Scientists at UCSF have uncovered how certain immune cells in the brain, called microglia, can effectively digest toxic amyloid beta plaques that cause Alzheimer’s. They identified a key receptor, ADGRG1, that enables this protective action. When microglia lack this receptor, plaque builds up quickly, causing memory loss and brain damage. But when the receptor is present, it seems to help keep Alzheimer's symptoms mild. Since ADGRG1 belongs to a drug-friendly family of receptors, this opens the door to future therapies that could enhance brain immunity and protect against Alzheimer’s in more people.

Extracellular vesicles (EVs) are tiny membranous structures that mediate intercellular communication. The role(s) of these vesicles have been widely investigated in the context of neurological diseases; however, their potential implications in the neuropathology subjacent to human psychiatric disorders remain mostly unknown. Here, by using next-generation discovery-driven proteomics, we investigate the potential role(s) of brain EVs (bEVs) in schizophrenia (SZ) by analyzing these vesicles from the three post-mortem anatomical brain regions: the prefrontal cortex (PFC), hippocampus (HC), and caudate (CAU). The results obtained indicate that bEVs from SZ-affected brains contain region-specific proteins that are associated with abnormal GABAergic and glutamatergic transmission.

A wound can leave a lasting imprint—even after it has healed. A new study in Current Biology finds that past injuries can quietly prime the body to overreact and be more sensitive to stress, pain and fear long after the damage is gone.

These findings may help explain how early injuries or trauma can set the stage for chronic pain conditions, where the nervous system remains hypersensitive long after the initial damage has healed. can set the stage for chronic pain conditions, where the nervous system remains hypersensitive long after the initial damage has healed.

Researchers at the University of Toronto Mississauga discovered that mice with a history of injury responded more intensely to the scent of a predator, an extremely stressful event for mice. These mice showed exaggerated fear and developed long-lasting pain in both hind paws, including the uninjured side. Strikingly, the symptoms lasted more than six months, long after the original injury had physically healed.

The implications of early telencephalic development in cortical disorders remain elusive. Here, the authors define risk gene dynamics and perturbation effects in neural stem cells, revealing vulnerability phases during early human corticogenesis.