Brain's immune system could treat Alzheimer's: Study
(NewsNation) — New research suggests enhancing the brain's own immune cells could help clear plaques associated with Alzheimer's disease.
Research indicates amyloid beta plaques, sticky clumps of protein that accumulate in the brain, contribute to Alzheimer's disease.
The main theory on Alzheimer's development is the amyloid cascade hypothesis, which suggests that the accumulation of amyloid beta plaques triggers a series of events, including the accumulation of tau proteins, which result in the symptoms of the disease.
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If the plaques could be cleared before tau proteins begin to accumulate, it could prevent cognitive decline.
The new findings, published in Nature Medicine, could help shift the future of treatment, leading to efforts to harness the brain's natural defenses against the disease.
Treatment for Alzheimer's remains limited. An earlier attempt at an Alzheimer's vaccine failed after the immune response caused dangerous brain swelling. There are FDA-approved antibody treatments, but they remain controversial, offering modest results while coming with potential side effects and high costs.
There are drugs that stimulate the immune system to remove amyloid beta plaques, said author David Gate, but he believes the data they gathered could make the drugs more effective.
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Scientists compared brain tissue from deceased people with Alzheimer's who received amyloid-beta immunization and those who did not. They found that not only did immune cells called microglia clear plaques, but they also helped restore the brain to a healthier level.
However, researchers also found that some microglia were more effective in plaques than others and that the region of the brain treated and the type of immunization played a role in how they worked.
Scientists currently have no way to target specific immune cells that are associated with plaque clearing, but scientists say methods of targeting cells in the brain are improving.
Copyright 2025 Nexstar Media, Inc. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.
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