The Genetic Relationship between Interleukin Genes in Alzheimer’s Disease

Copyright: © 2016 Mun MJ, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The contribution of genetics to Alzheimer’s disease (AD) risk and the pathological mechanisms of AD have been extensively investigated. Genetic polymorphisms in causative genes, including Amyloid precursor protein (APP), Presenilin 1 (PSEN1) and Presenilin 2 (PSEN2), are associated with the risk of early-onset AD (EOAD) [1] and Apolipoprotein E (APOE) has been linked to an increased risk of lateonset AD (LOAD) [2]. These genes all share a common function and affect amyloid beta (Aβ) production and clearance in the brain, which is an important factor in the pathogenesis of AD. AD is characterized by two neuropathological hallmarks: senile plaques and neurofibrillary tangles comprised of Aβ proteins, and the hyper phosphorylation of tau [3]. However, there is a strong correlation between neuroinflammation and the production of cytokines by immune cells. Interleukins (ILs), a group of cytokines, may actively participate in AD pathogenesis since they mediate a self-perpetuating cycle of neuroinflammation in AD [4]. Clinically, several cytokines including IL-1, IL-6, tumor necrosis factor-α (TNF-α) and transforming growth factor-β (TGF-β) have been shown to associate with AD [5]. In addition, ILs is associated with many autoimmune diseases [6]. Therefore, there have been extensive studies on the genetic association between ILs and AD [7-10].