Schizophrenia stems from abnormal brain development, which can begin even before birth. Yet symptoms typically don’t appear until later in life.
“For a long time, the brain is able to compensate for developmental errors and maintain relatively normal function. But at some point, it’s like a chain snapping — the brain can no longer compensate, and that’s when symptoms emerge. Until that point, however, prevention should be possible,” says one of the study’s first authors.
They investigated when this turning point occurs. By tracking brain development from the fetal stage to adulthood, they found that dramatic changes happen late in the brain’s development. Up until the transition from childhood to adolescence, molecular and functional changes in the brain were rather minor, likely explaining lack of symptoms before adolescence.
The researchers have worked with mice carrying a specific genetic mutation known as “15q13.3 microdeletion syndrome.” In humans, this syndrome is associated with epilepsy, schizophrenia, autism, and other neurodevelopmental disorders.
“We know that sleep is often disrupted in people with psychiatric disorders, so we chose to use sleep as a behavioral marker—something we could observe. We examined both the mice’s behavior and the activity of a specific type of brain cell. Our findings show that one particular cell type (γ-aminobutyric acid (GABAergic) projecting neurons) is significantly affected in the test animals compared to healthy mice,” explains the author.
These GABAergic rare brain cells are often overlooked because they make up only a tiny fraction of the brain’s total cell population. Nevertheless, they play a crucial role in regulating many brain functions.
The new study not only demonstrates a link between this specific type of brain cell and sleep — it also shows that the mice’s sleep patterns began to resemble those of healthy mice when researchers reduced the activity of the cell type in question.
Higher levels of fine particulate matter air pollution was associated with increased dementia severity and increased Alzheimer disease neuropathologic change.
Importance Exposure to fine particulate matter air pollution (PM2.5) may increase risk for dementia. It is unknown whether this association is mediated by dementia-related neuropathologic change found at autopsy.
Objective To examine associations between PM2.5 exposure, dementia severity, and dementia-associated neuropathologic change.
Design, Setting, and Participants This cohort study used data associated with autopsy cases collected from 1999 to 2022 at the Center for Neurodegenerative Disease Research Brain Bank at the University of Pennsylvania. Data were analyzed from January to June 2025. Participants included 602 cases with common forms of dementia and/or movement disorders and older controls after excluding 429 cases with missing data on neuropathologic measures, demographic factors, APOE genotype, or residential address.
Researchers at Karolinska Institutet in Sweden have identified a brain circuit that can drive repetitive and compulsive behaviors in mice, even when natural rewards such as food or social contact are available. The study has been published in the journal Science Advances and may contribute to increased knowledge about obsessive-compulsive disorder and addiction.
Both animals and humans can become stuck in certain behaviors, but exactly how this is regulated in the brain has been unknown. Now, researchers have been able to show that a specific nerve circuit in the brain can put behaviors into a kind of “repeat mode,” where mice continue to perform the same actions over and over again, even when there is no longer any reward.
The researchers investigated a neural circuit that runs from the nucleus accumbens, part of the brain’s reward system, to a region in the hypothalamus, which in turn is connected to the lateral habenula, an area that processes unpleasant experiences. By activating this circuit using optogenetics, a method in which nerve cells are controlled by light, the researchers were able to induce a negative state in mice that led to repetitive behaviors such as digging and sniffing—even when food or other rewards were available.
These images have been selected to showcase the art that neuroscience research can create.
As described by the authors: The cacophony voltage-gated calcium channel serves as the primary conduit for the calcium that triggers neurotransmitter release at countless synapses across the fruit fly (Drosophila) nervous system. To support this role at different synapse types, alternate splicing confers different biophysical properties upon cacophony. However, conventional techniques that might discriminate splice isoforms, such as antibodies, toxins, and pharmacological agents, are poorly suited for identifying splice isoforms across multiple neurons in a living nervous system.
This image demonstrates the transgenic expression of a bichromatic fluorescent exon reporter in most neurons of the fly brain. Green fluorescent protein (GFP) fluorescence was particularly bright relative to red fluorescent protein (TagRFP) in the α, β, and γ lobes of the mushroom body (MB), indicating a bias towards the inclusion of exon 11 at the expense of exon 10. Differences were also evident between neurons of the optic lobes.
Researchers at the Paul Scherrer Institute PSI have clarified how spermine—a small molecule that regulates many processes in the body’s cells—can guard against diseases such as Alzheimer’s and Parkinson’s: It renders certain proteins harmless by acting a bit like cheese on noodles, making them clump together. This discovery could help combat such diseases. The study has now been published in the journal Nature Communications.
Our life expectancy keeps rising—and as it does, age-related illnesses, including neurodegenerative diseases such as Alzheimer’s and Parkinson’s, are becoming increasingly common. These diseases are caused by accumulations in the brain of harmful protein structures consisting of incorrectly folded amyloid proteins. Their shape is reminiscent of fibers or spaghetti. To date, there is no effective therapy to prevent or eliminate such accumulations.
Yet a naturally occurring molecule in the body called spermine offers hope. In experiments, researchers led by study leader Jinghui Luo, in the Center for Life Sciences at the Paul Scherrer Institute PSI, have discovered that this substance is capable of extending the lifespan of small nematode worms, improving their mobility in old age, and strengthening the powerhouses of their cells—the mitochondria. Specifically, the researchers observed how spermine helps the body’s immune system eliminate nerve-damaging accumulations of amyloid proteins.
The CDC website now says: “The claim ‘vaccines do not cause autism’ is not an evidence-based claim…” Psychologist David Myers from Hope College summarizes the relevant evidence.
You are an educated reader, so I know that you know that vaccines do not cause autism. However, you probably have also read headlines such as the recent U.S. Health and Human Services release, “Autism Epidemic Runs Rampant.”
A meta-analysis of RCTs found high uptake (92%) but moderate adherence (62%) to mental health apps among participants with depression or anxiety; posttest attrition averaged 18% and follow-up attrition 28%. Trials that included reminders, human contact, and omitted gamification saw lower dropout rates.
Question What are the expected rates of uptake, attrition, and adherence in randomized clinical trials of mental health apps for depression and anxiety?
Findings This systematic review and meta-analysis of 79 randomized trials found high rates of app uptake (94%) and moderate adherence (62%) among participants with depression or anxiety. Posttest attrition averaged 17%, and follow-up attrition was 27%.
Meaning These findings highlight the need to optimize app design and trial protocols to improve engagement and reduce attrition in digital interventions for depression and anxiety.
Researchers at Tulane University, with a team of colleagues from eight other universities, have discovered a new nerve cell signaling mechanism that could transform our understanding of pain and lead to safer, more effective treatments.
The study, co-led by Matthew Dalva, director of the Tulane Brain Institute and professor of cell and molecular biology in the School of Science and Engineering and Ted Price at the University of Texas at Dallas, reveals that neurons can release an enzyme outside the cell that switches on pain signaling after injury. The work, published in Science, offers new insight into how brain cells strengthen their connections during learning and memory.
“This finding changes our fundamental understanding of how neurons communicate,” Dalva said. “We’ve discovered that an enzyme released by neurons can modify proteins on the outside of other cells to turn on pain signaling—without affecting normal movement or sensation.”