CP v2

Category: Psychology

  • Study of 1 300 golden retrievers finds shared genes tied to canine behavior and human anxiety risk

    Study of 1 300 golden retrievers finds shared genes tied to canine behavior and human anxiety risk

    Researchers analyzing the DNA of 1 300 golden retrievers have identified genetic regions linked to temperament traits such as trainability, activity level, fearfulness and dog-directed aggression. The work suggests some of the same genes associated with behavior in dogs are also implicated in human mental and cognitive traits.

    The study, published in Proceedings of the National Academy of Sciences, combined genome-wide data with detailed owner-reported behavioral profiles. Scientists say the results add evidence that dogs and humans can share biological pathways influencing emotional responses.

    How behavior was matched to DNA

    The team drew on the Golden Retriever Lifetime Study, a long-running project that follows dogs over time using health records and repeated questionnaires. Owners reported dozens of behaviors, which were grouped into categories to create measurable traits for genetic analysis.

    Researchers then scanned each dog’s genome and looked for genetic markers that were more common in animals showing specific behavioral patterns. This approach does not pinpoint a single cause of a behavior, but highlights biological systems that may shape stress sensitivity and learning.

    Overlap with human trait studies

    When the researchers compared their canine results with large human genetic datasets, they found 12 genes linked to golden retriever behavior that also appear in studies of human traits. Those traits include anxiety and depression risk as well as measures related to cognition and educational outcomes.

    One gene highlighted in the analysis, PTPN1, was associated with dog-directed aggression in golden retrievers and has also been reported in human research connected to intelligence and depression. The team also reported a variant tied to fear of other dogs that aligns with human findings on rumination and education-related measures.

    What this could mean for owners

    Scientists caution that genes do not predetermine a dog’s personality, and environment and training remain crucial. Still, they argue that recognizing inherited differences in stress reactivity may help explain why some dogs find everyday situations more challenging.

    The findings could also inform veterinary care, including how clinicians and owners interpret fear-based behaviors and when stress-reducing interventions may be appropriate. Researchers say dogs may serve as useful models for understanding the biology of emotional disturbance because they share human environments and show comparable behavioral variation.

  • Engineered psilocin compound hints at depression relief without hallucinations, early mouse study finds

    Engineered psilocin compound hints at depression relief without hallucinations, early mouse study finds

    Researchers have developed modified versions of psilocin, the active compound produced when the body metabolizes psilocybin, aiming to preserve potential antidepressant effects while reducing psychedelic-like symptoms. The work, published in the Journal of Medicinal Chemistry, adds to a fast-moving effort to make psychedelic-inspired medicines easier to use in routine care.

    Interest in psilocybin has grown as clinical trials explore its potential for major depressive disorder, treatment-resistant depression, anxiety linked to serious illness, and substance use disorders. Yet the hallmark altered state can complicate treatment settings, requiring intensive supervision and limiting who may be willing or able to receive it.

    Why scientists are redesigning psilocin

    The new research focuses on how strongly and how quickly psilocin reaches the brain and activates serotonin receptors, particularly pathways associated with mood regulation. The team tested five chemical variants designed to release psilocin more gradually, potentially reducing the rapid peak linked with more intense psychedelic effects.

    In lab experiments using human plasma and models of gastrointestinal absorption, one candidate stood out for stability and a slower conversion profile. The researchers selected that compound, referred to as 4e, for further testing as a proof of concept rather than a ready-to-use drug.

    What the mouse data suggests

    When given orally to mice, 4e delivered psilocin to the bloodstream and brain over a longer period, with lower peak levels than an equivalent dose of pharmaceutical-grade psilocybin. The compound still crossed the blood-brain barrier efficiently, suggesting it can reach the intended target tissue.

    To estimate psychedelic-like activity, the scientists tracked head-twitch responses, a standard rodent behavioral marker used in serotonin-based psychedelic research. Mice given 4e showed fewer head twitches than those given psilocybin, even though the compound continued to engage key serotonin receptors.

