Effects of Rhes Prenylation on Mouse Cognition in a 3-Nitropropionic Acid Animal Model of Huntington's Disease
Located on the short arm of chromosome 4, there exists a gene, IT15, responsible for the trinucleotide CAG expansion involved in the autosomal dominant neurodegenerative disorder known as Huntington’s disease (HD). The brain region associated with the most atrophy, the striatum, leads to expression...
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| Format: | Others |
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ScholarWorks@UNO
2015
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| Online Access: | http://scholarworks.uno.edu/td/1977 http://scholarworks.uno.edu/cgi/viewcontent.cgi?article=3031&context=td |
| Summary: | Located on the short arm of chromosome 4, there exists a gene, IT15, responsible for the trinucleotide CAG expansion involved in the autosomal dominant neurodegenerative disorder known as Huntington’s disease (HD). The brain region associated with the most atrophy, the striatum, leads to expression of severe motor dysfunction, the hallmark feature of HD. To a lesser degree, the cortex and hippocampus show earlier deterioration indicative of the cognitive deficits that occur prior to motor symptom onset. The brain regions associated with HD-induced neuronal death additionally selectively express the protein Rhes - the combination of Rhes and mutant huntingtin being cytotoxic. Using a 3-nitropropionic acid animal model of HD, we hypothesized that animals with preserved prenylation of Rhes would display cognitive and motor symptomology similar to genetic models of HD while animals administered statins or bisphosphonates would show inhibited Rhes prenylation and delayed cognitive symptoms. Experimental animals, however, did not perform differently than control animals on shallow water variants of the t-maze and MWM. |
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