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- W29386424 abstract "Huntington’s disease (HD) is a devastating neurodegenerative disease characterized by involuntary choreiform movements, psychiatric disturbances, behavioral changes, cognitive abnormalities of the frontal-type, as well as dementia (1). The age of onset is usually between the third and fifth decade of life, although juvenile ( 65 yr of age) cases do occur (2). HD is an autosomal dominant, fully penetrant, genetic defect on the short arm of chromosome 4, specifically at the IT 15 gene locus (3). The genetic defect on chromosome 4 results in an increased number of repeats (>39) encoding polyglutamine tracts (CAG). The gene encodes for the protein huntingtin. Intranuclear inclusions are found in cortical and striatal neurons in postmortem tissue of HD patients as a result of the polyglutamine-expanded N-terminal region of mutant huntingtin suggesting that aggregation of this protein may be involved in the pathogenesis of HD (4). Recently, CAG expansion has been shown to activate caspase-8, a known trigger of apoptotic cell death (5). However, the specific mechanism(s) by which the polyglutamine expansion damages and ultimately destroys neurons remains to be established." @default.
- W29386424 created "2016-06-24" @default.
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- W29386424 date "2003-01-01" @default.
- W29386424 modified "2023-09-23" @default.
- W29386424 title "Cyclosporin A Protects Striatal Neurons from Mitochondrial Dysfunction" @default.
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- W29386424 doi "https://doi.org/10.1007/978-1-59259-315-6_8" @default.
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