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Thursday, March 28, 2024 | Back issues
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Alzheimer’s Brain Plaque Busted by Antibody

(CN) — Researchers have discovered an antibody that reduces harmful brain plaques in Alzheimer's patients which may slow down or prevent the onset of the disease.

In a study published Wednesday in the journal Nature, researchers presented their work with aducanumab, a human monoclonal antibody — identical immune cells that are cloned from a unique parent cell — which selectively binds brain amyloid plaques to allow cells to remove the plaques.

Amyloid plaques typically develop 10 to 15 years before the emergence of initial symptoms of Alzheimer's, such as memory loss.

The team conducted a one-year long treatment with the antibody for a phase 1b study, resulting in nearly complete clearance of brain amyloid plaques in the 165 patients studied who had early-stage Alzheimer's disease.

"The results of this clinical study make us optimistic that we can potentially make a great step forward in treating Alzheimer's disease," study co-author Roger Nitsch said. "The effect of the antibody is very impressive. And the outcome is dependent on the dosage and length of treatment."

After treatment, the patients who received the highest dose of the antibody had the greatest reduction in amyloid plaques.

Using blood collected from elderly people up to 100 years old who demonstrated no cognitive impairment, the team was able to precisely isolate the immune cells whose antibodies are able to identify toxic beta-amyloid plaques but not the amyloid precursor protein that is present throughout the human body and likely plays a significant role in the development of nerve cells.

Aducanumab's effect in the study participants may be attributed to the antibody's specific capacity to bond with the abnormally folded amyloid protein fragment.

The positive results encouraged the researchers to investigate how the treatment affected the symptoms of the disease, which was not initially planned as a primary study objective. Using standardized questionnaires, the team assessed the cognitive abilities and everyday activities of the patients.

"Aducanumab also showed positive effects on clinical symptoms," Nitsch said. "While patients in the placebo group exhibited significant cognitive decline, cognitive ability remained distinctly more stable in patients receiving the antibody."

Some patients did suffer temporary amyloid-related imaging abnormality, an adverse effect that can be detected through MRIs. In a few cases, this was accompanied by temporary mild to moderate headaches.

The team believes that amyloid-related imaging abnormality is a measurable biological effect of amyloid clearance.

Aducanumab's benefits are currently being investigated by two large phase-three clinical studies, which will further evaluate safety and efficacy.

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