To obtain direct evidence supporting the theory that the postsynaptic density (PSD) in neuronal synapses is formed via phase separation, Chen et al. purified and characterized the native PSD from the mouse brain. Their results demonstrate that the native PSD has characteristic features of biological condensates formed via phase separation.
Procrastination, the tendency to unnecessarily delay or put off tasks even if this will have negative consequences, is a common behavior for many people. While occasionally delaying or putting off bothersome tasks is not necessarily problematic, severe and prolonged procrastination is closely tied to some neuropsychiatric disorders, including attention-deficit/hyperactivity disorder (ADHD) and anxiety disorders.
Unveiling patterns in the brain’s structure and genetic factors linked to procrastination could help to reliably uncover this tendency to postpone tasks in affected individuals. This could in turn inform the development of preventative strategies or interventions that tackle procrastination early, before it exacerbates other underlying mental health disorders.
Researchers at the Chinese Academy of Sciences and other institutes in China recently carried out a study aimed at shedding new light on the biological and genetic roots of procrastination. Their paper, published in Molecular Psychiatry, outlines specific patterns in the brain’s structure during adolescence that are linked to procrastination in adulthood.
The prenatal period is a critical window for brain development, yet few studies have examined the impact of air pollution exposure during pregnancy on child cognition. A new study led by the Barcelona Institute for Global Health (ISGlobal), in collaboration with the University of Barcelona (UB), shows that prenatal exposure to pollution is associated with lower cognitive performance in newborns.
These findings highlight the importance of reducing air pollution exposure, especially during pregnancy, to protect neurodevelopment.
The study, published in Environmental Pollution, included data from 168 mother-child pairs participating in the BiSC (Barcelona Life Study Cohort) project, conducted in Barcelona between 2018 and 2023.
Individuals with psychiatric disorders exhibiting seemingly similar symptoms often respond very differently to the same treatment, suggesting that distinct biological processes are at work beneath the surface of similar clinical presentations. Researchers have now identified a distinct immuno-inflammatory biomarker across major psychiatric disorders that can be detected using non-invasive brain imaging. Patients exhibiting this brain signature showed systemic inflammation and poorer response to standard treatments. The findings of the new study in Biological Psychiatry, published by Elsevier, lay the foundation for a biology-augmented diagnostic framework in psychiatry and detail the potential for biomarker-guided, anti-inflammatory precision therapies.
Neuroimaging links diverse biological mechanisms to clinical manifestations, providing compelling insights into the neural mechanisms underlying brain function implicated in psychiatric diseases. Through neuroimaging, shared neural correlates have been increasingly identified across major psychiatric disorders such as schizophrenia, major depressive disorder, and bipolar disorder. While subtypes within and across psychiatric diagnoses have been identified, the biological underpinnings remain unclear. This study aimed to uncover these hidden “biotypes,” focusing particularly on brain inflammation—a mechanism thought to drive illness in a subset of patients, but which is difficult to measure directly in the living brain.
The research was conducted in two independent cohorts. In the first stage, brain connectivity scans were combined with blood-based molecular (DNA methylation) data to identify a brain network pattern linked to immune system dysfunction. In the second longitudinal stage, investigators validated that patients with this brain marker had higher blood inflammation indices—such as neutrophil-to-lymphocyte ratios—and showed less improvement with conventional treatments during hospitalization.
The human brain contains billions of connected neurons that collectively support different mental functions, including the processing of sensory information, the encoding of memories, attention processes, and decision-making. For a long time, neuroscientists have assumed the position of specific neurons in the brain plays a key role in the brain’s connectivity and proper functioning.
Researchers at University of Geneva, INSERM, Ecole Polytechnique Fédérale de Lausanne and other institutes recently gathered evidence that contradicts this long-standing assumption, showing misplaced neurons can still retain their “identity,” connect with other neurons and support the processing of sensory information.
Their paper, published in Nature Neuroscience, could reshape the present understanding of developmental disorders and other conditions linked to the rearrangement of neurons or cortical malformations.
The shared pathways were linked to neuron maturation, synapse formation, and the control of gene activity. Further analysis pointed to a group of genes involved in organizing DNA and regulating which genes are switched on or off. These genes sit high in the regulatory chain, influencing many downstream processes previously linked to autism.
To test whether this network played an active role, the team reduced the activity of several key regulators using CRISPR-based methods in neural cells. This led to downstream changes similar to those seen in the autism models.
However, organoids from individuals with idiopathic autism showed less consistent changes, likely reflecting the complex and distributed genetic risk seen in most autism cases.
Lysosomes degrade damaged organelles and macromolecules to recycle nutrient components. Lysosomal storage diseases (LSDs) are linked to mutations of genes encoding lysosomal proteins and may lead to age-related disorders, including neurodegenerative diseases. But, how lysosomal dysfunction contributes to neurodegenerative diseases is not clear yet…
The researchers identify CLN3 (ceroid lipofuscinosis, neuronal 3), linked to Batten disease as a conserved lysosomal protein that regulates lysosomal chloride homeostasis, pH, and protein degradation.
Curcumin analog C1 is a natural compound with anti-inflammatory properties could enhance CLN3 activity and improve lysosomal function by activating TFEB. sciencenewshighlights ScienceMission https://sciencemission.com/CLN3-n-chloride-efflux-n-lysosomes
Wang et al. identify CLN3 as a conserved lysosomal protein that regulates lysosomal chloride homeostasis, pH, and protein degradation. Transcription factor EB (TFEB) activation enhances CLN3 function, revealing the TFEB-CLN3 signaling axis as a promising therapeutic target for lysosomal storage disorders.
As Rest of World reports, rising anxiety over the influence of AI, on top of already-grueling 90-hour workweeks, has proven devastating for workers. While it’s hard to single out a definitive cause, a troubling wave of suicides among tech workers highlights these unsustainable conditions.
Complicating the picture is a lack of clear government data on the tragic deaths. While it’s impossible to tell whether they are more prevalent among IT workers, experts told Rest of World that the mental health situation in the tech industry is nonetheless “very alarming.”
The prospect of AI making their careers redundant is a major stressor, with tech workers facing a “huge uncertainty about their jobs,” as Indian Institute of Technology Kharagpur senior professor of computer science and engineering Jayanta Mukhopadhyay told Rest of World.