By a News Reporter-Staff News Editor at Women's Health Weekly -- Investigators publish new report on Neurodegenerative Diseases. According to news reporting from Oxford, United Kingdom, by NewsRx journalists, research stated, "Epistasis between interleukin-10 (IL10) and aromatase gene polymorphisms has previously been reported to modify the risk of Alzheimer's disease (AD). However, although the main effects of aromatase variants suggest a sex-specific effect in AD, there has been insufficient power to detect sex-specific epistasis between these genes to date."
The news correspondents obtained a quote from the research from the University of Oxford, "Here we used the cohort of 1757 AD patients and 6294 controls in the Epistasis Project. We replicated the previously reported main effects of aromatase polymorphisms in AD risk in women, for example, adjusted odds ratio of disease for rs1065778 GG = 1.22 (95% confidence interval: 1.01-1.48, P=0.03). We also confirmed a reported epistatic interaction between IL10 rs1800896 and aromatase (CYP19A1) rs1062033, again only in women: adjusted synergy factor = 1.94 (1.16-3.25, 0.01). Aromatase, a rate-limiting enzyme in the synthesis of estrogens, is expressed in AD-relevant brain regions,and is downregulated during the disease. IL-10 is an anti-inflammatory cytokine. Given that estrogens have neuroprotective and anti-inflammatory activities and regulate microglial cytokine production, epistasis is biologically plausible."
According to the news reporters, the research concluded: "Diminishing serum estrogen in postmenopausal women, coupled with suboptimal brain estrogen synthesis, may contribute to the inflammatory state, that is a pathological hallmark of AD."
For more information on this research see: The sex-specific associations of the aromatase gene with Alzheimer's disease and its interaction with IL10 in the Epistasis Project. European Journal of Human Genetics, 2014;22(2):216-220. European Journal of Human Genetics can be contacted at: Nature Publishing Group, Macmillan Building, 4 Crinan St, London N1 9XW, England. (Nature Publishing Group - www.nature.com/; European Journal of Human Genetics - www.nature.com/ejhg/)
Our news journalists report that additional information may be obtained by contacting C. Medway, University of Oxford, John Radcliffe Hosp, Nuffield Dept. of Med, Oxford OX3 9DU, United Kingdom. Additional authors for this research include O. Combarros, M. Cortina-Borja, H.T. Butler, C.A. Ibrahim-Verbaas, R. de Bruijn, P.J. Koudstaal, C.M. van Duijn, M.A. Ikram, I. Mateo, P. Sanchez-Juan, M.G. Lehmann, R. Heun, H. Kolsch, P. Deloukas, N. Hammond, E. Coto and Alvare (see also Neurodegenerative Diseases).
Keywords for this news article include: Oxford, Europe, Dementia, Genetics, Tauopathies, United Kingdom, Brain Diseases, Alzheimer Disease, Risk and Prevention, Neurodegenerative Diseases, Central Nervous System Diseases
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