Mitochondrial Dysfunction, Endoplasmic Reticulum Stress, and Apoptosis in Alzheimer’s Disease
スポンサーリンク
概要
- 論文の詳細を見る
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 ER 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.
- 社団法人 日本薬理学会の論文
著者
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YAMADA Kiyofumi
Laboratory of Neuropsychopharmacology, Division of Pharmaceutical Sciences, Graduate School of Natur
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Takuma K
Laboratory Of Molecular Neuropharmacology Graduate School Of Pharmaceutical Sciences Osaka Universit
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Takuma Kazuhiro
Laboratory Of Neuropsychopharmacology Graduate School Of Natural Science And Technology Kanazawa Uni
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Yamada Kiyofumi
Laboratory Of Experimental Therapeutics Department Of Clinical Pharmacy Faculty Of Pharmaceutical Sc
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YAN Shirley
Departments of Surgery and Pathology, College of Physicians and Surgeons, Columbia University
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Stern David
Dean’s Office, Medical College of Georgia
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Takuma Kazuhiro
Laboratory Of Molecular Neuropharmacology Graduate School Of Pharmaceutical Sciences Osaka Universit
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Yan Shirley
Departments Of Surgery And Pathology College Of Physicians And Surgeons Columbia University
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Takuma Kazuhiro
Laboratory Of Medicinal Pharmacology Graduate School Of Pharmaceutical Sciences Osaka University
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Takuma Kazuhiro
Laboratory of Neuropsychopharmacology, Graduate School of Natural Science and Technology, Kanazawa University
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