Alzheimer’s drug slows mental decline in trial — but is it a breakthrough?

Alzheimer’s drug, researchers are celebrating this week’s announcement that a drug candidate for Alzheimer’s disease slowed the rate of cognitive decline for people in a clinical trial by 27%.

Others, however, remain hesitant, wanting to see data beyond what was disclosed in a 27 September press release. If the results stand up, the treatment called lecanemab would be the first of its kind to show a strong signal of cognitive benefit in a robust trial. “It’s such a win for our field,” says Liana Apostolova, a neurologist at the Indiana University School of Medicine in Indianapolis. Alzheimer’s drug, The results are “quite promising”, says Caleb Alexander, an internal-medicine specialist and epidemiologist at the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, and an advisory committee member for the US Food and Drug Administration (FDA). But, he adds, “we’ll have to see what the full analysis of the trial suggests”. Alexander and others also note that, although the results indicate that lecanemab does provide some clinical benefit, the degree to which it does so is small.

Developed by Eisai, a pharmaceutical company in Tokyo, and biotechnology firm Biogen in Cambridge, Massachusetts, lecanemab is a monoclonal antibody designed to clear clumps of protein from the brain that many think are a root cause of Alzheimer’s disease. Alzheimer’s drug, This theory, known as the ‘amyloid hypothesis’, holds that the protein amyloid-β accumulates into toxic deposits as the disease progresses, ultimately causing dementia. Whether or not lecanemab confirms the amyloid hypothesis remains to be seen, researchers say. “I don’t think one study will prove a very long-standing controversial hypothesis,” says Brent Forester, director of the Geriatric Psychiatry Research Program at McLean Hospital in Belmont, Massachusetts, who helped to run the clinical trial for lecanemab. “But one positive study supports the hypothesis.” Amyloid is “associated with the problem, but it isn’t ‘the’ problem”, says George Perry, a neurobiologist at the University of Texas at San Antonio and a sceptic of the amyloid hypothesis. “If you modulate it, of course you can have some small benefit.”

Source: This news is originally published by nature