An analysis of data from 17 clinical trials of two drugs presented as a “breakthrough” or “revolution” in the treatment of Alzheimer’s disease has found that they do not have a meaningful effect on slowing cognitive decline.

Researchers stated that the effects of the drugs donanemab and lecanemab did not lead to significant improvements in the quality of life of patients with dementia.

Some Alzheimer’s experts criticized the analysis, calling it methodologically flawed.

The controversial drugs target a sticky substance called beta-amyloid, which accumulates between brain cells in Alzheimer’s disease.

To detect and clear amyloid from the brain, scientists developed special antibodies similar to those the immune system produces to fight viruses and bacteria.

For many years, this approach did not produce results. However, trials of donanemab and lecanemab suggested that they may slow the rate of cognitive decline.

This finding was initially seen as revolutionary, as it marked the first time that drug treatments appeared able to slow brain degeneration in Alzheimer’s disease.

The Cochrane Collaboration, an international non-profit research network, analyzed 17 studies involving 20,342 participants, examining seven drugs designed to remove amyloid from the brain.

The researchers concluded that these and similar medications do slow the progression of Alzheimer’s disease, but not to a degree that produces a meaningful benefit for patients. In addition, these treatments are associated with risks such as brain swelling and bleeding, must be administered every two to four weeks, and are very expensive.

One of the report’s authors, Professor Edo Richard, a neurobiologist at Radboud University Medical Center in the Netherlands, who treats dementia patients in his clinic, commented: “I would tell them: ‘I don’t think these drugs are likely to help you, and they will probably be a heavy financial burden for you and your family.’”

At present, the UK’s National Health Service (NHS) does not purchase or provide these drugs, and an 18-month course of treatment in a private clinic costs around £90,000.

“I think it is extremely important to be honest with patients about what they should expect. I always try to be careful not to give people false hope,” he said.

Richard added that other approaches to Alzheimer’s treatment should now be explored, such as targeting inflammation in the brain.

The findings were also supported by long-standing critics of these drugs.

Professor Robert Howard of University College London (UCL) said it was “sad and unfair” for families affected by dementia that these treatments were promoted “without sufficient scientific justification, creating false hope.”

However, the Cochrane analysis itself sparked intense debate in the scientific community.

Many experts argue that differences in mechanisms between individual drugs are important, and that it is unfair to group older experimental therapies with newer ones that have shown proven efficacy.

The researchers maintain that all the reviewed drugs remove amyloid from the brain, and therefore their analysis reflects whether this overall approach is effective.

Professor Bart De Strooper of the UK Dementia Research Institute at UCL said the review “does not clarify the evidence, but rather obscures it.”

“Many early developments failed, but newer antibodies have brought modest but real clinical benefits,” he said.

“It is very important that we approach this review with full nuance, rather than using a sledgehammer to dismiss decades of innovative research,” said Dr Richard Oakley of the Alzheimer’s Society, a charity funding Alzheimer’s research.

In the UK, decisions on which drugs the NHS should purchase are made by the National Institute for Health and Care Excellence (NICE), which considers both cost and proven effectiveness. It previously judged that donanemab and lecanemab were not cost-effective, but in late March agreed to re-evaluate the data, taking into account the burden of dementia care on families.