A batch of new drugs that aim to clear the gunk out of the brains of Alzheimer's patients are providing the best hope yet that it might be possible to slow the disease.
But they're not even close to being a cure, experts said — and they're also not close to being on the market.
And, researchers admit, the benefits they see amount to numbers on a graph, not anything that patients or their loved ones might notice.
Researchers reported on the trials of three experimental drugs that use immune system weapons called monoclonal antibodies to clear the brain-clogging protein called amyloid.
They think their results show that the drugs might work if they use a high enough dose and if they treat patients in the very early stages of the disease, before their brains are too damaged.
Dr. David Knopman of the Mayo Clinic said he knew headlines would have his patients asking about when they can get the drugs.
"How am I going talk to my patients on Friday?" he said at a news conference. "These results aren't going to lead to something they can get next week. What you are hearing here represents solid advances."
The three drugs being highlighted at the Alzheimer's Association International Conference are called solanezumab, aducanumab and gantenerumab. (The "mab" at the end of the drug name stands for monoclonal antibody). They specifically attack amyloid.
Solanezumab, made by drug giant Lilly, disappointed patients, researchers and investors when it didn't seem to help patients in 2012. But the developers kept studying it, trying to see if it maybe offered a small benefit when given to people early. They compared people who got the drug right away in the trial to those who had been taking placebo - giving the drug to all the patients to see if there might be a difference.
They found one. When they looked at the combined memory and thinking test scores of all the volunteers three years later, those who got the drug early seemed to be doing better. Those who got it later could not seem to catch up. That suggests a small, hard-to-measure benefit.
"We should think about these drugs as slowing progression of an underlying disease," said Dr. Paul Aisen, director of the Alzheimer's Therapeutic Research Institute at the University of Southern California.
The the test scores don't translate into day-to-day life changes, Aisen said. "The cognitive measures do not have a direct relationship to clinically apparent benefit," he told reporters.
"We see … in mild subjects roughly a one-third slowing of decline."
Over the long-term, however, that could add up to many more days living at home, for instance, he said.
"The changes we are making are modest," said Knopman. "That is why you need to treat it really early, early, early."
Aducanumab, also known as BIIB037 and made by Biogen, appears to be clearing the amyloid from the brains of patients, researchers told the meeting. There's also some evidence that this might be improving test scores in the patients who got the very highest doses.
Biogen is moving ahead to a phase III study - the very last stage before seeking Food and Drug Administration approval. They'll test it in people who have very early Alzheimer's disease or who have what's called mild cognitive impairment - changes in memory and thinking that can lead to Alzheimer's.
Patients who got it did better on memory tests called the Clinical Dementia Rating or CDR and the Mini-Mental State Evaluation or MMSE, said Dr. Jeff Sevigny of Biogen.
"We observed statistically significant, dose-dependent slowing of decline on both MMSE and CDR," Sevigny told the news conference.
But again, nothing that patients would notice. And not all Alzheimer's experts agree that removing amyloid is affecting the underlying disease. "We can't say that yet," argued Dr. Rachelle Doody of Baylor College of Medicine.
Lilly's has also started a phase III clinical trial, although results are more than a year away.
A careful look at patients who took gantenerumab, another drug that failed in tests, showed it might just be that people were not given enough of it, said Dr. Philip Scheltens, director of the Alzheimer's Center at the VU University Medical Center in Amsterdam, Netherlands.
"Probably the doses were too low to be clinically efficient and effective," he said. But an analysis showed it was affecting a protein called tau, which some people believe might cause Alzheimer's and which does indicate brain cell damage.
Researchers will have to take care. High doses of the drugs also cause brain inflammation, which might indicate the drugs are working but which can cause headaches, dizziness and which, in other drug trials, were deadly.
"The data from these new analyses present exciting possibilities, and we look forward to the results of future studies in these experimental drugs," said Maria Carrillo, chief science officer of the Alzheimer's Association.
The researchers are keen to offer some hope, both for patients but also so that investors will continue to support development of new drugs. More than 5 million Americans have Alzheimer's, a number the Association projects will balloon to 28 million by 2050.
The Alzheimer's Association is asking Congress to fund more government research, which usually goes to early stage research hat drug companies are often reluctant to do.
"It takes big money, big time, to get us there," Knopman said.
Scheltens and other experts said no single drug will probably work. As with cancer and the AIDS virus, it will probably take a combination of drugs to help, he said. "I think Alzheimer's disease is a very complex disease," he said. "I think we ultimately will have no single method (to treat it)."
There are just a handful of Alzheimer's drugs on the market now, all approved more than a decade ago. They include Aricept, Namenda and Exelon, and they can treat symptoms for a while but do not affect the disease itself.