Well, the huntingtin gene gained a function that caused evasion of proteolysis and accumulation as inclusions. Aggregation efficiency of polyQ into the nucleus varies with severity and onset of disease. Note that aggregation in the cytoplasm is a cell-protective mechanism to evade huntingtin-induced cell death.
"When transfected into cultured striatal neurons, mutant huntingtin induced neurodegeneration by an apoptotic mechanism."
So, I guess your question is, where else besides the striatum?
"In the second family, several members had cerebellar signs as well as chorea and dementia; MRI and CT showed
olivopontocerebellar and striatal atrophy."
"Petersen et al. (2005) described a dramatic atrophy and loss of orexin (HCRT; 602358)-producing neurons in the lateral hypothalamus of R6/2 Huntington mice and in Huntington patients. Similar to animal models and patients with impaired orexin function, the R6/2 mice were narcoleptic."
"Although the HD mRNA and protein product show widespread distribution, the progressive neurodegeneration is selective in location, with regional neuron loss and gliosis in striatum, cerebral cortex, thalamus, subthalamus, and hippocampus. Reddy et al. (1998) created an experimental animal model in transgenic mice that showed widespread expression of full-length human HD cDNA with either 16, 48, or 89 CAG repeats. Only mice with 48 or 89 CAG repeats manifested progressive behavioral and motor dysfunction with neuron loss and gliosis in striatum, cerebral cortex, thalamus, and hippocampus."
http://omim.org/entry/143100
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Although I am sorry to say that the hypothesis of degeneration in the nbMeynert has been refuted
"The nucleus basalis of Meynert (nbM) provides most of the cholinergic input to the cerebral cortex. The loss of cortical choline acetyltransferase (CAT) activity in Alzheimer's disease (AD) and senile dementia of the Alzheimer's type (SDAT) appears to be related to a severe depopulation of the nbM in this dementia. In Huntington's disease (HD), by contrast, there is no loss of cortical CAT activity. The present quantitative study indicates that (1) there is no significant loss of neurons from the nbM in HD, and (2) that the previously described cytologic changes in the neurons of this nucleus in HD patients do not differ significantly from controls. These findings are consistent with the working hypothesis that the types of dementia associated with reductions of neocortical CAT activity are characterized by dysfunction or death of neurons in the nbM, but dementing disorders with normal neocortical CAT activity manifest no major abnormalities in this cholinergic nucleus of the basal forebrain."