A role for Kalirin-7 in corticostriatal synaptic dysfunction in Huntington's disease.

ABSTRACT: Cognitive dysfunction is an early clinical hallmark of Huntington's disease (HD) preceding the appearance of motor symptoms by several years. Neuronal dysfunction and altered corticostriatal connectivity have been postulated to be fundamental to explain these early disturbances. However, no treatments to attenuate cognitive changes have been successful: the reason may rely on the idea that the temporal sequence of pathological changes is as critical as the changes per se when new therapies are in development. To this aim, it becomes critical to use HD mouse models in which cognitive impairments appear prior to motor symptoms. In this study, we demonstrate procedural memory and motor learning deficits in two different HD mice and at ages preceding motor disturbances. These impairments are a

SUBMITTER: Puigdellivol M 

PROVIDER: S-EPMC4664166 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature