#Mog antibody disease treatment full

But those measures, like regular MRI scans to detect brain swelling, bring their own burdens. Because the number of patients who died in the trials is so small, it’s impossible to say whether these drugs cause more deaths than expected, and he thinks the safety measures in place will likely protect patients from severe side effects. Rojas, who has administered both drugs to patients in the clinical trials, is more sanguine about their safety. For the companies, she says, “there’s only downside” to interrogating the effects of their drugs further-so they might not do so.

#Mog antibody disease treatment full

But now that they are poised to obtain full FDA approval, Maria Glymour, a professor of epidemiology and biostatistics at the University of California, San Francisco, says she worries we may not ever have solid data. Much more research is needed to understand the long-term effects of anti-amyloid drugs. And though the data is limited, there’s some preliminary evidence that patients don’t see any additional slowing of their cognitive decline after finishing their course of lecanemab, and from this point decline at the same rate as untreated patients-making any relative benefits of the drug smaller over time. Within 18 months, both lecanemab and donanemab wiped most patients’ brains clear of excess amyloid beta, so taking the drugs for longer may not provide any additional benefit. But there’s little reason to think that should be the case. “That’s meaningful,” he says.įraming the effects as a percentage also subtly suggests that patients who took the drug could still be doing 35 percent better than their peers years later, says Howard. Julio Rojas, an associate professor of neurology at the University of California, San Francisco, says that half a point of slowing could let someone drive independently for several additional months. Patients, though, might notice things that escape doctors. Those changes could be almost unobservable to an outsider: In one study of people with Alzheimer’s, doctors reliably saw a difference in patients only when their CDR score changed by one point or more. On the CDR, 0.5 points is the difference between “slight” and “moderate” impairment in a single area, like memory or community relationships. Whether or not a drug with such modest benefits and weighty risks is “worth it” depends partly on how much one values a life lived with Alzheimer’s disease. At the same time, the risks are substantial: Several patients may have died as a result of taking these drugs. The 0.5- and 0.7-point differences on the CDR are averages, so the real impact may vary substantially between patients, and a half-point difference might be too small to be meaningful. But rolling out these drugs will need careful consideration.

Predictably, there’s been a lot of excitement about potentially altering the course of Alzheimer’s. In June 2021, the US Food and Drug Administration (FDA) gave the antibody aducanumab a preliminary form of authorization called accelerated approval, though the decision was mired in controversy-many experts believed there was no reason to think the drug would help patients. Those treatments are finally here in the form of anti-amyloid therapies-antibodies designed to target a protein called amyloid beta that accumulates into plaques in the brains of people with Alzheimer’s disease. “We didn’t realize we were going to have to wait more than 20.”

“The story was, within a few years, we should have drugs that will actually interfere with disease processes,” says Rob Howard, a professor of old-age psychiatry at University College London.

It seemed like disease-modifying drugs would be coming any day. True, the drugs didn’t slow the underlying disease, but they made a meaningful difference to symptoms. Nearly 30 years ago, when the first effective Alzheimer’s drugs were approved, optimism was in the air.