A panel of journalists joins Diane for analysis of the week's top international news stories.
Among the top 10 causes of death in the U.S. Alzheimer’s disease is the only one with no method to prevent, cure or even slow its progression. New research has generated hope among scientists and caregivers that treatment for the disease could come sooner than many dared to think possible. But there’s good reason to be cautious. The outcomes of studies on several promising drugs are due this year. Researchers fear pharmaceutical companies might halt the search for treatments if the results are disappointing. A major international conference on Alzheimer’s is in session this week in Vancouver, Canada. We’ll provide the latest news from the conference and efforts to find a cure.
- Reisa Sperling professor of neurology at Harvard Medical School and director of the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital.
- George Vradenburg co-founder and chairman of Us Against Alzheimer’s.
- Randall Bateman the Charles F. and Joanne Knight distinguished professor of neurology at Washington University School of Medicine and associate director of the Dominantly Inherited Alzheimer's Network (DIAN).
- Brigid Reynolds clinical care coordinator in the Memory Disorders Program at Georgetown University Medical Center.
MS. DIANE REHMThanks for joining us. I'm Diane Rehm. The Alzheimer's Association estimates one in eight Americans over the age of 65 has the disease. This weekend, Canada, researchers from around the world are meeting to present the latest findings on efforts to both understand and treat the disease.
MS. DIANE REHMJoining me in the studio to talk about the global effort against Alzheimer's: Brigid Reynolds of Georgetown University, joining us from a CBC radio studio in Vancouver, Dr. Randall Bateman of the Washington University School of Medicine in St. Louis, George Vradenburg of Us Against Alzheimer's, and Dr. Reisa Sperling of the Harvard Medical School, and Brigham and Women's Hospital. Do join us, 800-433-8850. Send us your email to email@example.com. Join us on Facebook or Twitter, and good morning to all of you.
DR. REISA SPERLINGGood morning, Diane.
MR. GEORGE VRADENBURGGood morning, Diane.
DR. RANDALL BATEMANGood morning.
REHMI'm going to start with you, George Vradenburg, if I may, since I'd be interested in your reaction to the mood you're seeing there in Vancouver among the Alzheimer's researchers.
VRADENBURGWell, I think the researchers have a great deal of hope that making significant new strides and understanding the basic causes and path of the disease. They are discovering new ways to be able to discern the development of the disease in ones' brains long before symptoms appear. But, on the other hand, they are constrained by limited resources from the federal government, which only allocates about $450 million a year to research compared to, for example, cancer at $6 billion.
VRADENBURGSo they're both surprised -- not surprised. They're both excited about the research developments and the diagnostic developments, but on the other side, you know, feeling frustrated that there's not an adequate resource devoted to the discovery of how to get a real drug to market.
REHMAnd, Dr. Sperling, to you, the Alzheimer's Association International Conference got underway over the weekend. I gather a couple of the findings that have been reported -- one to do with physical activity, the other concerned with gait changes. Explain that to us.
SPERLINGSo there's been some exciting news with the idea that, perhaps, physical activity might be protective in Alzheimer's disease, and we know that exercise at any stage of the illness is likely protective in the brain. There's been more encouraging results related to that. In terms of gait difficulties, although Alzheimer's disease really primarily affects cognition, there is also recent news to suggest that sometimes walking difficulties and immobility may actually be associated with early signs of the disease in individuals who will progress to develop dementia.
REHMAnd how useful is it for an Alzheimer's diagnosis, Dr. Sperling, to recognize changes in how a person walks? Isn't a change in gait a symptom of many other conditions as well, for example, Parkinson's?
SPERLINGAbsolutely. So, unfortunately, there are many changes in walking and gait speed as we get older, and these, of course, can cause disability for many different illnesses. But it is a major contributor to some of the disability that we see in patients with dementia and Alzheimer's disease. So I think it's important to take that into account and try to use physical therapy and other methods to get people as mobile as possible at any stage of the disease.
REHMWhat kind of exercise could help people with a cognitive impairment or those who are at risk for it, Dr. Sperling?
