Apoptosis in Alzheimer's disease - an update

Authors
Citation
S. Shimohama, Apoptosis in Alzheimer's disease - an update, APOPTOSIS, 5(1), 2000, pp. 9-16
Citations number
89
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cell & Developmental Biology
Journal title
APOPTOSIS
ISSN journal
1360-8185 → ACNP
Volume
5
Issue
1
Year of publication
2000
Pages
9 - 16
Database
ISI
SICI code
1360-8185(200002)5:1<9:AIAD-A>2.0.ZU;2-T
Abstract
Alzheimer's disease (AD) is the most common human neurodegenerative disorde r characterized by the progressive deterioration of cognition and memory in association with the presence of senile plaques, neurofibrillary tangles, and massive loss of neurons. Most cases of AD are late-onset and sporadic, but in some cases the disease is inherited as an autosomal dominant trait. Four different genes, the amyloid precursor protein, apolipoprotein E, and presenilins 1 and 2 have been implicated in the etiology of familial AD. It is now generally accepted that massive neuronal death due to apoptosis is a commmon characteristic in the brains of patients suffering from neurodege nerative diseases, and apoptotic cell death has been found in neurons and g lial cells in AD. This review summarizes the current findings regarding the evidence for apoptosis in AD and discusses the possible involvement of apo ptosis-regulating factors in the pathology of AD. Modification of the apopt otic cascade could be considered as a primary therapeutic strategy for the disease.