    What comes next before human trials

    The authors argue the results support a broader hypothesis that some therapeutic signaling may be separable from the most disruptive subjective effects. Even so, the study is early, relies on animal behavior proxies, and does not demonstrate antidepressant outcomes in people.

    Next steps typically include deeper safety profiling, dose-ranging studies, and clearer evidence of benefit in validated disease models before any clinical evaluation. The researchers also disclosed industry-linked funding and patent-related interests, which will be important to monitor as the work progresses.

    In parallel, human studies of psilocybin-assisted therapy continue to shape the field, including efforts to standardize dosing, supervision, and outcome measures. If non-hallucinogenic or low-hallucinogenic analogs prove effective, they could eventually broaden access by reducing the need for prolonged monitoring while still targeting serotonin-linked mechanisms relevant to depression.

  • Major Lancet review questions medicinal cannabis for anxiety and PTSD as trial evidence falls short

    Major Lancet review questions medicinal cannabis for anxiety and PTSD as trial evidence falls short

    A large review in The Lancet concludes there is no convincing evidence that medicinal cannabis improves symptoms of anxiety, depression or post-traumatic stress disorder. Researchers say the balance of data from randomized trials does not support routine prescribing for these mental health conditions.

    The analysis arrives as medical cannabis use has expanded rapidly in North America and elsewhere, including among people seeking relief from mood and trauma-related symptoms. The authors note that patient demand has often moved faster than the clinical evidence base.

    What the review examined

    The study pooled results from 54 randomized controlled trials conducted between 1980 and 2025, making it one of the broadest assessments of cannabinoids across mental health indications to date. It focused on both effectiveness and safety outcomes, comparing cannabis-based medicines with placebo or other controls.

    According to the authors, the evidence did not show meaningful improvements for anxiety, depression or PTSD when results were combined. They also cautioned that frequent use could be associated with harms, including psychotic symptoms and cannabis use disorder, and may delay more effective care.

    Potential benefits, but limited certainty

    The review found tentative signals that some cannabinoid preparations could help in a small number of other conditions, such as insomnia, tics or Tourette’s syndrome, autism-related symptoms, and cannabis use disorder. However, the authors stressed that the overall quality of evidence for these indications was low.

    They also pointed to areas where cannabis-based treatment is supported by stronger evidence, including specific epilepsy syndromes treated with cannabidiol, spasticity in multiple sclerosis, and certain types of pain. Even in these areas, they emphasized the need to match products and dosing to conditions studied in rigorous trials.

    Safety questions and regulation debate

    The authors said the findings should inform clinicians weighing prescriptions for mental health, particularly given varying product potency and formulations across markets. They argued that inconsistent regulation and marketing claims can leave patients with unclear expectations about benefits and risks.

    In substance use disorders, results differed by condition, with some evidence suggesting oral cannabinoid medicines may reduce cannabis smoking when combined with psychological therapy. But for cocaine-use disorder, the review reported increased cravings, indicating cannabis medicines should not be used for that purpose.

    Researchers called for clearer prescribing guidance and more high-quality trials that measure standardized mental health outcomes over longer follow-up periods. Until then, they said established, evidence-based treatments for anxiety, depression and PTSD should remain first-line care.

  • Ozempic and other GLP-1 drugs linked to lower depression and addiction risk in large Swedish study

    Ozempic and other GLP-1 drugs linked to lower depression and addiction risk in large Swedish study

    GLP-1 medications, such as semaglutide (Ozempic, Wegovy, and Rybelsus), commonly prescribed for diabetes and obesity may also be linked to better mental health outcomes, according to new research. The study found that people using these drugs had fewer psychiatric hospital visits and took less time off work due to mental health issues. The large-scale analysis was conducted by researchers from the University of Eastern Finland, Karolinska Institutet in Stockholm, and Griffith University in Australia.

