Researchers may have discovered a factor that contributes to racial discrepancies in developing Alzheimer’s disease (AD) or dementia, according to a study recently published in The Journal of Clinical Endocrinology and Metabolism.
Researchers led by Antonio C. Bianco, MD, PhD, of University of Chicago, point out that a common single nucleotide polymorphism in DIO2, Thr92AlaD2, is associated with a transcriptome typically found in neurodegenerative diseases in postmortem human brain tissue. The authors write that the metabolic and cognitive relevance of Thr92AlaD2 has been noted previously in different populations, but not always universally replicated. More recently, this same group reported that temporal lobe samples from Thr92AlaD2 carriers showed transcriptional alterations in processes typically associated with neurodegenerative diseases.
“In the current study,” the authors write, “we tested the hypothesis that carriers of the Thr92AlaD2 polymorphism have an increased risk for incident Alzheimer’s disease.” They also note that the epidemiology and tissue pathology of AD vary by ethnicity. For instance, African Americans (AAs) are more likely to have mixed tissue pathologies compared to clinically matched European Americans (EAs).
The study was performed at Rush University Medical Center. The researchers analyzed data from 3,054 AAs and 9,304 EAs; the primary population came from community-based cohorts from Chicago and northeastern Illinois, as well as religious clergymen from across the U.S. Secondary analyses came from a representative sample of the U.S. population. The team found that AAs with the Thr92AlaD2 polymorphism had 1.3 times higher odds of developing AD, and AAs from the secondary population with Thr92AlaD2 had increased odds of developing dementia and were 1.35 times more likely to develop cognitive impairment not demented (CIND). Meta-analysis showed that AAs with Thr92AlaD2 had 1.3 times increased odds of developing AD/dementia. EAs showed no association between Thr92AlaD2 and AD, dementia, or CIND.
“Our results show that in these large, well-characterized, population the Thr92AlaD2 polymorphism is associated with development of AD in AAs, but not EAs,” the authors conclude. “This, in addition to concurrent transcriptional evidence, supports the hypothesis that Thr92AlaD2 is a risk factor for neurodegenerative disease in AA.”