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Huntington Disease l: Introduction01:21

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Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...
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Cortical dysfunction in patients with Huntington's disease during working memory performance.

Robert C Wolf1, Nenad Vasic, Carlos Schönfeldt-Lecuona

  • 1Department of Psychiatry III, University of Ulm, Leimgrubenweg 12-14, 89075 Ulm, Germany. christian.wolf@uni-ulm.de

Human Brain Mapping
|January 4, 2008
PubMed
Summary

Huntington's disease (HD) patients exhibit impaired working memory (WM) with reduced brain activation in key cognitive control regions. These functional deficits occur even in areas with preserved gray matter volume.

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Area of Science:

  • Neuroscience
  • Cognitive Neuroscience
  • Neurology

Background:

  • Huntington's disease (HD) is a neurodegenerative disorder affecting executive functions.
  • Neural mechanisms underlying working memory (WM) deficits in HD remain poorly understood.
  • Previous studies suggest widespread cortical dysfunction in HD.

Purpose of the Study:

  • To investigate the functional neuroanatomy of working memory (WM) in patients with Huntington's disease (HD).
  • To identify specific brain regions and networks involved in WM deficits in HD.
  • To correlate functional brain activity with structural gray matter differences in HD.

Main Methods:

  • Event-related functional magnetic resonance imaging (fMRI) with a parametric verbal WM task.
  • Inclusion of 16 healthy controls and 12 mild to moderate stage HD patients.
  • Voxel-based morphometry (VBM) to assess gray matter atrophy and control for its effects.

Main Results:

  • HD patients demonstrated slower and less accurate performance on WM tasks across all load levels.
  • Reduced brain activation was observed in HD patients in prefrontal, parietal, putamen, and cerebellar regions at high WM loads.
  • VBM identified gray matter loss in the caudate, thalamus, parietal, and prefrontal regions, but these did not explain the observed functional activation differences during WM task performance.

Conclusions:

  • WM-related functional abnormalities in HD involve critical nodes within the WM network, including those for cognitive control and subvocal rehearsal.
  • Aberrant cortical function in HD can manifest in brain regions that are relatively preserved from significant atrophy.
  • These findings highlight distinct neural underpinnings of WM deficits in HD, independent of gross structural changes.