期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
卷 1772, 期 4, 页码 457-466出版社
ELSEVIER
DOI: 10.1016/j.bbadis.2006.10.002
关键词
Alzheimer; ataxia telangiectsia; cell cycle; neurodegeneration; APP mouse; atm-deficient mouse
资金
- NIA NIH HHS [P50 AG008012, P50 AG008012-16S2, AG08012] Funding Source: Medline
- NINDS NIH HHS [R01 NS020591, NS20591, R01 NS020591-23] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS020591] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P50AG008012] Funding Source: NIH RePORTER
Cell cycle events have been documented to be associated with several human neurodegenerative diseases. This review focuses on two diseases - Alzheimer's disease and ataxia telangiectasia - as well as their mouse models. Cell cycle studies have shown that ectopic expression of cell cycle markers is spatially and regional correlated well with neuronal cell death in both disease conditions. Further evidence of ectopic cell cycling is found in both human diseases and in its mouse models. These findings suggest that loss of cell cycle control represents a common pathological root of disease, which underlies the defects in the affected brain tissues in both human and mouse. Loss of cell cycle control is a unifying hypothesis for inducing neuronal death in CNS. In the disease models we have examined, cell cycle markers appear before the more well-recognized pathological changes and thus could serve as early stress markers-outcome measures for preclinical trials of potential disease therapies. As a marker these events could serve as a new criterion in human pathological diagnosis. The evidence to date is compatible with the requirement for a second hit for a neuron to progress cell cycle initiation and DNA replication to death. If this were true, any intervention of blocking 'second' processes might prevent or slow the neuronal cell death in the process of disease. What is not known is whether, in an adult neuron, the cell cycle event is part of the pathology or rather a desperate attempt of a neuron under stress to protect itself. (c) 2006 Elsevier B.V. All rights reserved.
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