The chemokine receptor CCR5-Delta32 gene mutation is not protective against Alzheimer's disease

Neurosci Lett. 2004 Aug 19;366(3):312-4. doi: 10.1016/j.neulet.2004.05.058.

Abstract

Chronic local inflammatory reaction involving reactive microglia is one of the major pathological events in Alzheimer's disease (AD). There is growing evidence that the chemokine receptor CCR5 is up-regulated in AD brain and plays a role in the recruitment and accumulation of microglia in senile plaques. A 32-base pair deletion in the CCR5 gene (CCR5-Delta32 mutant allele) confers resistance to HIV-1 infection by preventing expression of the receptor on the cell surface. Several other reports have shown a similar protective effect of CCR5-Delta32 mutation towards certain chronic inflammatory diseases. Given the potential importance of CCR5 in brain inflammation, we hypothesized that individuals carrying the CCR5-Delta32 allele would show a reduced risk of AD. So, we performed a case-control study in 376 Spanish AD patients and 369 healthy controls. The frequency of the CCR5-Delta32 allele in our AD sample was 7.8%, not significantly different from our control sample group (5.8%). The present study indicates that the CCR5-Delta32 allele is not a preventive factor for AD.

Publication types

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

MeSH terms

  • Aged
  • Aged, 80 and over
  • Alleles*
  • Alzheimer Disease / genetics*
  • Apolipoprotein E4
  • Apolipoproteins E / genetics
  • Female
  • Gene Deletion*
  • Gene Frequency
  • Genotype
  • Humans
  • Male
  • Middle Aged
  • Receptors, CCR5 / genetics*
  • Sequence Analysis, DNA / methods

Substances

  • Apolipoprotein E4
  • Apolipoproteins E
  • Receptors, CCR5