Neurobiological pathways to Alzheimer's disease: Amyloid-beta, TAU protein or both?

• Autor(a) principal: Paula,Vanessa de Jesus R. de
• Data de Publicação: 2009
• Outros Autores: Guimarães,Fabiana Meira, Diniz,Breno Satler, Forlenza,Orestes Vicente
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Dementia & Neuropsychologia
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1980-57642009000300188
• topic: TAU protein; amyloid precursor protein; beta amyloid; Alzheimer's disease.

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.