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Preclinical Huntington's disease: compensatory brain responses during learning
Andrew Feigin1, Maria-Felice Ghilardi, Chaorui Huang
1Center for Neurosciences, Institute for Medical Research, North Shore-Long Island Jewish Health System, 350 Community Drive, Manhasset, NY 11030, USA.
Annals of Neurology
|November 2, 2005
Summary
Motor sequence learning is impaired in presymptomatic Huntington's disease (p-HD) individuals. Enhanced brain activity in certain areas compensates for early Huntington's disease (HD) changes, but not enough to maintain normal performance.
Area of Science:
- Neuroscience
- Cognitive Neuroscience
- Neurodegenerative Diseases
Background:
- Motor sequence learning deficits are an early sign of Huntington's disease (HD).
- The underlying neural mechanisms of these early cognitive changes in presymptomatic Huntington's disease (p-HD) are not well understood.
Purpose of the Study:
- To investigate the neural basis of impaired motor sequence learning in p-HD.
- To identify brain regions involved in compensatory mechanisms during motor learning in p-HD.
Main Methods:
- Used H(2)(15)O positron emission tomography (PET) to measure brain activity during motor sequence learning tasks.
- Compared brain activation patterns between 11 p-HD subjects and 11 age-matched controls.
- Correlated brain activity with task performance to identify learning-related regions.
Main Results:
- p-HD subjects showed impaired motor sequence learning despite normal motor execution.
- Abnormally increased brain activation during learning was observed in the left mediodorsal thalamus and orbitofrontal cortex (OFC) in p-HD.
- Impaired learning performance in p-HD correlated with increased activation in the precuneus.
Conclusions:
- Enhanced thalamocortical pathway activation may compensate for early caudate degeneration in p-HD.
- This compensatory mechanism is insufficient to maintain normal motor sequence learning performance in the presymptomatic stage of HD.