The effectiveness of an effective anti-Alzheimer’s drug by the results of a clinical study

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An experimental treatment for Alzheimer’s disease developed by Eisai and Biogen slowed the decline of cognitive abilities in patients who participated in a clinical trial, according to new data published on Tuesday.

Scientists discussed, Wednesday, November 30, the detailed results of a clinical study on a new drug confirming its effectiveness in slowing the cognitive decline of patients with neurodegenerative Alzheimer’s disease, but also noted its sometimes severe adverse effects.

The complete results of this advanced clinical study (phase III) conducted on nearly 1,800 people followed for 18 months confirmed a 27% reduction in cognitive decline in patients treated with lecanemab, a drug developed by the Japanese pharmaceutical group Eisai and the American Biogenic.

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This “statistically significant” proportion, according to the two groups, had already been announced at the end of September. But the full study, published Wednesday in the New England Journal of Medicine, also specifies the incidence rates of adverse effects of lecanemab, sometimes serious and notably more frequent than in the group of patients on placebo.

Thus, 17.3% of patients treated with lecanemab suffered from cerebral hemorrhages, compared to 9% in the placebo group. And 12.6% of people who received this experimental drug suffered from cerebral edema, compared to just 1.7% in the placebo group.

However, the overall mortality rate is practically the same in the two groups of patients in the study (0.7% in people fed with lecanemab, 0.8% for those on placebo).

“A real treatment option”

“It’s the first drug to deliver a real treatment option for people with Alzheimer’s,” said Bart De Strooper, director of the UK’s Dementia Research Institute.

“Although the clinical benefits appear somewhat limited, they can be expected to become more apparent if the drug is administered over a longer period,” the professor revealed.

In Alzheimer’s disease, two key proteins – tau and another called beta-amyloid – gradually build up abnormally in the brain, causing brain cell death and brain shrinkage.

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This causes, among other things, memory loss and an increased ability to perform daily tasks. This disease is one of the main public health problems, affecting more than 40 million people worldwide.

Lecanemab targets deposits of beta-amyloid protein but only in the early stages of Alzheimer’s, which could prevent its use because this disease is often late onset.

With AFP


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