Alzheimer’s drugs don’t work—because it’s nothing to do with amyloid plaques in the brain

New Alzheimer’s drugs—hailed as breakthrough’ therapies—don’t work.

The drugs, donanemab (Kisunla) and lecanemab (Leqembi), are supposed to slow cognitive decline in early-stage Alzheimer’s by attacking beta amyloid, proteins that form into plaques in the brain and interfere with neural signalling.

Studies sponsored by the manufacturers showed they were working—but a review by independent researchers has concluded that the benefits were “well below” what was needed to make a difference to dementia patients’ lives.

The Cochrane Collaboration, which analyses medical data, looked at 17 studies involving 20,342 volunteers with mild cognitive decline, who were taking one of nine drugs that remove amyloid from the brain.  Overall, they concluded the approach does slow Alzheimer’s disease, but not by enough to make much difference to the day-to-day lives of patients.

“Unfortunately, the evidence suggests that these drugs make no meaningful difference to patients,” said lead author Francesco Nonino, neurologist and epidemiologist at the IRCCS Institute of Neurological Sciences of Bologna, Italy.

Any marginal gains are offset by dangerous side effects that include brain swelling and bleeding.

The drugs are also expensive.  In the UK, they’re not available under the NHS, and cost the patient around £90,000 a year to buy them privately; the National Institute of Health and Care Excellence (Nice) – which decides on the drugs the NHS will pay for – has rejected them for the same reasons cited by the Cochrane researchers.

The Cochrane review believes the amyloid theory is a false trail.  Although the drugs remove the plaques in the brain, patients aren’t showing any real improvement in their cognitive abilities.  Instead, Alzheimer’s research needs to focus on other possible causes, such as inflammation.

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