SPERLINGWell, I believe that exercise in particular that takes you outside and also improves your interaction with others might be really useful, so I recommend to my patients that they take a walk outside around the park or with their pet. And I actually like to recommend ballroom dancing because I think this teaches people new skills, has a social interaction and has some exercise as well. But, really, any form of physical exercise and social interaction may be protective.
REHMAnd turning to you, Dr. Bateman, tell us about the gene mutation study.
BATEMANThe Dominantly Inherited Alzheimer's Network is a study of people and families who carry a gene which causes Alzheimer's disease at a very early age, and so these people will begin to manifest the symptoms of Alzheimer's disease in their 30s, 40s and 50s and will have the same loss of cognition and memory and thinking and eventually independence. And it will lead to death at a young age. And so mutations in one of three genes causes this, as a rare form of Alzheimer's disease.
BATEMANHowever, it's highly instructive. It's informed the field over the past two decades and has led to much of the biomedical research, which is being used to develop drugs which are now currently in clinical trials. The study of the mutation carriers is reporting some of its first results both in a publication as well as here at the Alzheimer's Association International Conference, and the findings are very exciting and encouraging.
BATEMANAnd that we think we can now detect changes which occur in the brain and lead to Alzheimer's disease in these individuals 15, 20 or even more years before the first symptoms manifest. And what that does is it gives an opportunity, a time window in which we can potentially intervene.
REHMTell me exactly how this would be accomplished. How would you determine that these changes actually exist?
BATEMANCurrently, the study is ongoing, and people in the study come in and have a series of assessments called biomarker assessments, as well as clinical and cognitive measures, tests of their memory and thinking. They undergo a series of testing over typically three to four days, and then they would come back every one to three years.
BATEMANAnd in collecting this information, we track the different processes of Alzheimer's disease, including the memory. There's a protein buildup in the brain called amyloid or amyloid plaques, which can be measured with a specialized scan. And the brain shape and size and structure can be measured with an MRI, and other scans measure the rate of metabolism or glucose of the brain.
BATEMANAnd by tracking these different aspects of the disease, the team is able to put together those results and estimate what's changing and when and by how much. And so with that information, we are using that to design trials where we can take drugs, intervene in the process at its earliest stages, even before people have symptoms. And the goal there is to treat the underlying disease process in the brain and ultimately prevent those individuals from having cognitive impairment and dementia.
REHMAnd what you're saying is that you'd be particularly looking at individuals who have had Alzheimer's in the family, a parent or a sibling or watching that person even before symptoms begin to develop?
REHMAnd to you, Brigid Reynolds, you're one of the people who is doing these kinds of clinical test. Tell me about this.
MS. BRIGID REYNOLDSSo at Georgetown University, we're testing new treatments for Alzheimer's disease, and we're also involved in tests of new biomarker studies to better identify -- to compare across groups normal, mild cognitive impairment and Alzheimer's disease and track these biomarkers to help us develop new treatments.
REHMNow, are quite young people coming in for that kind of testing?
REYNOLDSWell, at this point, no. People that are coming in are typically 70 or older. It would be far too expensive to test younger people. And so we need to, you know, focus on people who are closer to developing the disease.
REHMAnd are you also testing people who've already shown some signs of impairment?
REYNOLDSYes. So for the clinical studies that we're doing, we are enrolling subjects with mild to moderate Alzheimer's disease.
REHMAnd, Brigid, give me an idea of how you perform those tests.
REYNOLDSHow we do an evaluation of someone...
REYNOLDS...coming in wondering if they have Alzheimer's disease?
REYNOLDSSo we always request that two people come, the patient and an informant or someone who knows them well because that is how we can get the best picture and the most information. And I think the most important aspect of the evaluation is the history: how things began, what were the first symptoms, and then how symptoms, cognitive symptoms, behavioral symptoms and function has changed.
REYNOLDSAnd then, of course, a physical exam is an important aspect of the evaluation. We do blood tests to make sure that other -- there aren't other things going on to contribute to the cognitive change, and also an MRI scan typically or a brain scan to make sure...
REHMOther things like what, Brigid?
