Berg, Henricus G. Ruhé, Henk A. Marquering, Liesbeth Reneman, and Matthan W. A. Caan.
-------------------------------------------------
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 #DepressionResearch #Amygdala #fMRI #Neuroimaging #KindlingTheory #UKBiobank #MentalHealthAwareness #BiomarkersInDepression #LongitudinalStudy #NeuroscienceAdvances
-
DATE: September 11, 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: Brain scans reveal how recurrent depression leaves a lasting mark on the amygdala
Brain scans reveal that elevated activity in the emotion-processing center is tied to a person’s history of recurrent depression, rather than their current mood. The large study, published in Psychological Medicine, suggests that each major depressive episode may leave a lasting biological mark that increases future vulnerability to the disease.
Major depressive disorder is a common psychiatric condition that affects millions of people worldwide. Currently, psychiatrists diagnose the condition based on clinical interviews and patient history. There are no biological markers, like a blood test or a brain scan, to guide treatment choices.
Functional magnetic resonance imaging, or fMRI, allows researchers to observe the brain in action by tracking blood-oxygen levels. When a brain region becomes active, it requires more oxygen, leading to localized changes in blood flow. The scanner detects these magnetic differences to map out neural activity.
Scientists often use this technology to study the amygdala, an almond-shaped structure deep inside the brain that processes fear and negative emotions. Early brain imaging research suggested that people with clinical depression have hyperactive amygdalae when looking at negative images. But a recent analysis of a massive dataset called the UK Biobank found no association between amygdala activity and current depression symptoms.
Jerke J. van den Berg, a biomedical researcher at the University of Amsterdam, and his colleagues designed a new study to better understand this discrepancy. They suspected that previous research might have missed the broader picture by only looking at a patient’s current mood. The researchers focused on a concept called the kindling theory.
The kindling theory proposes that an initial depressive episode makes the brain more sensitive to stress. After the brain has been sensitized by that first experience, it takes progressively less trauma to trigger a relapse. To test if the amygdala reflects this effect, the research team decided to look at a person’s lifetime history of depression, known as a trait, rather than their current symptoms, known as a state.
The researchers utilized data from the UK Biobank, a long-term population health study. They analyzed functional MRI scans from a subset of participants, totaling more than 11,000 individuals. While inside the scanner, participants completed a visual exercise called the Hariri task.
During the task, participants were shown a target image of an angry or fearful face at the top of a screen. They were then asked to select the matching face from two options at the bottom. This specific visual matching exercise is known to reliably stimulate the amygdala.
Brain activity can vary widely from person to person based on age, gender, and head movement during a scan. To account for this natural variation, the research team used a statistical technique called normative modeling. They analyzed scans from over 6,400 healthy participants to establish a baseline of expected amygdala activity. This works much like a pediatric growth chart, which maps out normal ranges for a child’s height and weight.
Next, the researchers evaluated how much the brain activity of nearly 5,000 other participants deviated from this baseline model. They categorized these individuals based on their self-reported mental health histories. The groups included healthy controls, people who had experienced a single depressive episode, those with moderate recurrence involving two to five episodes, and those with a high recurrence of six or more episodes.
For this initial cross-sectional analysis, the team focused strictly on participants who were currently in remission from their depression. The initial results were not statistically significant when the team analyzed the unaltered brain scans. However, once they applied the normative modeling technique to account for age and gender variations, a distinct pattern emerged.
The analysis revealed a measurable association between an individual’s history of depression and their amygdala response. Participants with a high recurrence of depressive episodes showed a heightened amygdala reaction to negative faces compared to healthy controls.
When the researchers looked at individuals actively experiencing a depressive episode, they found no distinct increase in brain activity compared to controls. This suggested that amygdala reactivity represents a long-term biological trait, rather than a temporary state reflecting current mood.
The researchers also wanted to know how medication might influence these brain signals. They noticed that a higher percentage of people in the severe recurrence group were taking antidepressants compared to those with a single past episode. They repeated their cross-sectional analysis, this time removing any participants who were actively taking antidepressant medications.
Excluding medicated individuals strengthened the observed differences between the healthy controls and the recurrent depression groups. The findings indicated that antidepressants might dampen the hyperactive amygdala signal associated with a history of recurrent depression. Because the medication reduced amygdala reactivity, including these participants in the initial data pool slightly masked the true extent of the brain changes.
To see how the brain changes over time, the team conducted a longitudinal analysis. They focused on a smaller group of participants who returned for a second brain scan roughly two and a half years after their initial visit. The researchers categorized these individuals based on whether they had suffered new depressive episodes between the two scans.
For this longitudinal evaluation, the team specifically analyzed people who were in remission during both of their imaging sessions. Participants who began the study with a history of just one depressive episode, but then experienced multiple new episodes before their second scan, exhibited an increase in amygdala reactivity over time.
