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

Document Type

Journal Article




Faculty of Health, Engineering and Science


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




This article was originally published as: 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, article in press. NOTICE: this is the author’s version of a work that was accepted for publication in Neurobiology of Aging (33), 1054-1056. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Neurobiology of Aging, article in press (2010) Original article available here.


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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