Access Restriction

Author André, Véronique M. ♦ Cummings, Damian M. ♦ Holley, Sandra M. ♦ Levine, Michael S. ♦ Cepeda, Carlos
Source Directory of Open Access Journals (DOAJ)
Content type Text
Publisher SAGE Publishing
File Format PDF
Date Created 2010-05-24
Copyright Year ©2010
Language English
Subject Domain (in LCC) RC321-571
Subject Keyword Neuropsychiatry ♦ Biological psychiatry ♦ Neurosciences ♦ Internal medicine ♦ Medicine
Abstract The discovery of the HD (Huntington's disease) gene in 1993 led to the creation of genetic mouse models of the disease and opened the doors for mechanistic studies. In particular, the early changes and progression of the disease could be followed and examined systematically. The present review focuses on the contribution of these genetic mouse models to the understanding of functional changes in neurons as the HD phenotype progresses, and concentrates on two brain areas: the striatum, the site of most conspicuous pathology in HD, and the cortex, a site that is becoming increasingly important in understanding the widespread behavioural abnormalities. Mounting evidence points to synaptic abnormalities in communication between the cortex and striatum and cell-cell interactions as major determinants of HD symptoms, even in the absence of severe neuronal degeneration and death.
ISSN 17590914
Age Range 18 to 22 years ♦ above 22 year
Educational Use Research
Education Level UG and PG ♦ Career/Technical Study
Learning Resource Type Article
Publisher Date 2010-03-01
e-ISSN 17590914
Journal ASN Neuro
Volume Number 2
Issue Number 2

Source: Directory of Open Access Journals (DOAJ)