McAninch EA, et al. - Experts assessed if the common single nucleotide polymorphism Thr92AlaD2 is related to incident Alzheimer disease (AD). Study findings suggested a relationship of Thr92AlaD2 with molecular markers known to cause AD pathogenesis in African Americans (AAs), interpreted to be a phenotype of elevated odds of developing AD/dementia in AAs in these populations. In incident AD, one factor contributing to racial discrepancies could be Thr92AlaD2.

Methods

• Researchers conducted a population-based study using human brain tissue microarray.
• The primary population was made up of community-based cohorts from Chicago and northeastern Illinois and religious clergymen from across the United States.
• For secondary analyses, a representative sample of the US population was used.
• The participants included 3,054 African Americans (AAs) and 9,304 European Americans (EAs).
• Main outcome measure was incident AD.

Results

• As per the findings, in the primary population, AAs with Thr92AlaD2 had 1.3 times [95% confidence interval (CI), 1.02 to 1.68; P=0.048] higher odds of developing AD.
• Results suggested that a trend toward increased odds of dementia was demonstrated by AAs from a second population with Thr92AlaD2 (odds ratio, 1.33; 95% CI, 0.99 to 1.78; P=0.06) and 1.35 times higher odds of developing cognitive impairment not demented (CIND; 95% CI, 1.09 to 1.67; P=0.006).
• Authors in the meta-analysis noted that AAs with Thr92AlaD2 still had 1.3 times increased odds of developing AD/dementia (95% CI, 1.07 to 1.58; P=0.008).
• Data demonstrated that the in EAs, no relationship was noted between Thr92AlaD2 and AD, dementia, or CIND.
• Transcriptional patterns linked to AD pathogenesis were identified by microarray of AA brain tissue.