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.