BOSTON, November 21, 2024 – Alzheimer’s disease disproportionately impacts African Americans, affecting them at roughly twice teh rate seen in White individuals. Now, the largest study of its kind focusing on African american brain tissue has pinpointed a gene, ADAMTS2, that appears to play a key role in the disease’s growth across racial lines, offering a potential new target for therapies.
New Genetic Clues in Alzheimer’s Disparity
Researchers identify a shared genetic factor in Alzheimer’s, potentially bridging the gap in understanding risk across racial groups.
- African Americans are disproportionately affected by Alzheimer’s disease.
- A new study analyzed brain tissue from over 200 African American donors.
- The ADAMTS2 gene showed considerably higher activity in those with Alzheimer’s.
- This gene also showed a similar pattern in a separate study of European ancestry individuals.
For years, scientists have known that Alzheimer’s doesn’t affect everyone equally.While genetics are involved, previous research ofen lacked sufficient representation from diverse populations, hindering a complete understanding of the disease’s complexities. This new work aims to change that.
Uncovering Genetic Patterns in African American Brains
Scientists at Boston University Chobanian & Avedisian School of Medicine analyzed gene expression data from the post-mortem prefrontal cortex tissue of 207 African american brain donors. The group included 125 individuals with pathologically confirmed Alzheimer’s disease and 82 individuals without the disease. These samples originated from 14 National Institutes of Health (NIH)-funded Alzheimer’s Disease Research Centers across the United States.
The research revealed numerous genes behaving differently in individuals with Alzheimer’s compared to those without. The ADAMTS2 gene stood out, exhibiting an activity level 1.5 times higher in the brain tissue of individuals with autopsy-confirmed Alzheimer’s disease.
Funding: This research was supported by NIH awards 081230, P01-AG003949, P30-AG062677, P30-AG062421; P30-AG 066507, P30-AG066511, P30-AG 072972, P30-AG066468, R01-AG072474, RF1-AG066107, U24-AG056270, P01-AG003949 , RF1-AG082339, RF1-NS118584, P30-AG072946; P01-AG003991, P30-AG066444, P01-AG026276, P30-AG066462, P30-AG072958, and P30-AG072978, as well as Florida Department of Health awards 8AZ06 and 20A22. The funding sources played no role in the study’s design, data collection, analysis, interpretation, or publication.
Disclosures: Mark Logue received grants from the NIH and Department of Veterans Affairs. Marla Gearing, Lee-Way Jin, richard Mayeux, Richard Perrin, Shih-Hsiu Wang and Lindsay Farrer received grants from the NIH. Melissa Murray received grants from NIH, was a paid consultant for Biogen Pharmaceuticals, and served on committees for the Alzheimer’s Association and International Conference on Alzheimer’s and Parkinson’s Diseases.Thor Stein received grants from the NIH and Department of Veterans Affairs, and an honorarium from Brown University. Andrew Teich received grants from the NIH, a contract from Regeneron Pharmaceuticals and an honorarium from Ono Pharmaceuticals, owns stock in Ionis Pharmaceuticals and Biogen Pharmaceuticals, and served on committees for the Department of Defense and the Alzheimer’s Association. The effort of Katarnut Tobunluepop and Zihan Wang was supported by NIH grants. Benjamin Wolozin received grants from the NIH, consulting fees from Aquinnah Pharmaceuticals and Abbingworth Ventures, honoraria for several lectures, and owns stock and is Co-Founder and CSO of Aquinnah Pharmaceuticals Inc. Other authors have no competing interests to report.
