Study reveals how sugar-protein interactions are critical for the placenta during early pregnancy, shedding light on complications like preeclampsia and restricted fetal growth.  

In Alzheimer’s disease—the leading cause of dementia—microglia, the brain’s immune defenders, can act as both protectors and aggressors, shaping how the disease progresses. Researchers at the Max Planck Institute for Biology of Ageing in Cologne and the Icahn School of Medicine at Mount Sinai in New York, in close collaboration with The Rockefeller University, The City University of New York and multiple international partners, have identified a distinct population of neuroprotective  microglia, that may point to a new therapeutic approach for Alzheimer’s disease. In a study published in Nature, the team reports that microglia with reduced expression of the transcription factor PU.1 and co-expression of the lymphoid-like receptor CD28 act to limit neuroinflammation and to slow amyloid-plaque build-up and neurotoxic tau protein spreading in the brain, the major hallmarks of Alzheimer’s pathology.