    Obesity and diabetes are both tied to a higher risk of mental health problems. At the same time, people with psychiatric disorders are more likely to develop metabolic conditions such as obesity and diabetes. Scientists have long been exploring how these conditions overlap and whether treatments for physical health might also influence mental well-being.

    To investigate this connection, researchers analyzed data from nearly 100,000 individuals, including more than 20,000 who had used GLP-1 medications. Participants were tracked using Swedish national health registers from 2009 to 2022.

    Reduced Depression Anxiety and Psychiatric Care

    The findings showed that GLP-1 medications, especially semaglutide, were associated with fewer psychiatric-related hospital visits and reduced sickness absence. During periods when people were taking semaglutide, the need for such care dropped by 42% compared to periods without GLP-1 use. The risk of depression was 44% lower, while anxiety disorders were reduced by 38%.

    Lower Risk of Substance Use and Suicidal Behavior

    The study also found a notable decrease in substance use disorders among semaglutide users. Hospital care and time off work related to substance use were 47% lower during treatment periods. In addition, GLP-1 receptor agonists were linked to a reduced risk of suicidal behavior.

    One of the study’s authors, Professor Mark Taylor from Griffith University, said the findings were not entirely unexpected: “An earlier study examining Swedish registers found the use of GLP-1 medications to be associated with a reduced risk of alcohol use disorder. Alcohol-related problems often have downstream effects on mood and anxiety, so we expected the effect to be positive on these as well.”

    Why Might These Drugs Affect the Brain

    Even so, the strength of the associations surprised the research team. “Because this is a registry-based study, we cannot determine exactly why or how these medications affect mood symptoms, but the association was quite strong. It is possible that, in addition to factors such as reduced alcohol consumption, weight loss-related improvements in body image, or relief associated with better glycemic control in diabetes, there may also be direct neurobiological mechanisms involved — for example, through changes in the functioning of the brain’s reward system,” said Research Director, Docent Markku Lähteenvuo from the University of Eastern Finland.

    Strong Evidence but More Research Needed

    The results were published in The Lancet Psychiatry, a leading journal in the field. While earlier studies on GLP-1 medications and mental health have produced mixed findings, many of those studies were smaller. This large registry-based analysis adds stronger evidence, though further research is still needed to fully understand the link.

  • New Swedish study flags delayed paternal depression surge around baby’s first year

    New Swedish study flags delayed paternal depression surge around baby’s first year

    Fathers in Sweden are less likely to receive a psychiatric diagnosis during their partner’s pregnancy and in the months right after their child is born. But this pattern reverses over time. A new study published in JAMA Network Open reports that diagnoses of depression and stress-related conditions rise about a year after childbirth. The research was led by scientists at Karolinska Institutet in Sweden and Sichuan University in China.

    “The transition to fatherhood often involves both positive experiences and a range of new stresses,” says Jing Zhou, PhD student at the Institute of Environmental Medicine, Karolinska Institutet, and co-first author of the paper. “Many cherish the intimate moments with their child, whilst at the same time the relationship with their partner may be affected and sleep quality may deteriorate, which can contribute to an increased risk of mental ill-health.”

    Study Tracks Over 1 Million Fathers Across Sweden

    The researchers analyzed data from more than one million fathers whose children were born in Sweden between 2003 and 2021. Using linked national registers, they followed when men received new psychiatric diagnoses, beginning one year before pregnancy and continuing until the child reached one year of age.

    Depression and Stress Diagnoses Increase After One Year

    The findings show that psychiatric diagnoses became less common during pregnancy and in the early months after birth compared with the year before pregnancy. By one year after birth, diagnoses related to anxiety and substance use had returned to levels seen before pregnancy. In contrast, depression and stress-related disorders showed a clear increase. These diagnoses rose by more than 30 percent compared with rates before pregnancy.

    “The delayed increase in depression was unexpected and underscores the need to pay attention to warning signs of mental ill-health in fathers long after the birth of their child,” says Donghao Lu, senior lecturer and associate professor at the Institute of Environmental Medicine, Karolinska Institutet, and the paper’s corresponding author.

