Mitochondrial Dysfunction, Endoplasmic Reticulum Stress, and Apoptosis in Alzheimer's Disease

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  • Takuma Kazuhiro
    Laboratory of Neuropsychopharmacology, Graduate School of Natural Science and Technology, Kanazawa University
  • Yan Shirley ShiDu
    Departments of Surgery and Pathology, College of Physicians and Surgeons, Columbia University
  • Stern David M.
    Dean’s Office, Medical College of Georgia
  • Yamada Kiyofumi
    Laboratory of Neuropsychopharmacology, Graduate School of Natural Science and Technology, Kanazawa University

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Abstract

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.<br>

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