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« Back to The Race to Cure Alzheimer’s main page    Transcript for: The Race to Cure Alzheimer’sANNOUNCER: Funding for Think Tank is provided by the T. Rowe Price Associates, an investment firm providing mutual funds, brokerage services, and retirement plan services. T. Rowe Price, invest with confidence, T. Rowe Price Investments, Incorporated.We’re Pfizer, we’re looking for the cures of the future, spending about $4-1/2 billion a year in search of new medicines for the 21st Century. Pfizer, life is our life’s work. Additional funding is provided by the Lynde and Harry Bradley Foundation, the John M. Olin Foundation, the Bernard and Irene Schwartz Foundation, the Smith Richardson Foundation, the Donner Canadian Foundation, and the Dodge Jones Foundation. (Musical break.) MR. WATTENBERG: Hello, I’m Ben Wattenberg. Alzheimer’s disease is the fourth leading cause of death in the United States, following heart disease, cancer, and stroke. It is a terrifying affliction that robs its victims of a sense of self, and of a meaningful relationship with the outer world. Recently however some major breakthroughs have brought hope to scientists seeking treatments and cures. What is being accomplished in the ongoing fight against Alzheimer’s. To find out Think Tank is joined by: Marcelle Morrison-Bogorad, associate director of the National Institute on Aging’s neuroscience and neuropsychology of aging program; Paul Aisen, professor of neurology and medicine at Georgetown University; and Judy Riggs, director of federal and state policy at the Alzheimer’s Association. The topic before the house, attacking Alzheimer’s, this week on Think Tank. (Musical break.) MR. WATTENBERG: Alzheimer’s disease, it is a malady that slowly and inevitably erodes brain function, progressing from forgetfulness to loss of ability to perform the simplest of household chores. But, in this age of rapid scientific advances there is progress. Researchers now know that Alzheimer’s causes the formation of abnormal structures in the brain called plaques and tangles. As they accumulate in affected individuals nerve cell connections are reduced, eventually the disease works its way into sections of the brain that control intellectual and physical functions. Armed with such knowledge in the last few years researchers in both the public and private sectors have been racing ahead. One breakthrough involves a vaccine, which has proven successful in mice. Some experts have said that we will shortly have available not one but several drugs capable of slowing, and perhaps even halting the progress of the disease. It is a race against time. The longer people live the more likely they are to contract Alzheimer’s. While one in ten persons over 65 have the disease, by age 85 nearly half do. There are currently 4 million cases of Alzheimer’s in America. Without a cure, as the baby boomers age that number is expected to rise from 4 million to 14 million by the year 2040. Ladies and gentleman, thank you for joining us. Marcelle, can you start us out and tell us what’s going on in the field that leads people to be excited and hopeful? MS. MORRISON-BOGORAD: I think the major reason that people are excited and hopeful is that we are very close to understanding how some of the basic science research is going to lead to drugs that might slow or halt the disease completely. So developing from all the basic research findings, there are several avenues of exploration that look like they’re giving results. One is the vaccine that you mentioned, which if it works is a tremendous and completely unexpected breakthrough. MR. WATTENBERG: Would a vaccine prevent someone from getting it, or halt it once you have it, or reverse it, or all of the above? MS. MORRISON-BOGORAD: Well, in mice I think it seems to halt it before they get it. So the vaccine stops plaques developing in mice models of Alzheimer’s disease. The vaccine halts the progression of plaque development when mice have already got the disease, and to a certain extent reverses it, as well. MR. WATTENBERG: Dr. Aisen, Paul, you are working actually on the front lines of these various testing procedures? MR. AISEN: I’m working on clinical trials, testing various treatments for the disease. Fortunately -- MR. WATTENBERG: At Georgetown University? MR. AISEN: Yes, I’m at Georgetown, and right now we’re conducting a nationwide trial to try to slow the progression of the disease in individuals who already have it. We’re taking one approach in this trial, one among many, we’re trying to use anti-inflammatory drugs to slow the slow the rate of progression, because one of the problems that occurs in the brain in Alzheimer’s disease, is that there’s a