The brain has its own immune system, which detects threats and mounts a defense. A growing body of evidence has shown that in Alzheimer’s disease, those immune cells are chronically overactivated, causing inflammation that damages the connections between brain cells. Now, in a preclinical study using human Alzheimer’s brain cells, scientists at Scripps Research have identified a molecular switch—and potential drug target—responsible for driving that chronic inflammation. 

UCLA researchers created a single-cell map of the developing human neocortex in Down syndrome during a critical window of prenatal brain development, finding that the condition alters the developmental tempo of neurogenesis.