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ShareScienceDaily (Feb. 23, 2009) — Dr. Mark Smith and colleagues at Case Western Reserve University found that dysregulated cell cycle control may contribute to neural cell death.
Neurodegeneration consists of the progressive loss of structure or function of neurons, often resulting in neural cell death. The causes of cell death in neurodegenerative diseases such as Alzheimer's and Parkinson's are incompletely understood. Mature neurons in healthy individuals do not divide; however, degenerating neurons express a protein, c-Myc (Myc), which regulates cell division.
Lee et al therefore explored the role of re-entry into the cell cycle, leading to cell division, in the neurodegenerative pathogenesis. They found that expression of Myc in forebrain neurons resulted in cell cycle re-entry. Furthermore, Myc expression resulted in neural cell death and cognitive defects. Neurodegeneration, therefore, may be a disease of dysregulated cell-cycle control, and cell-cycle regulators should be explored as future treatment targets.
Dr. Lee and colleagues "strengthen [their] hypothesis that neurodegeneration in [Alzheimer's disease], like cellular proliferation in cancer, is a disease of inappropriate cell cycle control." They "establish a model [that] provides a working platform to test genetic and pharmacologic approaches to block cycle re-entry" and thus explore new methods of treating neurodegenerative diseases.
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The above story is reprinted from materials provided by American Journal of Pathology, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Lee et al. The Neuronal Expression of MYC Causes a Neurodegenerative Phenotype in a Novel Transgenic Mouse. American Journal Of Pathology, 2009; 174 (3): 891 DOI: 10.2353/ajpath.2009.080583
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
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