destructive inflammatory action to the plaques that you mentioned. We think that if we can control the inflammation we can protect the brain cells against further damage. MR. WATTENBERG: Is there some evidence that some of the anti-inflammatory drugs, like Advil or something, have in fact reduced the incidence of Alzheimer’s? MR. AISEN: There is some evidence, there are a number of epidemiologic surveys which have examined this question, whether use of anti-inflammatory drugs such as ibuprofen, whether use of those drugs over a period of years reduces the risk of the disease. And those studies suggest that it may. MR. WATTENBERG: You’re beyond pure research, and into testing products? MR. AISEN: That’s right. We’ve been testing products for many years, the research has allowed us to focus on one particular step in the pathogenesis of the disease. MR. WATTENBERG: Judy, who is doing most of this? Is this the federal government, universities, the private sector, some combination thereof? MS. RIGGS: Well, it’s a combination. The Alzheimer’s Association, for example, has put almost $100 million into Alzheimer’s research and that’s all from the private sector. The drug companies spend a lot of money testing potential compounds. But, the real superstar in this is the National Institutes of Health. That’s where the money comes from. Led by the national institutes on aging, that’s where the basic science is, that’s -- I mean, it is the gold star in the federal government. And if it were not for the NIH none of the investment from the private sector would make a difference. MR. WATTENBERG: Just in reading some of the popular literature, is it correct that people with lower educational levels are more likely to be afflicted with Alzheimer’s? MR. AISEN: It seems to be. It seems to be that studies suggest that the more years of education you have the lower your risk of developing the disease. And the idea is that you build up a brain reserve, so that you’re less susceptible to symptoms caused by plaques and tangles that damage brain cells. MR. WATTENBERG: Is that sort of the general idea of use it or lose it, which you hear in a lot of aspects of medicine, anything muscular, I guess. MR. AISEN: That’s right. The idea is that this may apply to the brain, as well, and keeping your brain active through education, and continuing to stay vigorous, both physically but mentally, as well, can build up your reserve, and increase your resistance to neuro-degenerative diseases of the brain. MR. WATTENBERG: Your program is being funded by NIH. Why wouldn’t a private drug company say, Paul, this sounds great, do it for us, or do they? MR. AISEN: The goals overlap, the goals of the academic investigator, and the pharmaceutical investigator overlap. We’re both interesting in finding treatments or preventive measures to combat this disease. But, there are differences. Certain drugs have been around long enough so that they’re no longer protected, and drug companies may not be able to profit a great deal from the establishment of such drugs as a treatment. MR. WATTENBERG: In other words, if ibuprofen turned out to be the magic bullet, there’s not a whole lot of bucks in it for pharmaceutical companies? MR. AISEN: Exactly, so studies funded by NIH will look at any treatment out there, without regard to commercial potential. Whereas, a pharmaceutical company will have both altruistic and profit motives. MR. WATTENBERG: How much money does your agency put forth in research grants in the course of a year. MS. MORRISON-BOGORAD: Well, at the National Institute on Aging it’s about $350 million or so this past year. We don’t know exactly that figure, but it’s about that amount. MR. WATTENBERG: Who determines how much money goes to what disease. I mean, we’re here in Washington in a very political town, and we’ve seen in the last decade, or decade and a half the rise of sort of single disease, issue oriented groups. AIDS I guess being the predominant one. But, you’re doing it in Alzheimer’s, trying to focus attention and money on a single disease, as opposed to, am I right, general funding for NIH. And what do you all think of that? Does that make sense? MS. RIGGS: The way the Congress sets the priorities is to say, we’re going to put X amount of dollars into the National Institute on Aging, or the National Institute on Neurological Disease, or the National Institute on Mental Health. Those are the entities -- MR. WATTENBERG: But, when those institutes testify to Congress, they are indicating, and indicated to what diseases the Congress would like them to pay attention to. MS. RIGGS: Absolutely. Absolutely. And Congress has made Alzheimer’s disease a very high priority. But again, they don’t say to Marcelle and her