Abstract:
:Abnormal expansion of a polyglutamine tract in huntingtin (Htt) protein results in Huntington's disease (HD), an autosomal dominant neurodegenerative disorder involving progressive loss of motor and cognitive function. Contrasting with the ubiquitous tissue expression of polyglutamine-expanded Htt, HD pathology is characterized by the increased vulnerability of specific neuronal populations within the striatum and the cerebral cortex. Morphological, biochemical, and functional characteristics of neurons affected in HD that might render these cells more vulnerable to the toxic effects of polyglutamine-Htt are covered in this review. The differential vulnerability of neurons observed in HD is discussed in the context of various major pathogenic mechanisms proposed to date, and in line with evidence showing a 'dying-back' pattern of degeneration in affected neuronal populations.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Han I,You Y,Kordower JH,Brady ST,Morfini GAdoi
10.1111/j.1471-4159.2010.06672.xsubject
Has Abstractpub_date
2010-06-01 00:00:00pages
1073-91issue
5eissn
0022-3042issn
1471-4159pii
JNC6672journal_volume
113pub_type
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