The nucleus basalis in huntington’s disease

Arthur W. Clark, Irma M. Parhad, Susan E. Folstein, Peter J. Whitehouse, John C. Hedreen, Donald L. Price, Gary A. Chase

Research output: Contribution to journalArticle

41 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1262-1266
Number of pages5
JournalNeurology
Volume33
Issue number10
DOIs
StatePublished - Oct 1983

ASJC Scopus subject areas

  • Clinical Neurology

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    Clark, A. W., Parhad, I. M., Folstein, S. E., Whitehouse, P. J., Hedreen, J. C., Price, D. L., & Chase, G. A. (1983). The nucleus basalis in huntington’s disease. Neurology, 33(10), 1262-1266. https://doi.org/10.1212/wnl.33.10.1262