This brain change supported the kindling theory. It suggests that new depressive episodes incrementally alter how the brain processes negative emotional information, leaving a biological mark even after symptoms fade.
The study relied on a large dataset, but the researchers noted that the effect sizes were relatively small. These findings do not mean that a functional MRI scan can be used to diagnose depression in a clinical setting right now. The results are not robust enough to predict an individual’s exact risk of a relapse based on a single brain scan.
The data collection methods also presented certain limitations. The study depended on participants accurately recalling their own mental health histories, which can introduce memory biases. People might misremember exactly how many distinct depressive episodes they experienced over the course of their lives.
The mental health questionnaires also combined treatments for nerves, anxiety, and depression into a single metric. Because of this, the researchers could not strictly isolate the effects of anxiety disorders from the effects of clinical depression. Future studies will need to track larger groups of symptomatic individuals over extended periods of time to untangle these variables.
Scientists hope that advancing neuroimaging techniques will eventually reduce the normal fluctuations seen in brain scans. Over time, mapping the biology of recurrent depression could help psychiatrists tailor treatments to a patient’s individual history, moving away from the current trial-and-error approach to prescribing medication.
The study, “Normative amygdala fMRI response during emotional processing as a trait of depressive symptoms in the UK Biobank,” was authored by Jerke J. van den Berg, Henricus G. Ruhé, Henk A. Marquering, Liesbeth Reneman, and Matthan W. A. Caan.
-------------------------------------------------
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 #DepressionResearch #Amygdala #fMRI #Neuroimaging #KindlingTheory #UKBiobank #MentalHealthAwareness #BiomarkersInDepression #LongitudinalStudy #NeuroscienceAdvances
-
DATE: August 23, 2026 at 10:00AM
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: Survival of the wittiest: How humor and cleverness shaped human evolution
URL: https://www.psypost.org/survival-of-the-wittiest-how-humor-and-cleverness-shaped-human-evolution/
A new theoretical paper suggests that human cognitive and linguistic evolution was driven by early humans’ ability to be clever and humorous, an idea dubbed the “survival of the wittiest.” The analysis argues that the earliest stages of grammar provided a platform for verbal competition and sexual selection, gradually replacing physical violence with verbal agility. The research was published in PNAS Nexus.
For decades, discussions of human evolution have revolved around two dominant ideas. The first is Charles Darwin’s original concept of the survival of the fittest, which is often narrowly interpreted as physical strength or health. The second is the more recent hypothesis of the survival of the friendliest. This newer idea proposes that humans evolved primarily through selection for prosocial behavior and cooperation, which allowed early humans to form alliances and outcompete other groups.
Wayne State University linguist Ljiljana Progovac authored the new paper to offer an alternative viewpoint. Progovac argues that physical fitness and friendliness fail to capture the unique role that language played in human development. Being physically strong or socially cooperative are traits shared with many other animals, including bonobos and other primates. These traits alone do not explain the rapid and unique expansion of human cognition.
According to Progovac, focusing entirely on friendliness misses the competitive nature of human interaction. Evolution involves both cooperation and ruthless competition. To fully understand how our ancestors evolved into modern humans, researchers must account for the biological advantage of eloquence, imagination, and the ability to outwit rivals. This perspective centers on sexual selection, where traits that make an individual attractive to mates are passed down through successive generations.
To build this argument, Progovac analyzed linguistic structures that represent the earliest stages of grammar. Language leaves no physical bones behind, so researchers must rely on a process called reverse engineering. By peeling back the complex layers of modern syntax, linguists can reconstruct the most foundational building blocks of language. These foundational structures are referred to as living fossils.
In modern languages, these fossils appear as simple two-word combinations consisting of one verb and one noun. Examples in English include words like “killjoy,” “crybaby,” “pickpocket,” and “scatterbrain.” These basic compounds do not rely on complex grammatical rules. They lack the structural layers required to distinguish between subjects and objects or to establish tense.
These simple word pairs are remarkably consistent across entirely different language families. Progovac notes that similar verb-noun compounds exist in languages ranging from Serbian to Berber to Twi. Historically, these basic constructions have been used to create highly vivid, metaphorical nicknames. Often, these nicknames are derogatory or humorous, describing a person based on a prominent action or physical trait.
Progovac proposes that as early humans developed these two-word abilities, a new form of social competition emerged. Individuals who could quickly invent clever, insulting, or amusing names had a distinct social advantage. They could demean rivals and impress potential mates without resorting to physical combat. This quick-wittedness represented an enormous cognitive leap, showing that early language was not just for sharing information but for social maneuvering.
The biological benefits of this verbal agility are still visible in human populations today. In many traditional oral societies across the globe, the most eloquent speakers hold the highest social status. Individuals who can manipulate words effectively gain access to political power and better reproductive success. The ability to charm a mate through humor and metaphorical language proved to be highly adaptive over time.
