In mice, antibody removes amyloid, improves vessel function without raising risk of brain bleeds
Amyloid deposits (blue) in mouse brain tissue and blood vessels are reduced after treatment with an antibody that targets the protein APOE (right), a minor component of amyloid deposits, compared to a placebo antibody (left). Amyloid deposits in the brain increase the risk of dementia and strokes. Researchers at Washington University School of Medicine in St. Louis have identified an antibody that clears amyloid deposits from the brain without raising the risk of brain bleeds. (Image: Monica Xiong)
February 17, 2021 SHARE
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.
Researchers identify antibody that removes amyloid plaques without the risk of brain bleeds
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.
Amyloid deposits in the brain increase the risk of dementia and strokes. Researchers at Washington University School of Medicine in St. Louis have identified an antibody that clears amyloid deposits from the brain without raising the risk of brain bleeds.
Studies by a research team at Washington University School of Medicine in St. Louis indicate that a brain protein known as YKL-40 may link Alzheimerâs disease with dysfunction in circadian rhythms, suggesting that treatments that target the protein could slow the course of the disease. Their work, reported in
Science Translational Medicine, found that YKL-40 is both regulated by clock genes and involved in clearing away the potentially toxic build-up of Alzheimer’s proteins in the brain. The teamâs studies indicated that Alzheimer’s patients who carry a genetic variant that reduces YKL-40 levels maintain their cognitive faculties longer than those individuals without the variant.
Brain protein indicates a link between circadian rhythm dysfunction and Alzheimer s Disease
Fractured sleep, daytime sleepiness and other signs of disturbance in one s circadian rhythm are common complaints of people with Alzheimer s disease, and the problems only get worse as the disease progresses. But the reason for the link between Alzheimer s and circadian dysfunction is not well understood.
Researchers at Washington University School of Medicine in St. Louis say that a clue may lie in the brain protein YKL-40.
In a study published Dec. 16 in Science Translational Medicine, the researchers report that YKL-40 is both regulated by clock genes and involved in clearing away potentially toxic buildup of Alzheimer s proteins in the brain. Moreover, Alzheimer s patients who carry a genetic variant that reduces YKL-40 levels maintain their cognitive faculties longer than people without the variant, the scientists found.