Apoptosis in Alzheimer's disease--an update

• Published in: Apoptosis (London) 2000-02, Vol.5 (1), p.9-16
• Main Author: Shimohama, S
• Format: Article
• Language: English
• Subjects: Alzheimer Disease - pathology; Alzheimer's disease; Apoptosis; Brain - pathology; Brain Chemistry; DNA Fragmentation; Humans
• ISSN: 1360-8185; 1573-675X
• DOI: 10.1023/a:1009625323388

Alzheimer's disease (AD) is the most common human neurodegenerative disorder 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 neurodegenerative diseases, and apoptotic cell death has been found in neurons and glial cells in AD. This review summarizes the current findings regarding the evidence for apoptosis in AD and discusses the possible involvement of apoptosis-regulating factors in the pathology of AD. Modification of the apoptotic cascade could be considered as a primary therapeutic strategy for the disease.