colleagues at NIH, you have to spend X amount of dollars on Alzheimer’s disease. It is the science that comes to NIH that drives the funding. And that’s -- MR. WATTENBERG: Paul, do you agree with that? MR. AISEN: Well, I think it’s essential that you devote resources both to basic investigation, that’s not targeting a specific disease, and to specific diseases, and that you react the current situation, the current scientific environment. Now, it happens that right now in Alzheimer’s disease many of us believe that we’re on the brink of major breakthroughs. And it’s a result of many years of basic science research. Right now I think it makes sense to devote substantial resources to testing new treatments for Alzheimer’s disease specifically, because that’s where we are in studying the disease. MR. WATTENBERG: Would some of the treatments you’re working on allow the process to reverse itself, or is that permanent damage, I mean, one thinks of President Reagan, he’s pretty far advanced along this horrific path. Could some drug come along that would reverse that? MR. AISEN: It’s certainly possible. As Marcel said, in the mouse model one of the major breakthroughs in recent years has been the development of a mouse model of the disease, so there are now these mice that develop the plaques that are very similar to what occur in the brains of individuals with Alzheimer’s disease. And if you begin a vaccination program in these mice after they already have plaques they develop an immune response against this toxic peptide, and the plaques start to reduce -- to be re-sorbed, so there is some reversal of the pathology in mice that already have -- MR. WATTENBERG: So the brain function that involves remembering something when you stop remembering it, is that just damaged, or is that destroyed forever? MR. AISEN: Well, it’s a tough question. MS. MORRISON-BOGORAD: It’s a wonderful question. MR. WATTENBERG: Do you have a wonderful answer? MS. MORRISON-BOGORAD: Well, I think there are two answers. If the structure underlying the thought has gone, then I don’t think there is a reversal, but there’s some research now in normal aging which says that some of these crucial neurons in the brain, nerve cells, actually shrink, they don’t die. And if you give them certain boosting chemicals these neurons can pop back to life, and perhaps gin up your cognitive abilities again. Now, we don’t know if that’s true. We do know that they plump up again and seem to work better than they did before. MR. WATTENBERG: Is this a disease that in some ways is more devastating, in this sense, than the other major killers? I mean, if you have cancer or heart disease or a stroke, you may be suffering, you may be dying, but at least you are yourself. This is what you lose in Alzheimer’s. Is that better or worse, actually? MR. AISEN: It’s a very frightening disease, and you do lose yourself as the disease progresses. It starts out with just memory impairment, typically, difficulty encoding new information and without destroying the self, but it progresses over a period of years, typically over eight or ten years, the abnormalities spread throughout the brain, and all cognitive functions are affected, and you do destroy the self. That’s a horrible thing to watch in your loved one, and obviously it’s a devastating thing to go through. MR. WATTENBERG: Is the person who is a victim of Alzheimer’s, is he or she aware of what is happening to him or herself? MR. AISEN: Sometimes. MR. WATTENBERG: Sometimes? MR. AISEN: Sometimes, typically it’s people around them that are more aware. MR. WATTENBERG: I understand that. MR. AISEN: In fact, in general when someone comes into our program at Georgetown for evaluation of memory impairment, if they come in on their own worried that they can’t find their car, or lose their car keys, that’s less likely to be indicative of a serious problem. It’s when someone else has noticed a change, a family member or someone at work has noticed a change. That’s more suggestive of a real disease. MR. WATTENBERG: If everybody who lost their car keys was in trouble, you’d have more cases than there are people. MR. AISEN: So typically the individual is less aware of the problem than the people around that person. And I would also say that typically the disease is more devastating on family members than it is on the individual affected. MS. MORRISON-BOGORAD: That’s one of the major directions that research is heading right now, because we spent a long time trying to say what Alzheimer’s is, and from that basic research and research on the brains of people who died with Alzheimer’s, we know so much more about the disease, leading to treatments. But, now we’re saying, what happens earlier and earlier in the disease, when