Forty-eight previously unknown genetic regions linked to Alzheimer’s disease have been identified in a genetic analysis of approximately 2.8 million individuals, WELT reported.
Researchers evaluated data from 30 research groups involving 183,620 diagnosed Alzheimer’s patients and 74,131 proxy cases with an affected parent. Conducted by scientists at the University of Oslo and Oslo University Hospital, the study uncovered 127 DNA regions associated with disease risk.
Microglia, the immune cells of the brain, and specific neuron types showed distinct genetic signals in the data. Emil Uffelmann of Vrije Universiteit Amsterdam told Newsweek, “We have identified 48 new genomic regions associated with the risk of Alzheimer’s disease.”
Uffelmann also told Newsweek, “Our findings point to microglia, the immune cells of the brain, as well as to specific types of neurons, providing clues to biological mechanisms that could serve as therapeutic targets.” The analysis determined that common genetic variants account for roughly 16 percent of Alzheimer’s risk in people of European ancestry, exceeding previous statistical estimates of five to six percent.
The genetic signals concentrated heavily in microglia, which clear cellular debris and harmful substances from the nervous system. Several highlighted genes regulate the specific functions of these immune cells.
Researchers also identified certain nerve cells where specific genes displayed higher activity in microglia and lower activity in neuronal types. Edmundo Rodriguez-Frias of the Retreat of Broward in Florida told Newsweek, “Genetic variations can influence the corresponding protein levels and point to the role of these variants in the pathophysiology of the disease.”
The findings confirmed earlier research pathways concerning immune responses, amyloid processing, and lipid metabolism. Rodriguez-Frias told Newsweek that the newly identified genes “could shed light on the role of microglia and certain neurons in Alzheimer’s disease, which could be relevant for future therapies.”
Uffelmann said that common genetic variants contribute more to disease risk than previously recognized. He told Newsweek, “A better genetic risk prediction is promising, but remains for now a research tool and not a clinical one.”
Rodriguez-Frias stated, “The identification of genes that, when altered, can carry a higher or lower risk for developing the disease is only the first step on a long road toward a test or a drug from which patients can benefit.”
A proxy case involves an individual who does not have an Alzheimer’s diagnosis themselves but has a biological parent who developed the condition.
Researchers from the University of Oslo and Oslo University Hospital directed the analysis, working alongside international collaborators including scientists from Vrije Universiteit Amsterdam.
The 16 percent figure represents the statistical proportion of Alzheimer’s risk explained by common genetic variants across European populations, rather than a direct personal risk score for a single individual.