Earlier this month the U.S. Food and Drug Administration announced the approval of a new drug to treat Alzheimer’s disease, the first in almost 20 years. The drug, a protein with the tongue-twisting name of aducanumab (ad-yoo-can-yoo-mab), is touted as the first to slow the otherwise inexorable cognitive decline of Alzheimer’s.

The approval was naturally met with exuberant cheers from the drug’s maker, Biogen, and its investors, but also from many physicians, scientists and patient advocacy groups, who believe the approval of aducanumab represents the dawn of a new era in treating this most common form of dementia.

Many other doctors and researchers in the field, however, including myself, disagree, considering aducanumab’s approval to be a travesty and a tragedy. A travesty of medical science, as it assumes the drug should be effective despite lack of convincing evidence. And a tragedy for Alzheimer’s patients and their loved ones and caregivers, because at best the drug will only drag out the disease process.

No one will be cured. No one will become their old clear-thinking selves. No one will even have their slide to dementia halted. It may slow the decline, but the rate of slowing, and its significance in everyday life, remain unclear. My father died from Alzheimer’s 10 years ago. As hard as it was to watch him decline in this terrible way, I would not have recommended aducanumab for him.

Aducanumab is an antibody that binds to protein plaques in the brain. These deposits — made of a sticky protein called beta-amyloid — are characteristic of the disease. But whether amyloid plaques cause the disease or are coincidental markers remains unclear.

Studies of hereditary Alzheimer’s led to discovery of responsible genetic mutations, all of which directly affect beta-amyloid production. These findings appeared to confirm the “amyloid hypothesis” of Alzheimer’s disease, that clumping of beta-amyloid is the trigger of the disease process. As a corollary, blocking the production or clumping should prevent or slow this process.

But after nearly two decades, every drug candidate that targeted amyloid plaques failed to make people better. Biogen’s aducanumab seemed like the best bet to prove the amyloid hypothesis, as studies showed it clears amyloid plaques from patients’ brains. If aducanumab could slow or halt disease progression, it could help millions — and it would also prove that the long-held amyloid hypothesis was correct.

The results from two large clinical trials, however, were not promising. Biogen halted both trials after a so-called “futility analysis” suggested the drug was not effective. It seemed like aducanumab was another amyloid-targeting bust.

Months later, though, the company did an about-face: Post-hoc analysis of those at the early stage of disease who were in the highest-dose treatment group showed a marginal 22% slowing of decline — four months over an 18-month period — in one of the trials but not the other. On this basis, Biogen moved forward with a new drug application.

The bias favoring the results from only one of the two trials was called out by the FDA’s own advisory board, which stated emphatically that there was no clear evidence that aducanumab was effective. Nevertheless, under strong pressure from patient advocacy groups — desperate after many years of clinical trial failures — the FDA approved aducanumab for Alzheimer’s without any qualifications. The agency did demand, however, that Biogen carry out post-approval studies to show drug effectiveness, due in 2030.

In the meantime, Biogen and its investors will reap enormous profits. The drug, given monthly by infusion, is priced at $56,000 for a one-year treatment course. If Medicare pays, it could bankrupt the system. If Medicare does not, then only the wealthy will be able to afford treatment. But even if only 5% of the more than 6 million Alzheimer’s patients in the U.S. will pay for the drug, Biogen would rake in $17 billion a year. By 2030, that could easily amount to $150 billion total.

Biogen will get very rich, with little to no benefit to patients. Indeed, it may make them worse: the drug can cause brain swelling, among other adverse events. Other companies will jump on the bandwagon, working to develop their own antibodies to get a slice of the huge Alzheimer’s market. Precious resources will be diverted from other, more promising avenues of investigation.

In the face of this travesty and tragedy, the public should hold Biogen and the FDA accountable to show unambiguous effectiveness in controlled post-approval clinical trials. For the sake of the millions who will develop and die from Alzheimer’s in the coming years unless truly effective therapeutics are found.

— Michael S. Wolfe is the Mathias P. Mertes Professor of Medicinal Chemistry in the KU School of Pharmacy, where he leads a laboratory investigating the molecular basis of Alzheimer’s disease.