How Misfiring of Striatal Cholingeric Interneurons Can Explain Early Cognitive Deficits in Huntington's Disease
Material below summarizes the article Enhanced GABAergic Inputs Contribute to Functional Alterations of Cholinergic Interneurons in the R6/2 Mouse Model of Huntington’s Disease, published on February 24, 2015, in eNeuro and authored by Sandra M. Holley, Prasad R. Joshi, Anna Parievsky, Laurie Galvan, Jane Y. Chen, Yvette E. Fisher, My N. Huynh, Carlos Cepeda, and Michael S. Levine.
Huntington’s disease (HD) is an inheritable neurological disorder caused by a triplet repeat (CAG) expansion in the huntingtin (HTT) gene located in the short arm of chromosome four. Symptoms include uncontrollable dance-like movements (chorea), cognitive deficits, and psychiatric disturbances. Some of the early, or prodromic, symptoms include an inability to shift attention and other behavioral inflexibilities.
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