Acidification Deficiency of Autolysosomes Induces Neuronal Autophagic Amyloid-βPlaques in Alzheimer's Disease

Alzheimer's disease(AD),a degenerative disease of the central nervous system,is characterized by progressive cognitive dysfunction and behavioral impairment.AD has been linked to the formation of amyloid-β(Aβ)plaque deposits and neurofibrillary tangles(NFTs)in the brain[1].The aggregation of Aβmay repress the signal transmission of synapses between neurons,while tau tangles,the main components of NFTs,hinder the trafficking of nutrients and other molecules that are critical to normal function and neuronal survival.It has been reported that the deposition of Aβand the tangles of tau protein can activate microglia in the brain,during which balance cannot be maintained,chronic inflammation occurs,and the brain function of AD patients may be further impaired[2].As the mainstream theories,Aβand tau protein continue to be studied.Although researchers have mainly focused on the toxic effects of pathological factors such as Aβ,tau protein,and inflammatory factors,the physiological significance in pathological states and generative processes have rarely been considered.