Alzheimer's disease (AD),a degenerative neurological disorder,is the most common form of dementia among older people,whose symptoms include gradual memory loss,cognitive impairments and deterioration of language skills.Amyloid precursor protein (APP) is cleaved by serials of secretases and generates Aβ,sAPPα/β and APP intracellular domain (AICD).Aβ forms amyloid plaques,together with neurofibrillary tangles (NFTs) which is comprised with hyperphosphorylated tau,are hallmarks ofAD.Aβ,especially in its oligomeric form,plays important roles in AD,causing cell death,calcium influx,loss of spines and repression of long-term potentiation (LTP)[1].However,recent studies indicate that in addition to Aβ,other fragments of APP after its cleavage,such as AICD,play essential roles in AD as well.In this article,the function of AICD and its underlying mechanisms will be reviewed.