RT Journal Article SR Electronic T1 Associations of cytokine genes with Alzheimer's disease and depression in an elderly Korean population JF Journal of Neurology, Neurosurgery & Psychiatry JO J Neurol Neurosurg Psychiatry FD BMJ Publishing Group Ltd SP 1002 OP 1007 DO 10.1136/jnnp-2014-308469 VO 86 IS 9 A1 Hee-Ju Kang A1 Jae-Min Kim A1 Sung-Wan Kim A1 Il-Seon Shin A1 Sung-Woo Park A1 Young-Hoon Kim A1 Jin-Sang Yoon YR 2015 UL http://jnnp.bmj.com/content/86/9/1002.abstract AB Background Inflammatory processes regulated by cytokines are important in the aetiology of Alzheimer's disease (AD) and depression. Differences in transcriptional activities associated with several genetic polymorphisms affect cytokine production. We investigated the involvement of alleles associated with higher production of proinflammatory and lower production of anti-inflammatory cytokines in AD and depression in a community-dwelling sample of elderly individuals.Method A total of 732 community-dwelling elders were clinically evaluated for AD applying the NINCDS-ADRDA criteria and for depression applying the Geriatric Mental State Schedule. Genotyping was performed for six proinflammatory (interleukin (IL)-1β −511C/T and +3953C/T, IL-6 −174G/C, IL-8 −251T/A, tumour necrosis factor (TNF)-α −850C/T) and two anti-inflammatory (IL-4 +33T/C, IL-10 −1082G/A) cytokines. The sums of risk alleles of proinflammatory and anti-inflammatory cytokine genes were estimated. Age, gender, education and apolipoprotein E genotype were considered covariates.Results TNF-α −308G/A and IL-8 −251T/A were significantly associated with AD and IL-1β +3953C/T with late-life depression, while the significance of these associations was lost after Bonferroni correction. A greater number of risk alleles producing proinflammatory cytokines was significantly associated with AD, but not with depression, after adjustment for the covariates. No association was found between an increased number of risk alleles for anti-inflammatory cytokine production and either AD or depression.Conclusions The present findings support the inflammatory hypothesis in the aetiology of AD as measured by several cytokine genes associated with increased proinflammatory cytokine production.