REYNOLDSThe blood tests, things that can be treated that can cause memory problems, like thyroid or low B12.
REHMAll right. Brigid Reynolds is clinical care coordinator at the Memory Disorders Program at the Georgetown University Medical Center. We'll take a short break here. I do invite you to join us. I look forward to hearing from you.
REHMAnd welcome back. We're talking about new and indeed exciting research into Alzheimer's. Three people are at an Alzheimer's convention of researchers and interested parties in Vancouver.
REHMThree of them are on the line with us: Dr. Randall Bateman -- he is at the Washington University School of Medicine in St. Louis -- Reisa Sperling is professor of neurology at Harvard Medical School and director of the Center for Alzheimer's Research and Treatment at Brigham and Women's Hospital, and George Vradenburg, chairman and co-founder of Us Against Alzheimer's. Here in the studio, Brigid Reynolds, clinical care coordinator of the Memory Disorders Program at the Georgetown University Medical Center.
REHMThe lines are open. We do invite you to join us. George Vradenburg, there are studies going on with drug companies like Eli Lilly and Pfizer. Now, tell me how important those studies are and where they're being conducted.
VRADENBURGWell, they're being conducted all over the country through multiple sites, and they are very important, and they will report out their results some time in the next -- just the next few months. And these are the latest stage drug trials, so this will be a determinant of whether or not one of these companies has discovered a means of intervening that actually will modify the course of the disease.
VRADENBURGAnd if so, they will apply to the FDA for approval of that treatment for release to the American public, and they might do so as early as the end of the year. What is intriguing about them is that they are testing a beta amyloid intervention in people who have a mild to moderate symptoms of the disease, and in one case, MCI, a mild cognitive impairment. And so there is great hope that one of those drug candidates or treatment candidates will be successful.
VRADENBURGBut there is also great concern that the drug -- the treatment candidates may be being applied to patients in a more advanced state when their brains have already deteriorated as a result of this disease. So as...
REHMIn which case, the drugs would not be effective.
VRADENBURGThat's correct. But they may not -- and I use the may judiciously here. It may be that you could apply the same drugs much earlier in the course of the disease, as Dr. Bateman is pointing out, before symptoms appear. And because they have a mild disease-modifying effect, while they wouldn't work in mild to moderate victims, they may work in slowing down the disease significantly, and thus deferring the onset of symptoms.
VRADENBURGSo we are looking forward with great anticipation to the report of their results in detail, which will occur in October, although they may report out the top line results sooner than that.
REHMI see. George Vradenburg, why did you become involved in this fight against Alzheimer's?
VRADENBURGWell, my wife's mother passed away from this disease about 20 years ago, and I saw it up close and personal. It is a long, slow, progressive decline. And while some might romantically refer to it as the long goodbye, it is anything but that. It is -- destroys the identity. It destroys the ability of a person to recognize family members. It destroys an individual's ability to manage their own daily life and, indeed at the end, their own functioning.
VRADENBURGSo it is a cruel, cruel disease that slowly takes away your loved one. And you see them dying before your eyes, and you can do nothing. So when this happened to my wife's mother, she and I set out to basically to do what we could do to stop the disease.
REHMAnd, Dr. Sperling, to what extent is there evidence of hereditary factors within Alzheimer's?
SPERLINGSo I think there is evidence of hereditary factors at multiple levels. So certainly there are some rare genes that are what we call deterministic, and those genes, such as Randy Bateman just spoke of, unfortunately confer nearly 100 percent likelihood of developing Alzheimer's disease dementia at a young age. But we also know that there are hereditary genetic factors that modulate the risk of developing Alzheimer's disease in late onset cases.
SPERLINGAnd most recently, there was a report of a genetic factor that might be protective, and this is a very rare gene. But it was also in a gene that was related to the development of amyloid protein, and this suggests that perhaps there are protective genes that we can discover and perhaps even develop drugs to help us modulate the products of those genes and prevent Alzheimer's disease dementia.
REHMWell, Dr. Bateman, if you're looking at early onset, will the same findings help to modulate the effects of Alzheimer's in those who get the disease late in life?
