alzheimer

parp

alzheimer_55461

alzheimer_108136

dressings

debriefing

alzheimer_34652

alzheimer_115240

vigorous

bees_66826

alzheimer_83063

radiation exposure

tuned mass

upper triangular

precursor protein

beta-amyloid

foraging areas

amyloid deposition

ad pathogenesis

Molecules

The amyloid hypothesis of Alzheimer's disease has long been the predominant theory, suggesting that Alzheimer's disease is caused by the accumulation of amyloid beta protein (Aβ) in the brain, leading to neuronal toxicity in the central nervous system (CNS). Because of breakthroughs in molecular medicine, the amyloid pathway is thought to be central to the pathophysiology of Alzheimer's disease (AD). Currently, it is believed that altered biochemistry of the Aβ cycle remains a central biological feature of AD and is a promising target for treatment. This review provides an overview of the process of amyloid formation, explaining the transition from amyloid precursor protein to amyloid beta protein. Moreover, we also reveal the relationship between autophagy, cerebral blood flow, ACHE, expression of LRP1, and amyloidosis. In addition, we discuss the detailed pathogenesis of amyloidosis, including oxidative damage, tau protein, NFTs, and neuronal damage. Finally, we list some ways to treat AD in terms of decreasing the accumulation of Aβ in the brain.

Amyloidosis in Alzheimer’s Disease: Pathogeny, Etiology, and Related Therapeutic Directions