Abstract:
:Huntington's disease (HD), a dominantly inherited neurodegenerative disease, is defined by its genetic cause, a CAG-repeat expansion in the HTT gene, its motor and psychiatric symptomology and primary loss of striatal medium spiny neurons (MSNs). However, the molecular mechanisms from genetic lesion to disease phenotype remain largely unclear. Mouse models of HD have been created that exhibit phenotypes partially recapitulating those in the patient, and specifically, cortico-striatal disconnectivity appears to be a shared pathogenic event shared by HD mouse models and patients. Molecular studies have begun to unveil converging molecular and cellular pathogenic mechanisms that may account for cortico-striatal miscommunication in various HD mouse models. Systems biological approaches help to illuminate synaptic molecular networks as a nexus for HD cortio-striatal pathogenesis, and may offer new candidate targets to modify the disease.
journal_name
Curr Opin Neurobioljournal_title
Current opinion in neurobiologyauthors
Veldman MB,Yang XWdoi
10.1016/j.conb.2017.10.019subject
Has Abstractpub_date
2018-02-01 00:00:00pages
79-89eissn
0959-4388issn
1873-6882pii
S0959-4388(17)30230-1journal_volume
48pub_type
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