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Bhattacharya touts NIH study on brain aging
Research identifies a midlife shift in brain immune cells that may influence dementia risk.
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Malvika Choudhary - Tue, 04, Aug 2026
- 13:42 EDT
- 33
Dr. Jay Bhattacharya, National Institutes of Health (NIH) Director and acting director of the Centers for Disease Control and Prevention (CDC), arrives to testify before a U.S. House Appropriations Labor, Health and Human Services, Education, and Related Agencies Subcommittee oversight hearing on the National Institutes of Health, on Capitol Hill in Washington, D.C., U.S., March 17, 2026. / REUTERS/Elizabeth Frantz/File Photo
NIH Director Jay Bhattacharya announced findings from an NIH-funded study that identified a previously unknown change in the aging human brain that could improve understanding of dementia and cognitive decline.
In a video statement, Bhattacharya said the research uncovered a previously unrecognized remodeling of the brain's immune cell landscape in the hippocampus, a region critical for learning and memory.
Also Read: NIH Chief Bhattacharya unveils policy to halt high-risk research
The study found that resident immune cells known as microglia progressively decline between approximately ages 50 and 75 and are replaced by immune cells with elevated inflammatory signatures that resemble cells originating outside the brain.
New NIH-funded research has uncovered an aspect of human brain aging that reshapes our approach to age-related cognitive decline and dementia risk.
— Jay Bhattacharya, MD, PhD (@NIHDirector_Jay) August 3, 2026
This knowledge will be critical as we work toward developing earlier detection methods and more effective treatments.
Read the… pic.twitter.com/fSlFS6cV1M
The findings challenge the long-held belief that microglia continuously renew throughout a person's lifetime.
Researchers also found deterioration in cells that maintain the blood-brain barrier, a protective structure that regulates what enters the brain. In addition, the study identified widespread disruptions in genome architecture across multiple brain cell types, linking these structural changes to shifts in gene regulation and cellular identity during aging.
The research analyzed postmortem hippocampal tissue from 40 neurologically healthy adults between the ages of 20 and 95 using advanced single-cell genomic and epigenetic techniques. It was conducted by scientists from the University of California, San Diego, the New York Genome Center and the University of California, Irvine.
Bhattacharya said the findings could reshape scientists' understanding of human brain aging and help explain why the risk of dementia increases with age.
He said future studies will investigate what drives the loss of resident microglia and determine whether the immune-cell transition directly contributes to Alzheimer's disease and other age-related neurological disorders. He added that the research could support earlier detection of disease and the development of more effective treatments.
The study was supported by the NIH's National Institute on Aging and the NIH Common Fund's 4D Nucleome program and was published as part of a collection of studies in Science and Science Advances.
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