BATEMANYes, we think so. And that's based on the similarities between the two diseases. The early onset form with the mutation is not identical to the more common late onset form in that the early onset folks have a mutation which is causing their disease, whereas most people with later onset disease past 60 or 65 years old typically don't have mutations.
BATEMANBut in our studies and at this meeting, there is converging evidence that the processes which lead to the disease and the changes which are occurring in the brain and the clinical symptoms and the presentation of this disease is largely similar between the two forms. And one of the things that scientists and researchers use in the study of Alzheimer's disease and the development of therapeutics are models which use the mutations found in these early onset families.
BATEMANSo it's those mutations which really allow us to develop these drugs, which are now in clinical trials. And there is a logic that the drugs that are developed on these mutations, in fact, may be most likely to work in the early onset population with those mutations. But the drugs target a part of the process which is similar or the same between the two diseases.
REHMSo, George Vradenburg, you talked earlier about the small amount of money that the government has put into Alzheimer's research. Why do you think those figures are so small in comparison to, for example, cancer or any of the other big killers in the country?
VRADENBURGWell, I think some of this is historic. We made significant investments in cancer starting in the '70s and heart in the '80s and HIV/AIDS in the late '80s, early '90s. And then Congress and, I think, the whole nation went a different tact, and they basically started -- they started a process of doubling the amount of money allocated to NIH rather than selecting investments in particular diseases.
VRADENBURGAnd that is where the -- Congress is right now. They are still on the belief that they ought to try to maximize the resource going to NIH but have no role, they believe, in making strategic allocation decisions across diseases. Now, that, I think, theory is beginning to get challenged again because we have set the pattern in which we've invested in different disease conditions back in the early to mid-'90s. We have not made any strategic adjustments based upon the discoveries that have occurred since then.
VRADENBURGSo we have made significant progress in, for example, in HIV/AIDS, and yet HIV/AIDS continues to get about $3 billion a year in annual investments, whereas in Alzheimer's, a disease that only really began to get real attention in the early '90s, that disease has been underinvested in. So we have not, as a political process, been able to adjust based upon burden of disease or other strategic factors, but are constrained by simply the allocation decisions that were in place in the mid-'90s.
REHMBut as you look at the population and evaluate the numbers of individuals who are likely to be affected by Alzheimer's, it would seem that, clearly, more money is needed.
VRADENBURGWell, I think that's exactly right, Diane. But, in fact, you live in a time of fiscal -- I'm not going to defend Congress on this -- but a time of fiscal stress. It's difficult to take money away from cancer or heart or HIV/AIDS and allocate it to Alzheimer's because of the deep investment of the research community in those diseases and the advocacy groups which you build up around it. And, having said that, you're absolutely right.
VRADENBURGThe number of people that have this disease today is roughly five to 5.5 million. That is going to triple. At the same time, we're going to lose 10 million baby boomers to this disease through death over the next -- in the coming decades. And if you really believed an enemy of the United States had a weapon that was going to destroy 10 million people over the course of the next few decades, you can imagine the kind of resources we would marshal against that enemy.
VRADENBURGAnd we are not marshaling those resources against this enemy. And at the same time, we're investing $200 billion a year in care for those who have the disease. And it seems almost, to this ex-businessman, ludicrous to think that you're only investing $450 million to try and offset a cost of over $200 billion, growing every year and, by 2050, will be $1 trillion a year. So the -- it's like sitting here in the 1950s and say, we ought to be investing in more iron lungs and leg braces when, in fact, Salk said, no, we would invest in a cure.
VRADENBURGAnd we, today, don't have a whole lot of polio health care costs, right, because we, in fact, found it a cure. That's where the investment should be made. In my view, we need to make a strategic allocation of resource to this disease because of the fiscal reasons, but also, most importantly, because of the numbers of people who are going to be adversely impacted.
REHMDr. Sperling, if you are, say, 25 and you have a parent with Alzheimer's, what test, if any, should you seek out?
SPERLINGWell, I think if your parent developed Alzheimer's disease in the late-onset form -- so after age 60 or 65 -- at this point, we really don't recommend a specific test such as a genetic test or one of these biomarkers, but instead would tell you at age 25 to be as physically and mentally active as possible because certainly keeping yourself healthy would be healthy for the brain.
