The deletion variant of α2b-adrenergic receptor is associated with decreased risk in Alzheimer's disease and mild cognitive impairment

J Neurol Sci. 2013 May 15;328(1-2):19-23. doi: 10.1016/j.jns.2013.02.003. Epub 2013 Mar 15.

Abstract

A common genetic polymorphism of the α2b-adrenergic receptor (ADRA2B) resulting in a deletion of three glutamic acids located on the third intracellular loop of the protein, has been associated with memory formation enhanced by emotional events. Additionally, there are several studies documenting the involvement of this polymorphism in other types of cognition, such as episodic memory. The aim of this study was to investigate the possible relationship of this genetic variance with a common memory affecting disease, Alzheimer's disease. Our study was carried out in a total number of 311 Greek subjects, including 119 sporadic AD patients, 95 MCI cases and 97 controls. Genomic DNA was extracted from whole blood and the fragments containing the polymorphism were amplified by PCR analysis. A genotypic analysis of the APOE polymorphism was also carried out. A significant difference in the frequency of the ADRA2B genetic variation among the three groups was observed. Specifically, the deletion variant is more prevalent in controls than in AD and MCI patients. Our data demonstrate for the first time an independent contribution of the ADRA2B genetic polymorphism to memory impairment and we further suggest a possible protective role of the deletion variant against the disease development.

MeSH terms

  • Aged
  • Alzheimer Disease / genetics*
  • Apolipoprotein E4 / genetics
  • Cognitive Dysfunction / genetics*
  • Female
  • Gene Frequency
  • Genetic Association Studies
  • Genotype
  • Greece
  • Humans
  • Male
  • Middle Aged
  • Neuropsychological Tests
  • Polymorphism, Genetic*
  • Psychiatric Status Rating Scales
  • Receptors, Adrenergic, alpha-2 / genetics*
  • Sequence Deletion / genetics*

Substances

  • ADRA2B protein, human
  • Apolipoprotein E4
  • Receptors, Adrenergic, alpha-2