can we catch it? What are the first signs? If a person is 50 years old, is there any test we can give them, can we do imaging on their head, can we give them a psychological test, can we give them a genetic test that will sort of help us understand -- MR. WATTENBERG: Isn’t there a big argument about that, that until you have a cure it’s sort of almost sadistic to perform these tests and say, boy, you’re going to get it, without saying -- MS. MORRISON-BOGORAD: But, you can’t wait until you have a cure before you do all this research to determine how to find out who is going to get it. MR. WATTENBERG: Research in samples, but it would not be wise, or so goes the argument, to do it on the general public, to say you ought to get a screening for Alzheimer’s, is that correct? MS. MORRISON-BOGORAD: No. It’s like two streams or research converging on the goal of giving the drug before they get the disease. MR. WATTENBERG: We have a dissenter? MR. AISEN: No. MS. RIGGS: No. MR. AISEN: I don’t disagree. But, it is essential that we diagnose the disease earlier. We do have treatments now. We have drugs that help. We have important ways of improving the quality of life of individuals and their families with treatments that we have now. MR. WATTENBERG: Such as? MR. AISEN: Such as choline esterase inhibitors, which improve memory, and clinical status in individuals who have the disease. We now know that the use of antioxidants, such as vitamin E, helps to slow down the clinical progression. MS. RIGGS: One of the places where science is going right now, which is so exciting. You mentioned at the beginning of the show the $14 million people who will have Alzheimer’s disease by the middle of the century. Those are today’s baby boomers, those are us. And what the scientists are saying, I think, is that the process that leads to Alzheimer’s disease starts in the brain at least 10 maybe 20 years before you get the symptoms of the disease. So if I’m going to have Alzheimer’s disease in 15 or 20 years, which is when I would be at the age of risk, something is happening up here right now. And that, I think, is the excitement about these trials. If we can figure out a way to slow down the process before the symptoms appear, then I might have the changes going on in my brain, but I’ll never be disabled by Alzheimer’s disease. And if we can do that, that’s excitement. MR. WATTENBERG: Judy mentioned the word exciting, are you excited when you go into the office? MR. AISEN: Yes, I think this is a very exciting time. I think that seven years ago we had no treatments whatsoever. We now have drugs that really provide help to individuals and their families, and there are many exciting drugs that are entering clinical testing. It does take years to bring a drug from pre-clinical identification to proof that it’s effective in humans. MR. WATTENBERG: The ones you’re talking about, the anti-inflammatory, the vitamin E, things like that, they are all sort of outside of this profit making sphere that you were talking about. Are there some things -- I imagine there are, just read about it in the stock market, what are the drug companies looking at, and is it in the sort of older, big pharma kind of companies, or is it in the biogenetic area? MS. RIGGS: I think it’s in both. MR. AISEN: It is in both. We mentioned earlier some of the exciting leads that are being pursued by pharmaceutical companies, and one is the idea of a vaccine, and several companies are looking at potential vaccines to allow the body to clear these fragments before they do damage. The development of secretase inhibitors, this is a class of drug that seems to reduce the generation of these toxic fragments. And these would be new drugs that are being perceived by the -- MR. WATTENBERG: These would be classic blockbusters if they succeed. MR. AISEN: That’s right. MS. RIGGS: These large scale clinical trials are really the best hope for finding a way to prevent the disease. So we need to start those trials as fast -- I mean, the drug companies are out there where there’s a potential for a blockbuster drug doing them as fast as the ideas are there. And we need to be able to do that in the public sector, as well, just as fast as those ideas are there, so we get the answer as soon as we can, and that’s what the race is all about. MR. WATTENBERG: Is there some possibility that some of the things that we ingest in the normal course of our lives -- I mean, one hears it sometimes about antacids that those could be causative agents in Alzheimer’s, or is that just sort of a fairytale? MR. AISEN: There has been interest in investigating these questions. There are likely to be environmental factors that contribute to the risk of the disease. But, in fact, aluminum