AI Article Synopsis

  • Interleukin (IL)-1beta is a key proinflammatory cytokine linked to Alzheimer's disease (AD) and also plays a role in cardiovascular issues.
  • The study investigated genetic variations in the CASP1 gene, which is involved in the activation of IL-1beta, within a sample of 628 Spanish AD patients and 722 controls.
  • Results showed no significant differences in the genetic variations between AD cases and controls, suggesting that CASP1 genetic variations do not contribute to AD risk in this population.

Article Abstract

Background: Interleukin (IL)-1beta is a potent proinflammatory cytokine markedly overexpressed in the brains of patients with Alzheimer's disease (AD), and also involved in development of atherosclerosis and coronary artery disease. Caspase-1 (CASP1), formerly called IL-1beta converting enzyme (ICE), mediates the cleavage of the inactive precursor of IL-1beta into the biologically active form. CASP1 genetic variation (G+7/in6A, rs501192) has been associated with susceptibility to myocardial infarction and cardiovascular death risk. We examined the contribution of this gene to the susceptibility for AD.

Methods: We examined genetic variations of CASP1 by genotyping haplotype tagging SNPs (htSNPs) (rs501192, rs556205 and rs530537) in a group of 628 Spanish AD cases and 722 controls.

Results: There were no differences in the genotypic, allelic or haplotypic distributions between cases and controls in the overall analysis or after stratification by age, gender or APOE epsilon4 allele.

Conclusion: Our negative findings in the Spanish population argue against the hypothesis that CASP1 genetic variations are causally related to AD risk.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2837022PMC
http://dx.doi.org/10.1186/1471-2350-11-32DOI Listing

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