Scientists have identified dozens of previously unknown genetic risk factors for Alzheimer’s disease in one of the largest studies of the disease to date. The findings offer new clues about which brain cells and biological processes might contribute to the disease.
The study, which pooled data from 30 research groups, analyzed the genetic data of about 2.8 million people, including 183,620 with an Alzheimer’s diagnosis. The researchers identified 127 regions of human DNA associated with the risk of developing the disease, 48 of which had not previously been discovered in this context.
One of the study’s authors, Emil Uffelmann of Vrije Universiteit Amsterdam in the Netherlands, said News week: “We identified 48 new regions of the genome linked to Alzheimer’s disease risk, and our results point to microglia, immune cells in the brain, as well as specific types of neurons. These results provide clues to biological mechanisms that could become therapeutic targets.
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“Our study also shows that common genetic variants contribute much more to Alzheimer’s disease risk than previously estimated, meaning that large genetic studies still have much to discover. Better prediction of genetic risk is promising, but for now it remains a research tool, not a clinical tool.”
Published in Nature and led by the Norwegian University of Oslo and Oslo University Hospital in collaboration with an international consortium, the research gives scientists a more detailed picture of the biology underlying Alzheimer’s disease and identifies potential avenues for future treatments.
New brain clues
Major discovery strengthens evidence for the role of microglia, immune cells that help remove harmful substances and damaged cellular material from the brain. Researchers found genetic evidence implicating microglial activation and recruitment of immune cells.
The study also identified genes linked to important brain processes, including evidence of their involvement in the processing of amyloid, a protein that can accumulate in the brain after the onset of Alzheimer’s disease.
Following this, the researchers also identified, for the first time, several specific types of neurons enriched in genetic signals associated with Alzheimer’s risk, opening another avenue for studying the development of the disease.
The findings also suggest that common genetic variants account for about 16 percent of differences in Alzheimer’s risk between people, nearly three times previous estimates of about 5 percent. The researchers said the higher figure was largely the result of a statistical method that better accounts for APOE, a gene with an unusually large influence on Alzheimer’s risk.
This 16 percent figure applies to the population level, and it does not mean that genes account for 16 percent of an individual’s risk of Alzheimer’s disease, nor can a genetic test determine whether a person will develop the disease. Age, environment and other biological and personal factors also influence risk.
What the results could mean for treatment
Dr. Edmundo Rodriguez-Frias, medical associate at Retreat of Broward in Florida, said News week that genes are a gateway to understanding Alzheimer’s disease.
“Genetic variation can modulate corresponding protein levels and indicate the role of these variants in disease pathophysiology,” Rodriguez-Frias said. “And the newly implicated genes could shed light on the role of microglia and certain neurons in Alzheimer’s disease, which could be relevant for future therapies.
“Identifying genes that may, when altered, confer greater or lesser risk of developing disease is just the first step in a long journey toward a test or drug that patients can benefit from.”
Alzheimer’s disease is the leading cause of dementia, with more than 150 million cases of dementia predicted worldwide by 2050. The newly identified genetic associations could help scientists build laboratory models and study potential targets for drugs, but they do not prove that targeting particular genes will produce effective treatments.
Further research is needed to establish which associations are causal and whether the intervention is safe and effective.
Reference
Uffelmann, E., Wightman, DP, Bahrami, S. et al. (2026). The genetics of Alzheimer’s disease converge toward microglial and neuronal dysregulation. Nature. https://doi.org/10.1038/s41586-026-11206-y.
Contact Newsweek editors on this story: Kara Dolman and Tony Phillips.
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