Parkinson's Disease Research Today is a free monthly online journal that collates and summarizes the latest research about Parkinson's Disease, including details on symptoms, treatment, genetics, medication.

Inflammatory cytokine gene polymorphisms and increased risk of Parkinson disease.

Wahner AD, Sinsheimer JS, Bronstein JM, Ritz B

Department of Epidemiology, UCLA School of Public Health, University of California, Los Angeles, CA 90095-1772, USA. awahner@ucla.edu

BACKGROUND: The proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and IL-1beta (interleukin 1beta) have a role in neuroinflammation, and functional polymorphisms in the TNF-alpha and IL-1beta genes may affect susceptibility to Parkinson disease (PD). OBJECTIVE: To investigate whether functional DNA polymorphisms of the TNF-alpha and IL-1beta genes affect the risk of PD. DESIGN: Population-based case-control study. SETTING: Three rural California counties (Fresno, Tulare, and Kern). PARTICIPANTS: Two hundred eighty-nine incident idiopathic PD cases and 269 population control subjects, marginally matched by age, sex, and race/ethnicity. MAIN OUTCOME MEASURES: Genotypes of IL-1beta-511 and TNF-alpha-308. RESULTS: We observed a greater than 2-fold increased risk of PD among carriers of the homozygous variant genotype of IL-1beta-511 (odds ratio [OR], 2.26; 95% confidence interval [CI], 1.27-4.02) and the homozygous variant genotype of TNF-alpha-308 (OR, 2.49; 95% CI, 0.90-6.85) and an almost 3-fold increased risk among carriers of the homozygous variant genotype for either or both polymorphisms (OR, 2.92; 95% CI, 1.66-5.16). CONCLUSIONS: A smaller magnitude of PD risk increase among carriers of the heterozygous genotype for either or both polymorphisms suggests a gene-dosing effect (OR, 1.45; 95% CI, 0.97-2.16; P<.001 for trend). Results were not sensitive to exclusion of all nonwhite subjects or to adjustment for nonsteroidal anti-inflammatory drug use or smoking.

Published 12 June 2007 in Arch Neurol, 64(6): 836-40.
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