Interactions between PPAR-α and inflammation-related cytokine genes on the development of Alzheimer’s disease, observed by the Epistasis Project

International Journal of Molecular Epidemiology and Genetics

Rachel Barber¹  Cornelia M van Duijn¹  Patrick G Kehoe¹  Onofre Combarros¹  Olivia Belbin¹  Panos Deloukas¹  Reinhard Heun¹  Eliecer Coto¹  Monique Breteler¹  Kristelle Brown¹  Carla A Ibrahim-Verbaas¹  Donald R Warden¹  Heike Kölsch¹  Victoria Alvarez¹  Kevin Morgan¹  Gordon K Wilcock¹  Michael G Lehmann¹  Donald J Lehmann¹  Ignacio Mateo¹  Maaike Schuur¹  Mario Cortina-Borja¹  A David Smith¹  Yurii S Aulchenko¹  Naomi Hammond¹ 

关键词: AD;    genetics;    epistasis;    inflammation;    interleukin;    steroid receptors;    PPAR-alpha;    sporadic;    genetic interaction;   

DOI  :  

学科分类：流行病学

来源: e-Century Publishing Corporation

【 摘 要 】

Neuroinflammation contributes to the pathogenesis of sporadic Alzheimer’s disease (AD). Variations in genes relevant to inflammation may be candidate genes for AD risk. Whole-genome association studies have identified relevant new and known genes. Their combined effects do not explain 100% of the risk, genetic interactions may contribute. We investigated whether genes involved in inflammation, i.e. PPAR-α, interleukins (IL) IL- 1α, IL-1β, IL-6, and IL-10 may interact to increase AD risk.

【 授权许可】

Unknown