OBJECTIVE: The increased production of proinflammatory mediators such as cytokines and prostaglandins may interact at multiple levels with neurodegeneration in Alzheimer disease (AD). This study was undertaken to evaluate the possible role of interferon-γ (IFN-γ) T+874A, cytoplasmic phospholipase A₂ (cPLA2) BanI, and cyclooxygenase-2 (COX-2) G-765C polymorphisms in AD. METHODS: The study included 237 probable patients with AD who met the diagnostic criteria of National Institute of Neurological and Communicative Disorders and Stroke-AD and Related Disorders Association, and 245 probands in the healthy comparison (HC) group. RESULTS: No significant difference in mean age or in the distribution of genders between AD and HC groups was found. The COX-2 G/G genotype was significantly more frequent in the AD, when compared with the HC group. There was no significant correlation between IFN-γ or cPLA2 genotypes and AD. CONCLUSIONS: Our findings indicate that the COX-2 G/G genotype is associated with AD and support the involvement of COX-2 in AD etiology.
OBJECTIVE: The increased production of proinflammatory mediators such as cytokines and prostaglandins may interact at multiple levels with neurodegeneration in Alzheimer disease (AD). This study was undertaken to evaluate the possible role of interferon-γ (IFN-γ) T+874A, cytoplasmic phospholipase A₂ (cPLA2) BanI, and cyclooxygenase-2 (COX-2) G-765C polymorphisms in AD. METHODS: The study included 237 probable patients with AD who met the diagnostic criteria of National Institute of Neurological and Communicative Disorders and Stroke-AD and Related Disorders Association, and 245 probands in the healthy comparison (HC) group. RESULTS: No significant difference in mean age or in the distribution of genders between AD and HC groups was found. The COX-2 G/G genotype was significantly more frequent in the AD, when compared with the HC group. There was no significant correlation between IFN-γ or cPLA2 genotypes and AD. CONCLUSIONS: Our findings indicate that the COX-2 G/G genotype is associated with AD and support the involvement of COX-2 in AD etiology.