The Cochrane Collaboration concluded that amyloid-removing Alzheimer's disease drugs slow disease progression but not sufficiently to produce a meaningful clinical benefit for patients, following a systematic review of 17 studies involving 20,342 participants. The review found that while clinical trials of donanemab and lecanemab showed they slowed cognitive decline, the drugs are unlikely to benefit patients in a clinically meaningful way.

The drugs target beta amyloid, a sticky substance that accumulates in the spaces between brain cells in Alzheimer's disease. Engineered antibodies designed to mimic the body's immune response can bind to and remove beta amyloid from the brain, and clinical trials had represented the first demonstration that a drug could slow brain tissue destruction in the disease. However, the drugs carry risks of brain swelling and bleeding, must be administered every two to four weeks, and have a high cost.

In the United Kingdom, amyloid-removing drugs are only available through private payment, making them unaffordable for most people. The National Health Service does not cover the drugs, and an 18-month course costs £90,000 privately. The National Institute for Health and Care Excellence previously rejected these drugs for NHS coverage and is reviewing the evidence to consider the burden on unpaid carers.

Prof. Edo Richard, a professor of neurology, said he would counsel patients against the treatments. "I would tell them, I think you will probably not benefit from these drugs and they're burdensome for you and your family. I think it's extremely important that we're honest to our patients about what they can expect, I'm always wary to avoid giving people false hope." Richard also said that alternative treatment approaches for Alzheimer's disease, including targeting brain inflammation, need to be explored.

Prof. Robert Howard, a professor at University College London, said that hyping these drugs without robust scientific support was unfair to families affected by dementia and raised false hopes. Dr. Richard Oakley, a researcher at the Alzheimer's Society, urged caution in interpreting the findings. "It's essential that we interpret this review with nuance and avoid taking a sledgehammer to decades of pioneering scientific study," Oakley said.

Several studies published over the past few years arguing that amyloid-β is the central driver of Alzheimer's disease have been retracted, and some scientists have been indicted for fraud related to amyloid-β research. The journal Neurobiology of Aging retracted a 2011 paper claiming that a form of amyloid-β was responsible for memory loss in the disease. No drugs targeting amyloid-β have produced significant clinical benefits in patients to date.

Research into amyloid's role in Alzheimer's stretches back decades. In 1984, researchers identified amyloid-β accumulating in the plaques of patients' brains. In 1999, Elan Pharmaceuticals developed a vaccine against amyloid-β that cleared brain plaques in transgenic mice carrying a mutated human APP gene, but a clinical trial of the vaccine in 360 patients with mild to moderate Alzheimer's disease was suspended after several participants developed brain inflammation.