As people age, a normal brain protein known as amyloid-beta often starts to collect into harmful amyloid plaques in the brain.
Such plaques can be the first step on the path to Alzheimer’s dementia.
When they form around blood vessels in the brain, a condition known as cerebral amyloid angiopathy, the plaques also raise the risk of strokes.
Several antibodies that target amyloid plaques have been studied as experimental treatments for Alzheimer’s disease.
Such antibodies also may have the potential to treat cerebral amyloid angiopathy, although they haven’t yet been evaluated in clinical trials.
But all of the anti-amyloid antibodies that have successfully reduced amyloid plaques in Alzheimer’s clinical trials also can cause a worrisome side effect: an increased risk of brain swelling and bleeds.
In a new study, researchers found an antibody that could remove amyloid plaques from brain tissue and blood vessels without increasing the risk of brain bleeds.
The antibody targets a minor component of amyloid plaques known as apolipoprotein E (APOE).
The findings suggest a potentially safer approach to removing harmful amyloid plaques as a way of treating Alzheimer’s disease.
The research was conducted by a team at Washington University School of Medicine in St. Louis.
The team says that Alzheimer’s researchers have been searching for decades for therapies that reduce amyloid in the brain.
Anti-amyloid antibodies work by alerting the immune system to the presence of unwanted material—amyloid plaques—and directing the cleanup crew—inflammatory cells known as microglia—to clear out such debris.
By targeting APOE in a different way, the current finding seems to be effective at removing amyloid from both the brain tissue and the blood vessels, while avoiding potentially dangerous side effects.
The side effect, amyloid-related imaging abnormalities, is visible on brain scans. Such abnormalities indicate swelling or bleeding in the brain caused by inflammation and can lead to headaches, confusion, and even seizures.
In clinical trials for anti-amyloid antibodies, roughly 20% of participants develop the symptoms.
One author of the study is David Holtzman, M.D.
The study is published in Science Translational Medicine.