Increased cerebral activity in Parkinson's disease patients carrying the DRD2 TaqIA A1 allele during a demanding motor task: a compensatory mechanism?

Genes Brain Behav. 2007 Aug;6(6):588-92. doi: 10.1111/j.1601-183X.2006.00290.x. Epub 2006 Nov 27.

Abstract

Previous studies suggest that neuroimaging techniques are useful for detecting the effects of functional genetic polymorphisms on brain function in healthy subjects or in patients presenting with psychiatric or neurodegenerative conditions. Former evidence showed that individuals carrying risk alleles displayed broader patterns of brain activity during behavioural and cognitive tasks, despite being clinically comparable to non-carriers. This suggests the presence of compensatory brain mechanisms. In the present study, we investigated this effect in Parkinson's disease (PD) patients carrying the DRD2 TaqIA A1 allelic variant. This variant may confer an increased risk of developing the disease and/or influence the clinical presentation. During a complex sequential motor task, we evidenced by functional magnetic resonance imaging that A1 allele carriers activated a larger network of bilateral cerebral areas than non-carriers, including cerebellar and premotor regions. Both groups had similar clinical and demographic measures. In addition, their motor performance during the functional magnetic resonance experiment was comparable. Therefore, our conclusions, pending replication in a larger sample, seem to reflect the recruitment of compensatory cerebral resources during motor processing in PD patients carrying the A1 allele.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological / genetics
  • Aged
  • Arousal / physiology
  • Attention / physiology*
  • Brain / metabolism*
  • Brain Mapping*
  • Case-Control Studies
  • Chi-Square Distribution
  • Female
  • Gene Frequency
  • Humans
  • Magnetic Resonance Imaging
  • Male
  • Middle Aged
  • Motor Skills / physiology*
  • Neural Pathways / metabolism
  • Parkinson Disease / genetics*
  • Parkinson Disease / metabolism
  • Receptors, Dopamine D2 / genetics*
  • Receptors, Dopamine D2 / metabolism

Substances

  • Receptors, Dopamine D2