Memory deficits in the transgenic rat model of Huntington's disease

Behav Brain Res. 2012 Feb 1;227(1):194-8. doi: 10.1016/j.bbr.2011.11.009. Epub 2011 Nov 15.

Abstract

Memory deficits are common in patients with Huntington's disease (HD) and have a substantial impact on the quality of life of patients and their relatives. A good model resembling the human memory deficits is needed for research purposes. In this study we investigated the memory function of the transgenic rat model of Huntington's disease (tgHD) in the object location (OLT) and the object recognition task (ORT). Several studies have shown that the recent developed tgHD rat model resembles the human phenotype of HD. Impairments of spatial and object recognition memory in the OLT and ORT, however, have to our knowledge not yet been reported in this transgenic model. Our findings show that in both early and late stages of the disease the tgHD rats have clear deficits for both visuospatial and visual object memory. Since HD patients are known to be impaired in both types of memory, these results confirm the validity of this tgHD rat as a model for the human HD phenotype.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Animals
  • Discrimination, Psychological / physiology
  • Disease Models, Animal
  • Humans
  • Huntingtin Protein
  • Huntington Disease / complications*
  • Huntington Disease / genetics
  • Male
  • Memory Disorders / etiology*
  • Memory Disorders / genetics
  • Mutation / genetics*
  • Nerve Tissue Proteins / genetics*
  • Neuropsychological Tests
  • Nuclear Proteins / genetics*
  • Rats
  • Rats, Sprague-Dawley
  • Rats, Transgenic
  • Recognition, Psychology / physiology

Substances

  • HTT protein, human
  • Huntingtin Protein
  • Nerve Tissue Proteins
  • Nuclear Proteins