    Timing Support for Fathers’ Mental Health

    The researchers note that their results are based on clinical diagnoses, meaning men who did not seek care may not be included. Even so, the study highlights when fathers may be most vulnerable during early parenthood.

    “By identifying periods of increased vulnerability, healthcare providers and other stakeholders can more easily offer support,” says Jing Zhou. “Postnatal depression is often discussed for new mothers, but fathers’ well-being is also important, both for themselves and for the whole family.”

    The study was conducted in collaboration with Sichuan University in China and Uppsala University in Sweden. It was funded by Karolinska Institutet’s strategic research area in epidemiology and biostatistics, the Swedish Research Council and the European Research Council. The researchers report no conflicts of interest.

  • Scientists pinpoint metformin’s brain pathway, offering new clues for targeted type 2 diabetes treatment

    Scientists pinpoint metformin’s brain pathway, offering new clues for targeted type 2 diabetes treatment

    After more than 60 years as a first-line drug for type 2 diabetes, metformin is yielding a clearer explanation for how it lowers blood sugar. Researchers report that part of its glucose-lowering effect depends on a specific brain circuit, not only the liver or the gut.

    The study, led by Baylor College of Medicine and international collaborators, was published in Science Advances. It focuses on the ventromedial hypothalamus, a brain region known to help regulate whole-body metabolism.

    A protein switch in the hypothalamus

    The team centered on Rap1, a small signaling protein active in the ventromedial hypothalamus. They found that clinically relevant metformin dosing relied on suppressing Rap1 activity in this brain area to reduce blood glucose.

    To test the mechanism, the researchers used mice engineered to lack Rap1 in the ventromedial hypothalamus and then fed them a high-fat diet to model diabetes. In those mice, low-dose metformin did not improve blood sugar, while insulin and GLP-1–based drugs still worked.

    Why tiny brain doses mattered

    In another experiment, researchers delivered extremely small amounts of metformin directly into the brains of diabetic mice. Even at doses thousands of times lower than typical oral exposure, blood glucose fell markedly, supporting a central nervous system effect.

    The study also identified SF1 neurons in the ventromedial hypothalamus as key responders, becoming activated when metformin reached the brain. Electrophysiology data suggested metformin increased activity in most of these neurons, but only when Rap1 signaling was intact.

    What it could mean next

    The findings add to a growing view that metformin’s benefits may come from multiple organs working together, with the brain reacting at comparatively low drug levels. The authors argue that mapping this pathway could help guide future diabetes therapies that more precisely target glucose control.

    The researchers also pointed to broader interest in metformin’s neurological effects, including ongoing questions about brain aging. They plan to examine whether the same Rap1-linked signaling helps explain other observed effects of the drug beyond diabetes.

  • MIT study links GRIN2A mutation to slower reality updating in schizophrenia, pointing to a treatable brain circuit

    MIT study links GRIN2A mutation to slower reality updating in schizophrenia, pointing to a treatable brain circuit

    Researchers at MIT report that a mutation in the gene GRIN2A may interfere with how the brain updates beliefs when new information arrives, a cognitive difficulty often seen in schizophrenia. In mouse experiments, the change was tied to slower, less adaptive decision-making in a shifting environment.

    Schizophrenia affects about 1% of people and has a strong genetic component, though the biology connecting risk genes to symptoms has been hard to pin down. Large genomic studies have identified many associated variants, but many sit in non-coding DNA, making their functional impact difficult to interpret.

    From genetic signal to mechanism

    To narrow in on mutations that directly alter proteins, the team drew on large-scale exome sequencing that compares protein-coding regions across people with schizophrenia and unaffected controls. That work has helped highlight a smaller set of genes where rare disruptive mutations can substantially increase risk.

    GRIN2A stands out because it encodes a subunit of the NMDA receptor, a key component of glutamatergic signaling involved in learning, plasticity and cognitive control. NMDA receptor dysfunction has long been considered relevant to schizophrenia, but linking specific mutations to circuit-level effects has remained challenging.

