Engineered immune cells targeted and reduced the toxic protein plaques that drive Alzheimer’s disease in a recent study. Alzheimer's and related dementias represent a growing crisis within the Department of Veterans Affairs medical system.
Researchers at Washington University School of Medicine in St. Louis, Missouri, the academic partner of the VA St. Louis Health Care System, engineered the cells for the study published Feb. 9 in the Proceedings of the National Academy of Sciences (PNAS). It represents the first time CAR-T cell therapy, a technique developed to fight cancer, has been applied to a neurodegenerative disease.
Why It Matters to Veterans
The VA’s Veterans Health Administration estimates that roughly 10% of VA patients ages 65 and older have dementia, and the VA's Office of Policy and Planning has projected a 22% increase in the number of VA patients with dementia between 2020 and 2033, from approximately 276,000 to 335,000.
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More than half of all VA patients are 65 or older. Veterans face elevated risk factors that the general population does not: Large-scale longitudinal studies have found that veterans with post-traumatic stress disorder are at 50% to 60% greater risk of developing dementia, and the risk associated with traumatic brain injury may be even higher. A January 2026 study published in Frontiers in Dementia found that veterans carry higher aggregate prevalence of nearly every modifiable dementia risk factor, including diabetes, chronic pain, smoking, depression, sleep disturbances and hearing loss.
Research from the VA's own Million Veteran Program has shown that PTSD and TBI interact with genetic risk factors for Alzheimer's, meaning that service-connected conditions may compound the biological vulnerability to the disease. As the post-9/11 generation ages into the peak risk window for dementia, the need for new treatment approaches is not theoretical. It is a coming wave that the VA is already preparing for.
What CAR-T Cells Are and What the Study Did
CAR-T cell therapy works by removing a patient’s own T cells, a type of immune cell, and genetically modifying them to recognize and attack a specific target. The technique has transformed treatment for certain blood cancers. The WashU team, led by neuroimmunologist Dr. Jonathan Kipnis, applied the same principle to Alzheimer’s by engineering T cells to recognize amyloid beta, the protein that forms the plaques widely considered central to the disease.
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Researchers removed T cells from healthy mice, modified them to target amyloid beta, and injected them into six-month-old mice that had been genetically engineered to develop Alzheimer’s-like amyloid plaques. The mice received three injections spaced 10 days apart. Ten days after the final injection, the treated mice showed significantly greater reduction in amyloid plaques compared to mice that received unmodified T cells. The brains of treated mice also showed reduced activation of microglia and astrocytes, two cell types associated with the neuroinflammation that accompanies Alzheimer’s.
What Comes Next
The study is early. It was conducted in mice, not humans, and the researchers have noted that significant work remains to determine safety, dosing and whether the approach can translate to the far more complex human brain.
Kipnis has said the team plans to explore how the engineered cells improve brain health beyond plaque reduction and to test the approach in mouse models of other neurodegenerative diseases, including ALS and Parkinson’s.
The research builds on Kipnis’s earlier discovery of the brain’s meningeal lymphatic system and his recent work showing that T cells with neuroprotective properties can aid spinal cord recovery.
For veterans living with the cognitive effects of TBI or facing the onset of Alzheimer’s, the work is years from a clinic. But it adds to a growing body of research emerging from the WashU-VA St. Louis corridor that is pushing the boundaries of what the immune system can do for the brain.
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