Psychotic symptoms in Alzheimer's disease are not influenced by polymorphic variation at the dopamine receptor DRD3 gene

Neurosci Lett. 2004 Sep 16;368(1):33-6. doi: 10.1016/j.neulet.2004.06.052.

Abstract

It has been suggested that genetic influences unmasked during neurodevelopment to produce schizophrenia may appear throughout neurodegeneration to produce AD plus psychosis. Risk of schizophrenia and psychosis in Alzheimer's disease (AD) has been linked to polymorphic variation at the dopamine receptor DRD3 gene implying similar causative mechanisms. We tested this association in a large cohort of Alzheimer's disease patients with a diagnosis of probable AD of 3 years or more duration from the relatively genetically homogenous Northern Irish population. We assessed relationships between genotypes/alleles of the DRD3 BalI polymorphism and the presence or absence of psychotic symptoms (delusions, hallucinations) in AD patients during the month prior to interview and at any stage during the dementia. No significant associations were found when delusions and hallucinations were cross-tabulated against S and G alleles and SS, SG and GG genotypes. Logistic regression failed to detect any influence of APOE, gender, family history or prior psychiatric history. In conclusion, we were unable to confirm previously reported associations between the DRD3 BalI polymorphism and psychotic symptoms in AD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Alleles
  • Alzheimer Disease / genetics*
  • Alzheimer Disease / psychology*
  • Cohort Studies
  • DNA / genetics
  • Delusions / psychology
  • Female
  • Genotype
  • Hallucinations / genetics
  • Hallucinations / psychology
  • Humans
  • Logistic Models
  • Male
  • Mutation / genetics
  • Psychotic Disorders / etiology*
  • Psychotic Disorders / genetics*
  • Receptors, Dopamine D2 / genetics*
  • Receptors, Dopamine D3

Substances

  • DRD3 protein, human
  • Receptors, Dopamine D2
  • Receptors, Dopamine D3
  • DNA