Tuesday 4 October 2022 01:30 AM Will the new Alzheimer's drug ward off brain decline? trends now
Could the tide finally be turning in the hunt for an effective treatment for Alzheimer’s disease? That was the suggestion from a story last week about a new drug, lecanemab, which seems to improve symptoms of early Alzheimer’s.
For decades, scientists have been working on drugs to treat the condition without much success, so understandably there was excitement after the pharmaceutical companies behind lecanemab — Eisai and Biogen — announced that it slowed early Alzheimer’s, specifically cognitive decline, by 27 per cent over 18 months in a trial of 1,795 people.
However, while this was greeted as an ‘historic moment’, the trial data is not yet available for independent scrutiny — and previous experience with similar medicines suggests we should be cautious.
The preliminary lecanemab data is unique as it shows the drug can slow down disease progression
Last year, Good Health reported on aducanumab, the first new medicine for Alzheimer’s in two decades to be approved by the U.S. regulator, the Food and Drug Administration (FDA).
The approval was controversial because despite clearing plaque in the brain (seen as a hallmark of Alzheimer’s), the drug did not significantly improve symptoms.
In addition, more than 35 per cent of the trial participants experienced brain side-effects, including swelling, reported a study in the journal JAMA Neurology earlier this year, which analysed data from a number of trials.
There are also ongoing investigations into a very small number of patients who died after taking aducanumab. Lecanemab works in a similar way to aducanumab (but seems to target a slightly different type of amyloid) — and the preliminary data suggests the rate of side-effects, such as brain swelling or bleeding, was 21.3 per cent in the lecanemab group and 9.3 per cent in the placebo group; something the developers described as ‘within expectations’.
Both aducanumab and lecanemab clear the brain of plaque, formed of a build-up of a sticky protein called amyloid — this has been linked to dying nerve cells.
Until now, most drugs that target the amyloid, including aducanumab, haven’t led to a clinical benefit, i.e. improved