    Decision task reveals slower adaptation

    In the study’s behavioral task, mice chose between two levers with different reward sizes and different effort costs that changed over time. Typical mice shifted to the more efficient option once the higher-reward choice became too costly, reflecting flexible updating as conditions evolved.

    Mice carrying the GRIN2A-related mutation took longer to commit, continuing to alternate between choices after the balance of effort and reward had effectively changed. The researchers interpret the pattern as reduced ability to incorporate new evidence quickly, leaving prior expectations to dominate behavior for longer.

    A circuit that can be nudged

    Brain measurements pointed to altered activity in the mediodorsal thalamus and its connections with the prefrontal cortex, a pathway central to executive function and decision-making. The team reports that this thalamocortical circuit appeared to represent changing option values differently in the mutated mice.

    Using optogenetics to activate neurons in the mediodorsal thalamus, the researchers were able to push behavior toward the more adaptive pattern seen in control animals. While only a subset of patients would be expected to carry GRIN2A mutations, the results suggest the same circuit could contribute to cognitive symptoms across broader groups.

    The authors frame the work as a step toward treatments that target cognition, an area where many patients continue to experience impairment even when hallucinations or delusions are reduced. Next efforts focus on identifying druggable nodes in the thalamus–prefrontal pathway that might restore more flexible updating without invasive methods.

  • Gut microbiome study points to inflammatory sugars as a potential trigger for ALS and frontotemporal dementia

    Gut microbiome study points to inflammatory sugars as a potential trigger for ALS and frontotemporal dementia

    Researchers at Case Western Reserve University say they have identified a gut-driven immune mechanism that may help explain why brain damage progresses in amyotrophic lateral sclerosis and frontotemporal dementia. The work focuses on specific sugars produced by certain gut bacteria and how they may spark harmful inflammation.

    The study, published in Cell Reports, links bacterial glycogen molecules to immune activation that can injure neurons in models of ALS and FTD. The authors suggest the pathway could become both a diagnostic clue and a target for treatments aimed at the gut rather than the brain alone.

    How the proposed gut pathway works

    According to the researchers, some gut microbes can generate an inflammatory form of glycogen, a complex sugar, that appears to provoke immune responses tied to neurodegeneration. In the study’s patient samples, 70% of 23 people with ALS or FTD showed elevated levels of the implicated bacterial glycogen, compared with about one-third of people without the conditions.

    Aaron Burberry, an assistant professor at Case Western Reserve School of Medicine, said the team found that these microbial sugars can trigger immune reactions that ultimately damage brain cells. The results point to a potential way to interrupt the process by reducing or degrading the inflammatory glycogen.

    Why genes may not be the whole story

    The findings could be especially relevant for carriers of the C9orf72 mutation, the most common known genetic cause of ALS and FTD. Many carriers never develop disease, and the study adds evidence that environmental factors such as the gut microbiome may influence whether symptoms emerge.

    The researchers propose that certain bacterial communities may act as a switch that worsens inflammation in genetically susceptible people. That idea aligns with a growing body of research connecting immune activity, the microbiome, and neurodegenerative disease risk.

    What comes next for treatment research

    In experiments described by the team, lowering levels of the harmful glycogen improved brain health measures and extended lifespan in model systems. Alex Rodriguez-Palacios, also at Case Western, said reducing these sugars was associated with better outcomes, supporting efforts to design therapies that target the compounds in the gut.

    The group plans larger studies to track microbiome changes in ALS and FTD patients, including before and after disease onset where possible. Burberry said the results support clinical trials testing whether glycogen-degrading approaches could slow progression, though timelines and trial designs will depend on additional validation.

  • Loss of Smell May Signal Early Alzheimer’s: New Study Points to an Immune Trigger

    Loss of Smell May Signal Early Alzheimer’s: New Study Points to an Immune Trigger

    A subtle decline in the sense of smell could be among the earliest detectable changes linked to Alzheimer’s disease, potentially emerging well before clear memory problems. New research from Germany suggests the shift may be driven by the brain’s immune cells damaging key odor-processing connections.

