Mitochondrial dysfunction, endoplasmic reticulum stress, and apoptosis in Alzheimer's disease

Kazuhiro Takuma, Shirley Shi Du Yan, David M. Stern, Kiyofumi Yamada

研究成果: ジャーナルへの寄稿総説査読

128 被引用数 (Scopus)

抄録

Alzheimer's disease (AD) is the most common neurodegenerative disorder of late life characterized by insidious, chronic, and progressive memory impairment in association with the accumulation of senile plaques, neurofibrillary tangles, and massive loss of neurons. Apoptosis is believed to be an important contributor to progression and pathology of neurodegeneration in AD. There is considerable evidence that amyloid β-peptide, a major component of senile plaques, has the capacity to activate intracellular apoptosis pathways leading to neuronal cell death. AD-related mutations in genes coding presenilins are also shown to cause neuronal apoptosis, by directly and indirectly regulating apoptotic signaling cascades. Recent evidence suggests that two intrinsic pathways, mitochondrial dysfunction and endoplasmic reticulum stress, are central in the execution of apoptosis in AD. This review summarizes recent progress of research in this field focused on the molecular mechanisms involved in neuronal apoptosis mediated by organelle dysfunction.

本文言語英語
ページ(範囲)312-316
ページ数5
ジャーナルJournal of Pharmacological Sciences
97
3
DOI
出版ステータス出版済み - 03-2005
外部発表はい

All Science Journal Classification (ASJC) codes

  • 分子医療
  • 薬理学

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