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Goddammit, We Still Can't Cure Alzheimer's Disease

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Last summer, a promising trial of a new antibody treatment was shown to totally stop cognitive decline in four Alzheimer's patients over the course of three years, giving researchers hope that the disease could be slowed or even cured. This year, it was expanded into a double blind placebo test and administered to nearly 100 times more Alzheimer's patients. It proved ineffective. Goddammit.

The failed study was announced yesterday by Baxter, and did not show any difference between placebo patients and those given the drug. It follows two other studies—and huge disappointments—from last year that tried and failed to attack amyloid protein (amyloid plaques and tau protein both need to be present in the brain for a positive diagnosis).

An estimated 5.1 million Americans have Alzheimer's—35 million worldwide—and it's the sixth leading cause of death in the nation. Of course, we don't fear Alzheimer's as a particularly cruel disease because of its death count, but because of its tragic effect on the living. It's maybe the most heartbreaking affliction we have. Active Alzheimer's cases are only expected to rise with the aging population, as the risk of Alzheimer's doubles every five years after the age of 65, and the US's 65-and-older population will itself double to 88.5 million between 2010 and 2050. We need to figure something out, soon.


Despite the recent disappointing results, there are some other promising studies out there, too. Simply getting enough sleep might reap benefits down the road, or taking a pill to chemically enlargen a part of your brain that shrinks in patients with dementia or clinical depression could help. Pacemaker-like implants have even been looked at, and are promising. But we still don't know what's going wrong in these studies.


It might be that scientists need to look elsewhere, away from just amyloid protein. Maybe tau, which is instrumental in the cognitive mess made of NFL players' brains, will be looked at more closely soon. Maybe a type of blocking agent for both, or something else. It's hard to say, because all we're looking at for now is a bunch of failed attempts, on patients who might even be too far along with the disease to help. By the time symptoms begin to show, the disease could be more aggressive and harder to control. We just don't know.

There are some promising advancements in diagnosing the disease—the UCLA-developed FDDNP[18] PET scan marker that attaches to both tau and amyloid, for instance—but they are still prohibitively expensive for anyone not experiencing any symptoms. There are other types of tests for brain disease, like computerized cognitive testing, but all require symptoms to begin to manifest, which may be too late.


Look, this is just how science works, and "try harder, jerks" is the least helpful of the many sentiments that come up in discussions about for-now incurable diseases. Science tried something, and it didn't work. That's OK. Soon, it will try something else, and that might succeed where everything else has not, or it could be that it won't. It won't stop trying; Sisyphus will get that damn boulder on top of that hill. But for now, we're rolling right back to where we started, and that's terribly disappointing. It's OK to just say that this sucks. [Technology Review]


Image: Shutterstock/Andrii Muzyka