is not apparently a risk factor. There was concern because -- MR. WATTENBERG: So if I take Rolaids, I’m okay, we think? MR. AISEN: Correct. MS. RIGGS: But it is interesting. That’s an important point, because you hear a lot about -- MR. WATTENBERG: You hear a lot about a lot these days, you can’t pick up the pages of a newspaper or magazine without hearing about all the great breakthroughs and then when you start sifting through it, it gets much more complicated, which is why we try to do some programs like this. MS. RIGGS: That’s right. And people are frightened if they have Alzheimer’s disease in their family. I know my mother was my age when she started showing the signs of Alzheimer’s. But, it’s interesting the fact that there are risk factors, but it doesn’t necessarily mean you’re going to get the disease. And NIA is funding some very exciting work in twins to try to figure out, here are people who have exactly the same genetic make up, and one person gets the disease, and the other doesn’t. And why is that happening? I mean, there is some mix between genetics and environment that is really triggering what causes Alzheimer’s disease. MS. MORRISON-BOGORAD: What we think a the moment is that late Alzheimer’s disease there’s a mixture of genetic risk factors and your chance of getting it is dependent on which of these bad or good risk factors you inherit from your parents. But, there’s also the environmental thing. Perhaps having high blood pressure when you’re in mid-life might put you at risk for Alzheimer’s, perhaps having high levels of cholesterol will put you at risk for Alzheimer’s. There are studies, epidemiology studies suggesting the high blood pressure also cholesterol. And there are studies in mice which suggests that if you give mice a high cholesterol diet these transgenic Alzheimer mice, they develop more plaques on the brain. So there are definitely going to be environmental factors, which are going to be easy to do, if we all decide we want to do them, that might actually reduce the risk. And then there will be the genetic thing, the thing you were born with, the genetics interacting with the environment, to say you’re likely to get Alzheimer’s by 65, 75. MR. WATTENBERG: In ten years, is Alzheimer’s going to be something that we’ve whipped, that we say that’s one of those diseases that we don’t have to really worry about anymore. MS. MORRISON-BOGORAD: Not quite, but nearly. I think where we’re at right now we never would have believed we would be at 20 years ago. MR. WATTENBERG: What is your view on that, Judy? MS. RIGGS: Ten years from now, I hope we’ve kept a lot of those 14 million people from getting Alzheimer’s disease. But, I think it’s important to understand, there will be those people for whom the answers come too late. And they’re still going to need a lot of treatment, and a lot of care, and so we have to deal with both issues. MR. AISEN: I think that if we devoted adequate resources, I think that ten years would be a reasonable target for defeating this problem. I think it would be reasonable target. We’re making good progress now. I think if we increased the effort, if there were a significant increase in the scale of federal funding for this research, I believe that in ten years we would have come a very long way to defeat this disease. MR. WATTENBERG: All right. We’ve got to leave it here. Thank you very much, Paul Aisen, Marcelle Morrison-Bogorad, Judy Riggs, and thank you. Please remember to send us your comments via email. For Think Tank, I’m Ben Wattenberg. ANNOUNCER: We at Think Tank depend on your views to make our show better. Please send your questions and comments to New River Media, 1219 Connecticut Avenue, Northwest, Washington, D.C. 20036, or email us at thinktank@pbs.org. To learn more about Think Tank, visit PBS Online at pbs.org. And please let us know where you watch Think Tank. This has been a production of BJW, Incorporated, in association with New River Media, which are solely responsible for its content. Funding for Think Tank is provided by the T. Rowe Price Associates, an investment firm providing mutual funds, brokerage services, and retirement plan services. T. Rowe Price, invest with confidence, T. Rowe Price Investments, Incorporated. We’re Pfizer, we’re looking for the cures of the future, spending about $4-1/2 billion a year in search of new medicines for the 21st Century. Pfizer, life is our life’s work. Additional funding is provided by the Lynde and Harry Bradley Foundation, the John M. Olin Foundation, the Bernard and Irene Schwartz Foundation, the Smith Richardson Foundation, the Donner Canadian Foundation, and the Dodge Jones Foundation. (End of program.) 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