학술논문

Neurobiological pathways to Alzheimer's disease: Amyloid-beta, TAU protein or both?
Document Type
article
Source
Dementia & Neuropsychologia. September 2009 3(3)
Subject
TAU protein
amyloid precursor protein
beta amyloid
Alzheimer's disease.
Language
English
ISSN
1980-5764
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline, including memory loss, behavioral and psychological symptoms and personality changes. The neuropathological hallmarks of AD are the presence of neuritic (senile) plaques (NP) and neurofibrillary tangles (NFT), along with neuronal loss, dystrophic neurites, and gliosis. Neuritic plaques are extracellular lesions and their main constituent is the amyloid-b42 peptide (Ab42). Neurofibrillary tangles are intracellular lesions that are mainly composed of hyperphosphorylated TAU protein. In this article, we review the major hypotheses concerning the physiopathology of AD, focusing on the b-amyloid cascade as primary events (supported by the "baptists") and cytoskeletal abnormalities secondary to the hyperphosphorylation of protein TAU (as advocated by the "Tauists"). We further provide an integrative view of the physiopathology of AD.