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Abstract
Huntington’s disease, a fatal neurodegenerative disorder, is caused by the expansion of the polyglutamine (polyQ) tract near the N-terminus of huntingtin protein (htt). Expanded polyQ domains are correlated with a tendency to aggregate into oligomers and fibrils, species that are likely neurotoxic. The number of polyQ repeats is directly associated with the severity and age of onset of Huntington’s disease. The htt protein has several proposed functions, many of which are related to interactions with lipid membranes.
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