Gene tied to Alzheimer's runs hot in Black and white brains alike, Boston study finds

An analysis of more than 200 African American brain donors found a gene called ADAMTS2 sharply overactive in Alzheimer's cases, and the same gene independently topped a comparable study of white patients, researchers say.

A gene called ADAMTS2 showed 1.52 times higher expression in Alzheimer's disease brain tissue than in tissue from people without the disease, according to a study of 207 postmortem prefrontal cortex samples from African American donors published in Alzheimer's & Dementia, the journal of the Alzheimer's Association. The finding, reported by researchers at Boston University led by Jonathan Logue and colleagues, emerged as the single most statistically significant gene difference in what the authors describe as the largest Alzheimer's gene-expression study yet conducted in African American brain tissue (p = 2.96x10-8).

The result matters because Alzheimer's disease occurs at roughly twice the rate in African Americans compared with white Americans, a gap researchers attribute partly to social and health factors that remain incompletely understood at the biological level. Few African American donors have been included in postmortem Alzheimer's studies historically, leaving open whether the molecular changes driving the disease in this population mirror or diverge from those documented mainly in white patients. When the Boston University team compared their results with a separate, previously reported gene-expression study of European-ancestry brain donors, ADAMTS2 again ranked among the top differentially expressed genes, a pattern the researchers call substantial concordance between the two ancestry groups.

Boston University geneticists, quoted in a university news release accompanying the paper, said the shared elevation of ADAMTS2 across both Black and white brain tissue points to a common biological process in Alzheimer's disease and raises the gene's priority as a subject for further research into whether it could serve as a therapeutic target. That characterization, however, describes a rationale for future investigation, not a demonstrated treatment pathway; the paper itself is a gene-expression comparison in autopsy tissue, not a clinical trial or a test of any intervention.

The study was observational and cross-sectional, comparing gene activity in brain tissue collected after death from people with and without confirmed Alzheimer's pathology. It identified an association between higher ADAMTS2 expression and Alzheimer's status, but postmortem tissue analysis cannot establish whether the elevated gene activity contributes to the disease, results from it, or reflects some other factor common to both. The researchers themselves frame the finding as a starting point for mechanistic and therapeutic-target research, not as evidence for any drug, supplement, or intervention.

Researchers say the next step is determining what ADAMTS2, a gene involved in collagen processing, actually does in the Alzheimer's brain, and whether altering its activity has any effect in laboratory models before any relevance to patients could even be considered.