Thank you. I'm very pleased to be here.
My ultimate endeavour is to make you join us in thinking this is the right time to put more money into research. My specialty is taking the mystique out of mystical things, and if you don't mind, I'm going to do this with Alzheimer's disease.
I will remind you that 100 years ago, Dr. Alzheimer had a patient with what was then called senile dementia. It was later called Alzheimer's disease. She was only 49, by the way, and when she died a few years later, he did something that was relatively unprecedented at that time; he looked at her brain in the microscope and he saw things he did not see in the normal brain. It was as if you'd taken a pot of pepper and shook it all through the brain. You had all these little dots that you saw in the microscope, and he called them the “plaques”. Then he looked inside the nerve cells, which you also can't see by eye but you can see in the microscope. They were as if you had a ball of wool inside that started to unravel, which he cleverly called “tangles”. The plaques and the tangles that he described are often called the hallmarks of Alzheimer's disease.
Since then, in that 100 years, we've discovered that the plaques, first of all, are made of a protein. It's called beta amyloid—it doesn't matter whether you remember the name or not—and it's a normal protein. We all have it in our brains, but in Alzheimer's disease the concentration of this protein goes up, and as it goes up, the molecules start to stick together until enough of them stick together and they deposit down as a plaque. The tangles he saw in the nerve cells tend to come afterwards. Finally, it was discovered that the real toxicity that was going on was not due to the plaques as such but due to the molecules even before they had stuck together and formed the plaques. In fact, as they start sticking together, they become toxic.
I hope this background will allow you to understand why research has had one primary objective in Alzheimer's disease, and that is to get rid of this suspect protein, this amyloid that accumulates. If you get rid of that, you won't get the toxic effect on the nerve cells, you won't get the tangles, the nerve cells won't get sick and die, and we won't get the dementia.
That's what the dementia and the brain has been all about in Alzheimer's disease, until the last year and a half to two years. We're at a crossroads now. I'll explain this by telling you about two or three phenomena, and you'll see immediately what the point is.
First of all, they looked at a lot of very old people, people in their nineties and hundreds, who did not have a dementia. They did not have a dementia, but they looked at their brains and they were full of plaques and tangles. If a pathologist had looked at their brain, he would have said they had Alzheimer's disease. Well, they had Alzheimer's disease of the brain, but they didn't have a dementia. The dementia is what we're concerned with—the sort that Debbie just spoke about. That's what we're worried about: the dementia. I don't care what's in my brain as long as I don't have a dementia.
The second observation comes from 10 years ago. One way to get rid of this suspect protein was to make a vaccine against it. A vaccine, essentially, is to create antibodies in the body. They circulate in the body. They recognize the dangerous molecule or virus, or whatever it is you're trying to get rid of. They neutralize it and then the cells of the immune system carry off the neutralized product.
So they made a vaccine. The vaccine worked well on animal models, so they tried it on humans. They ran it for two years, and then some of the people started to get a potentially lethal inflammation of the brain. All over the world the vaccine studies were stopped. But the people didn't die; they continued on. Then some of them started to die, and when they looked into their brains, the vaccine had worked. The plaques had virtually disappeared. To all intents and purposes, they'd cured Alzheimer's disease, but the dementia was unchanged.
There are more and more examples where we're seeing that these classical signs of Alzheimer's disease in the brain don't necessarily match up to the thing we're worried about, which is the dementia. Although this sounds very dismaying, we have now realized there were three or four other things that Alzheimer didn't see in the brain that were looked at—some people have always worked on them—which are also characteristic of Alzheimer's disease, but they haven't been the primary target of the research. Now they're coming into focus as what should be a very urgent target for research, not just to get rid of this amyloid, which has driven the research, as I say, for the last 10 years, but to attack these other areas.
To give you just one example of these other areas, for every nerve cell in your brain, there are 10 cells called glia cells; I call them the caregiver cells. They are the cells with all the intelligence in the brain. The nerve cells are kind of dummies, really; they can't do much at all. Compared to a skin cell, a nerve cell is a real idiot. But the reason it does so well is because of these caregiving cells. They tell it everything. They tell it to grow, they tell it to stop growing, they tell it to make branches, they tell it to make new connections.
So the glia are really the bright guys in the brain, and it's now been discovered that they are impaired in Alzheimer's. If they were the primary target of the disease, you can understand why the nerve cells get sick and die. This is just one example of a new approach to research, and it's very exciting.
Now in the Alzheimer Society, one of our main thrusts is to produce the researchers of tomorrow. We have a very active training program. Those researchers are absolutely primed now to begin their careers with this new thrust into Alzheimer's research, which I believe is going to produce the cure—along with the original thrust. But of course we can't do it unless they have the money to do the research.
Right now, 40% of 100 hundred applicants to most agencies get funded—although the agencies would like to fund the other 60%. It happens with us; it happens with CIHR. That's where we need it.
And they're young, they're ready to go, they're bursting with enthusiasm, and they're dedicated to Alzheimer's research--but they can't get the money.
I think I'll leave you with that thought as to how we can really combat this disease by just injecting money into the research.