BACE1 and Alzheimer disease: A study by Schnöder et al. showed that partial deletion of the p38α MAPK reduces Aβ generation by BACE1 degradation [83], while Colié et al. reported that the downregulation of p38α in AD in vivo model improves memory, reduces Aβ deposits, and modulates astrogliosis, microglia activation, and neurogenesis [10].