    The study, led by scientists at the German Center for Neurodegenerative Diseases (DZNE) and Ludwig Maximilian University of Munich, focuses on microglia, immune cells that help maintain brain health. Researchers report that in early Alzheimer’s, microglia may begin dismantling nerve fibers needed for normal smell perception.

    How the brain’s smell circuit changes

    The team examined communication between the olfactory bulb, which processes odor signals, and the locus coeruleus, a brainstem region involved in sensory regulation and other core functions. Long nerve fibers from the locus coeruleus help tune activity in the olfactory bulb, supporting normal smell processing.

    According to the researchers, early Alzheimer’s-related alterations make these fibers appear abnormal to microglia. In response, microglia break down the connections, which could help explain why smell deficits can appear early in the disease course.

    An eat-me signal on neurons

    The study points to changes in the nerve fiber membrane as a likely trigger. A molecule called phosphatidylserine, typically kept on the inner side of the cell membrane, was observed on the outside, where it can act as an immune cue.

    Microglia are known to respond to this kind of signal during normal synaptic pruning, a process that removes unused or impaired connections. The researchers suggest that in early Alzheimer’s, abnormal neuron activity may prompt this membrane shift, leading microglia to remove fibers that are still needed.

    Evidence from mice, tissue, and PET scans

    To support the mechanism, the scientists combined results from Alzheimer’s-like mouse models with analyses of human brain tissue and PET imaging data from people diagnosed with Alzheimer’s or mild cognitive impairment. Together, these lines of evidence point to immune-driven damage occurring at an early stage.

    The findings also connect to a growing push for earlier diagnosis, as newer Alzheimer’s treatments are generally aimed at earlier phases of the disease. Researchers say a better understanding of smell-related changes could help identify people who should receive further testing before cognitive symptoms become pronounced.

    Smell loss can have many causes, including aging, infections, allergies, and other neurological conditions, so it is not a stand-alone diagnostic sign. Still, the study strengthens the case that changes in olfaction may offer a practical early clue worth taking seriously in Alzheimer’s research and clinical follow-up.

  • Study of the hippocampus suggests newborn brains start densely wired, then prune connections for sharper memory

    Study of the hippocampus suggests newborn brains start densely wired, then prune connections for sharper memory

    The hippocampus, a brain region essential for forming memories and mapping space, may develop in a way that challenges the long-held idea of the mind as a blank slate. New research from the Institute of Science and Technology Austria suggests key memory circuits begin life with unusually dense wiring that is later trimmed and refined.

    In a study published in Nature Communications, scientists examined how a major hippocampal network changes after birth in mice. The team focused on CA3 pyramidal neurons, cells widely seen as central to storing and retrieving memories.

    How the CA3 circuit develops

    Using patch-clamp recordings and high-resolution imaging, researchers compared the CA3 network across early postnatal stages, adolescence, and adulthood. The methods allowed them to measure tiny electrical signals and map how strongly neurons were connected at different ages.

    The results pointed to an early-life circuit that is highly connected and seemingly random, followed by a gradual shift toward fewer but more organized links. Rather than adding connections over time, the network became more efficient by losing many of its initial ones.

    Pruning may boost memory efficiency

    Lead researcher Peter Jonas said the pattern fits a pruning model in which the system starts full and then becomes streamlined. The researchers argue that an initially exuberant network could help the hippocampus quickly integrate different kinds of sensory information into usable memories.

    If the brain started with far fewer built-in links, the team notes, neurons would first need more time to find and connect to each other, potentially slowing early information processing. The study adds to broader evidence that brain development often involves overproduction of connections followed by activity-dependent pruning.

    While the work was conducted in mice, the hippocampus is highly conserved across mammals, making the findings relevant to ongoing debates about how genetics and experience shape learning. The authors say future research will need to clarify what signals drive which connections are kept or removed, and how this process relates to memory performance.