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Effects Of Pharmacological De-Prenylation Of Rhes On Motor Behavior In A Beta-Nitropropionic Acid Animal Model Of Huntington's Disease, Ashley Whitmarsh
Effects Of Pharmacological De-Prenylation Of Rhes On Motor Behavior In A Beta-Nitropropionic Acid Animal Model Of Huntington's Disease, Ashley Whitmarsh
University of New Orleans Theses and Dissertations
Huntington’s disease (HD) is a heritable, neurodegenerative disorder characterized by motor, cognitive, and psychiatric disturbances. The progressive disease is caused by an unstable CAG expansion within the gene that normally encodes for the huntingtin protein (Htt). The expanded mutant form of Htt (mHtt) is expressed ubiquitously throughout patients’ bodies; however, neuronal degeneration is prominent only in the corpus striatum and, to a lesser extent, the cortex. The Ras homolog Rhes is also preferentially localized to the striatum. The putative co-factor Rhes has been shown to act with mHtt to cause neuronal death. Simvastatin, a lipid lowering drug, and zoledronate, a …
Effects Of Rhes Prenylation On Mouse Cognition In A 3-Nitropropionic Acid Animal Model Of Huntington's Disease, Diana Hobbs
Effects Of Rhes Prenylation On Mouse Cognition In A 3-Nitropropionic Acid Animal Model Of Huntington's Disease, Diana Hobbs
University of New Orleans Theses and Dissertations
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. …