The paper also reviews experimental evidence from neuroimaging to support this evolutionary timeline. In a prior functional magnetic resonance imaging experiment, researchers tracked brain activity while participants read ancient verb-noun combinations compared to more modern, complex words. The older compounds evoked a more visceral reaction in the brain than modern words.
The experimenters found that processing the older, fossil-like compounds activated the right side of the fusiform gyrus in the brain. This specific brain region is directly involved in face perception and face recognition. Finding that the same brain area handles both face recognition and basic verb-noun processing supports the idea that the earliest grammar was closely tied to naming individuals and attaching linguistic labels to faces.
A related brain imaging experiment looked at how the brain processes simple sentences compared to hierarchical, modern sentences. The simpler sentences resulted in less activity in the Broca’s area and the basal ganglia. The basal ganglia are deep brain structures involved in motor control and learning.
Over the course of human evolution, the connections between the Broca’s area and the basal ganglia became much denser. The gradual mastery of more complex language likely drove the physical evolution of these brain networks. This aligns with genetic changes unique to humans and Neanderthals, including variations in the FOXP2 gene, which is associated with speech and language development.
By replacing physical fighting with verbal dueling, quick-wittedness played a direct role in reducing physical aggression among early humans. Humor and laughter act as natural stress antagonists, lowering cortisol levels in the body. This biological response connects the survival of the wittiest with the concept of human self-domestication. Over time, societies selected for individuals who could use words to defuse tension or assert dominance, leading to a species that prizes cognitive contests over lethal battles.
While this perspective offers a robust framework for understanding language origins, measuring the evolutionary impact of humor and wit relies heavily on reconstructing the past. Researchers must reverse-engineer modern languages and rely on brain imaging proxies, which cannot definitively prove how ancient ancestors behaved in their daily lives. Brain scans of modern humans only provide an approximation of ancient cognitive processes.
Future studies could test this hypothesis by examining how individual variations in cognitive conditions process these fossil grammars. By observing how brains with different neurological setups handle early grammatical structures, scientists can better map the exact neural pathways that allowed language to flourish.
The study, “Survival of the wittiest (not friendliest): The art and science behind human linguistic and cognitive evolution,” was authored by Ljiljana Progovac.
URL: https://www.psypost.org/survival-of-the-wittiest-how-humor-and-cleverness-shaped-human-evolution/
-------------------------------------------------
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 #SurvivaloftheWittiest #HumorEvolution #LanguageOrigins #EarlyGrammar #VerbalCompetition #SexualSelection #Neuroimaging # FOXP2 #SocialManeuvering #EvolutionOfCognition
-
Exploring the Brain: A Journey Through Neuroimaging and Neural Dynamics
#BrainScience #Neuroimaging #Neuroscience #BrainHealth #Microglia #Synapses #Endocannabinoid #Neurochemistry #BrainArchitecture #Memory #Cognition #MoodRegulation #Neurotherapy #BrainConnectivity #MentalHealth #NeuroscienceExplained
-
Exploring the Brain: A Journey Through Neuroimaging and Neural Dynamics
#BrainScience #Neuroimaging #Neuroscience #BrainHealth #Microglia #Synapses #Endocannabinoid #Neurochemistry #BrainArchitecture #Memory #Cognition #MoodRegulation #Neurotherapy #BrainConnectivity #MentalHealth #NeuroscienceExplained
-
Exploring the Brain: A Journey Through Neuroimaging and Neural Dynamics
#BrainScience #Neuroimaging #Neuroscience #BrainHealth #Microglia #Synapses #Endocannabinoid #Neurochemistry #BrainArchitecture #Memory #Cognition #MoodRegulation #Neurotherapy #BrainConnectivity #MentalHealth #NeuroscienceExplained
-
Exploring the Brain: A Journey Through Neuroimaging and Neural Dynamics
#BrainScience #Neuroimaging #Neuroscience #BrainHealth #Microglia #Synapses #Endocannabinoid #Neurochemistry #BrainArchitecture #Memory #Cognition #MoodRegulation #Neurotherapy #BrainConnectivity #MentalHealth #NeuroscienceExplained
-
🧠 #Brain age proposed as a #biomarker to improve diagnosis and treatment for patients suffering from #neurodegenerative diseases using #DeepLearning & #BigData.
📃 Grant Proposal: https://doi.org/10.3897/rio.11.e156738
-
Timely synopsis of emerging #neuroimaging evidence linking #loss anticipation in the #insula to #stimulant use relapse by Jennifer Stewart of the Laureate Institute (thanks for the shout-out! #neuroscience, #addiction)...
https://www.sciencedirect.com/science/article/pii/S0006322323016256