Functional effects of genetic polymorphism in inflammatory genes in subjective memory complainers

Authors

• Simon Lau, Edith Cowan University
• Kristyn Alissa Bates, Edith Cowan University
• Hamid R. Sohrabi, University of Western Australia
• Mark Rodrigues, Edith Cowan University
• Georgia Martins, Edith Cowan University
• Satvinder S. Dhaliwal, Curtin University
• Kevin Taddei, Edith Cowan UniversityFollow
• Simon M. Laws, Edith Cowan UniversityFollow
• Ian J. Martins, Edith Cowan UniversityFollow
• Francis L. Mastaglia, University of Western Australia
• Jonathan K. Foster, Edith Cowan University
• Jacqueline K. Phillips, Murdoch University
• Ralph N. Martins, Edith Cowan University

Document Type

Journal Article

Keywords

[RSTDPub]

Publisher

Elsevier

Faculty

Faculty of Health, Engineering and Science

School

School of Exercise, Biomedical and Health Science / Centre of Excellence for Alzheimer's Disease Research and Care

RAS ID

10543

Grant Link

http://purl.org/au-research/grants/nhmrc/595392

Comments

Lau, S. , Bates, K. A., Sohrabi, H. R., Rodrigues, M., Martins, G., Dhaliwal, S.S., Taddei, K. , Laws, S.M., Martins, I. J., Mastaglia, F.L., Foster, J. K., Phillips, J.K., & Martins, R. N. (2012). Functional effects of genetic polymorphism in inflammatory genes in subjective memory complainers. Neurobiology of Aging, 33 (6),1054-1056.

Article available here

Abstract

A number of genetic risk factors have been identified for Alzheimer’s disease (AD) including genes involved in the inflammatory response (interleukin 1A, [IL-1 (-889)], interleukin 1B (IL-1 [ 3953]), and tumor necrosis factor (TNF [-308 and -850]). We investigated the prevalence and functional consequences (baseline cognitive performance, plasma cytokine levels) of possession of these putative genetic risk factors within a group of subjective memory complainers (SMC, n 226) and age and sex matched noncomplainers (NMC, n 167). We observed no effect of any of the genetic factors investigated on cognitive performance. Further, there was no difference in the frequency of the disease-associated alleles, or cytokine levels between subjective memory complainers and noncomplainer participants. There was no relationship between TNF polymorphisms and TNF levels. There was a significant increase in plasma IL-1 levels in those homozygous for the disease-associated allele (i.e., IL-1 3953 TT). Follow-up longitudinal assessments on this cohort will provide insight as to how these polymorphisms may affect the risk of cognitive decline over time.

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