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Association of interleukin-1 beta polymorphisms with idiopathic Parkinson's disease
Patrick L McGeer1, Koji Yasojima, Edith G McGeer
1Kinsmen Laboratory of Neurological Research and the Movement Disorders Center, University of British Columbia, Vancouver, B.C., Canada. mcgeerpl@interchange.ubc.ca
Abstract:
Activated microglia surround degenerating substantia nigra neurons in Parkinson's disease (PD). Such microglia produce high levels of interleukin-1 beta (IL-1 beta) and interleukin-1 alpha (IL-1 alpha). T and C alleles exist for the IL-1 beta-511 regulatory region as well as for the IL-1 alpha-889 regulatory region. The T genotypes of both have been reported to increase the risk of Alzheimer's disease (AD) (Arch. Neurol. 58 (2001) 1790). Since the lesions of PD and AD have similar neuroinflammatory characteristics (Neurology 38 (1988) 1285), we genotyped 100 PD and 100 control postmortem brains for the same polymorphisms. We found a significant increase of the IL-1 beta T genotype in PD cases compared with controls (chi(2)=9.65, P=0.0019). A significant increase was not found for the IL-alpha T genotype (chi(2)=1.32, P=0.23), although there was a trend towards more frequent expression of the T allele.