A worldwide quest is under way to find new treatments to stop, slow or even prevent Alzheimer's disease, and the Alzheimer's Association is playing a leading role. Since awarding our first grants in 1982, we have given more than $300 million to over 2,100 best-of-field proposals. We have been part of every major advancement in Alzheimer's research during the past 30 years.
We recently spoke with Dr. Dave Morgan, a renowned researcher whose work has received Association support. His confidence in science's ability to conquer Alzheimer's gives us reason to hope – for answers, for treatments and ultimately, for a cure.
There are three levels at which we can treat a disease: Prevention, treatment and cure. Prevention is easiest, because people aren't sick yet and there's no physical damage. Prevention is where we can make the most impact. I believe the tools necessary to prevent Alzheimer's disease are within reach.
That doesn't mean people won't get the disease – not everyone will find out they're at risk and not everyone will take the medicines available to them. But, my hope is that in the not-too-distant future, if you're willing to get a PET scan or spinal tap to determine if you're at risk, you'll be able to take drugs to delay the onset of the disease and presumably prevent it in your lifetime.
Please take a moment to read Dr. Morgan's message and help us move the fight forward.
What causes Alzheimer's?
I can say that with confidence in part because scientists have reached a consensus during the past 20 years – the majority believes that the initiating factor for Alzheimer's disease is the accumulation of a substance called beta-amyloid. Amyloid deposits that build up in the spaces between nerve cells are called "plaques." Most people develop some plaques as they age, but those with Alzheimer's tend to develop far more.
For the past 20 years, my lab has focused most of its work on animal models, trying to identify ways to produce plaques in rats or mice. Because we've succeeded, we're now trying to develop effective treatments effective in mice that may translate into human clinical studies. We were one of first groups to show that a vaccine, using the amyloid peptide, could reduce amyloid in the brain and reverse memory loss.
While we found that the drugs worked well in mice, they didn't work well in people. We were treating the humans too late; by the time the first Alzheimer's symptoms appeared, human brains had all the amyloid they'll ever have. We're going to start testing drugs at an earlier stage, even before people show symptoms. New discoveries allow us to detect amyloid in the brain even before clinical symptoms appear. We'll start these tests this summer.
We need resources, not miracles
We don't need miracles to prevent this disease – what we need are the resources to complete these challenging and expensive clinical trials.
The analogy of Alzheimer's to AIDS is an interesting one: About 20 years ago, AIDS advocates launched a campaign to gain federal funding for research, and it worked. The amount of money put into AIDS research was incredible – about $3 billion to this day, which helped lead to effective treatments for the disease.
On the other hand, Alzheimer's has received significantly less federal funding than AIDS, yet it affects far more people and costs our nation 10 times as much. We've seen from the AIDS example that unevenness in funding can be overcome – and it can't come too soon.
During the last three or four years, there's no doubt in my mind we've made a lot of scientific progress in the fight against Alzheimer's. The pace has picked up and we're on the cusp of finding preventive therapies. It's a fascinating time to be a researcher in this field – and a promising one.