| Cell cycle re-entry mediated neurodegeneration and its treatment role in the pathogenesis of Alzheimer's disease. | |
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MedLine Citation:
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PMID: 19114068 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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As one of the earliest pathologic changes, the aberrant re-expression of many cell cycle-related proteins and inappropriate cell cycle control in specific vulnerable neuronal populations in Alzheimer's disease (AD) is emerging as an important component in the pathogenesis leading to AD and other neurodegenerative diseases. These events are clearly representative of a true cell cycle, rather than epiphenomena of other processes since, in AD and other neurodegenerative diseases, there is a true mitotic alteration that leads to DNA replication. While the exact role of cell cycle re-entry is unclear, recent studies using cell culture and animal models strongly support the notion that the dysregulation of cell cycle in neurons leads to the development of AD-related pathology such as hyperphosphorylation of tau and amyloid-beta deposition and ultimately causes neuronal cell death. Importantly, cell cycle re-entry is also evident in mutant amyloid-beta precursor protein and tau transgenic mice and, as in human disease, occurs prior to the development of the pathological hallmarks, neurofibrillary tangles and amyloid-beta plaques. Therefore, the study of aberrant cell cycle regulation in model systems, both cellular and animal, may provide extremely important insights into the pathogenesis of AD and also serve as a means to test novel therapeutic approaches. |
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Authors:
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Hyoung-Gon Lee; Gemma Casadesus; Xiongwei Zhu; Rudy J Castellani; Andrew McShea; George Perry; Robert B Petersen; Vladan Bajic; Mark A Smith |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review Date: 2008-12-09 |
Journal Detail:
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Title: Neurochemistry international Volume: 54 ISSN: 0197-0186 ISO Abbreviation: Neurochem. Int. Publication Date: 2009 Feb |
Date Detail:
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Created Date: 2009-02-23 Completed Date: 2009-05-01 Revised Date: 2010-12-03 |
Medline Journal Info:
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Nlm Unique ID: 8006959 Medline TA: Neurochem Int Country: England |
Other Details:
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Languages: eng Pagination: 84-8 Citation Subset: IM |
Affiliation:
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Department of Pathology, Case Western Reserve University, Cleveland, OH, USA. hyoung-gon.lee@case.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Alzheimer Disease
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pathology*,
therapy* Amyloid beta-Peptides / metabolism, physiology Cell Cycle / physiology* Cell Death / physiology Humans Nerve Degeneration / pathology* Oxidative Stress / physiology Presenilins / metabolism, physiology tau Proteins / metabolism, physiology |
| Grant Support | |
ID/Acronym/Agency:
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R01 AG028679-01A2/AG/NIA NIH HHS; R21 AG030096-02/AG/NIA NIH HHS; R21 AG031364-02/AG/NIA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Amyloid beta-Peptides; 0/Presenilins; 0/tau Proteins |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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