Please use this identifier to cite or link to this item: http://hdl.handle.net/1959.14/169624
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- Title
- Functional effects of genetic polymorphism in inflammatory genes in subjective memory complainers
- Related
- Neurobiology of aging, Vol. 33, Issue 6, (2012), p.1054-1056
- DOI
- 10.1016/j.neurobiolaging.2010.09.003
- Publisher
- Elsevier
- Date
- 2012
- FoR/RFCD Code(s)
-
110900 Neurosciences
110300 Clinical Sciences
- Author/Creator
- Lau, Simon
- Author/Creator
- Bates, Kristyn Alissa
- Author/Creator
- Foster, Jonathan K
- Author/Creator
- Phillips, Jacqueline K
- Author/Creator
- Martins, Ralph N
- Author/Creator
- Sohrabi, Hamid R
- Author/Creator
- Rodrigues, Mark
- Author/Creator
- Martins, Georgia
- Author/Creator
- Dhaliwal, Satvinder S
- Author/Creator
- Taddei, Kevin
- Author/Creator
- Laws, Simon M
- Author/Creator
- Martins, Ian J
- Author/Creator
- Mastaglia, Francis L
- Description
- A number of genetic risk factors have been identified for Alzheimer's disease (AD) including genes involved in the inflammatory response (interleukin 1A, [IL-1α (-889)], interleukin 1B (IL-1β [+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-1β levels in those homozygous for the disease-associated allele (i.e., IL-1β +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.
- Description
- 3 page(s)
- Subject Keyword
- 110900 Neurosciences
- Subject Keyword
- 110300 Clinical Sciences
- Resource Type
- journal article
- Organisation
- Macquarie University. Australian School of Advanced Medicine
- Identifier
- http://hdl.handle.net/1959.14/169624
- Identifier
- ISSN:0197-4580
- Identifier
- mq-rm-2010005579
- Language
- eng
- Reviewed
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