Researchers find a promising approach to remove amyloid plaques in Alzheimer's disease

Apr 3 2024Washington University School of Medicine Alzheimer's disease starts with a sticky protein called amyloid beta that builds up into plaques in the brain, setting off a chain of events that results in brain atrophy and cognitive decline. The new generation of Alzheimer's drugs -; the first proven to change the course of the disease -; work by tagging amyloid for clearance by the brain's immune cells.

The approach could have implications beyond Alzheimer's. Toxic clumps of brain proteins are features of many neurodegenerative conditions, including Parkinson's disease, amyotrophic lateral sclerosis and Huntington's disease. Encouraged by the study results, researchers are exploring other potential immunotherapies – drugs that harness the immune system – to remove junk proteins from the brain that are believed to advance other diseases.

For reasons that are still unknown, the researchers found that, in mice and people with Alzheimer's disease, microglia that surround plaques produce and position LILRB4 on their cell surface, which inhibits their ability to control damaging plaque formation upon binding to APOE.

Drugs that target amyloid plaques directly can cause a potentially serious side effect. In Alzheimer's patients, amyloid proteins build up on the walls of the arteries in the brain as well as other parts of brain tissue. Removing plaques from brain blood vessels can induce swelling and bleeding, a side effect known as ARIA. This side effect is seen in some patients receiving lecanemab, a drug approved by the Food and Drug Administration to treat Alzheimer's.

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