SPERLINGNow, if you have a parent who developed Alzheimer's disease at a younger age, in their 40s or 50s, and have a family history that would be suggestive of one of these rare genetic mutations, as in the Dominantly Inherited Alzheimer Network study, then there are specific genetic tests that can tell you whether you have one of those mutations. But they are quite rare, and I think, at this point, unless there's a clear family history, we don't recommend that type of genetic testing.
REHMAnd you're listening to "The Diane Rehm Show." So, Brigid Reynolds, if someone came to you and said, my parent had early-onset Alzheimer's, I'd like to find out whether I am vulnerable to the same process, what would you say and do?
REYNOLDSWell, as Dr. Sperling was saying, there is genetic testing that can be done for early-onset Alzheimer's disease. But, again, that form of Alzheimer's disease is extremely rare. I would encourage people to remain informed. There is a -- an organization, the Alzheimer's Prevention Initiative by Banner Health out in Arizona, where you can become a member of a registry and receive more information and possibly volunteer for a prevention trial at some point.
REHMYou know, we've had several emails this morning, asking whether there is any validity to the claim that coconut oil can help restore memory in Alzheimer's patients. Apparently, that story is going around on the Internet. Brigid, what are you hearing?
REYNOLDSI have been asked the question about coconut oil on numerous occasions. The evidence for, I believe, in the double-blind, placebo-controlled clinical trials for new treatments -- and there hasn't been a trial such as that conducted with coconut oil, so I would not recommend that people take coconut oil.
REHMBut has there been anecdotal evidence that somehow it's worked for some people?
REYNOLDSYeah. So there is some anecdotal evidence, but there's nothing that you can take that's not without some potential for harm. So, you know, you need more solid evidence outside of anecdotal stories to...
REHMDr. Bateman, Dr. Sperling, what do you make of this coconut oil report?
BATEMANI think, you know, over the years, there are a great many things that are reported to potentially have some benefit. And in general, I think we see these things come and go, and under a careful study, they typically don't pan out to actually offer benefit.
BATEMANThat being said, you know, if a additional nutrient or supplement is not harmful, and I tell my patients, if you're interested in taking it, you want to try it, as long as it's not harmful, I don't see any major caveat in it except the expense. And I think people do try these. I've had several patients who have informed me they've been taking it, and none that I know of have reported any significant benefit from it.
REHMAll right. And to you, Dr. Sperling, you mentioned physical activity. What are some of the types of exercises that could help people with cognitive impairment or who are at risk for it?
SPERLINGWell, some of the study suggests that walking as little as six miles a week may be somewhat protective in slowing rates of cognitive decline or brain shrinkage or atrophy. But there are other studies that suggest that that exercise needs to be at a level where you really increase your heart rate. And that would be going to a gym and to an aerobic class or swimming very vigorously or perhaps bike riding.
SPERLINGI think that this is something that each patient or person at risk should really discuss with their own doctor so that they do this in a healthy way. But in general, I think exercising 20 to 30 minutes a day for at least four to five times a week would be ideal in slowing the progression of Alzheimer's disease.
REHMReisa Sperling, she is professor of neurology at the Harvard Medical School. She's also involved in Alzheimer's research and treatment at Brigham and Women's Hospital.
REHMAnd we're back in this hour, discussing Alzheimer's disease, a conference going on right now in Vancouver, dealing with the possibility of new drugs, dealing with new forms of identification and the hope for treatment. We are going to open the phones now, 800-433-8850, first to York, Penn. Good morning, Steven.
STEVENGood morning, Diane. I love your show.
STEVENI watched my mother melt away from Alzheimer's at the age of -- she started at the age of probably 60. And my dad is now 90. He started melting away with Alzheimer's at 88, and he's -- I have a long family history, and I'm 58. I exercise seven days a week on an elliptical machine. I try to keep my mind sharp as much as I can, but I see myself having a lot of problems. I'm losing lots of things, and I'm -- and, you know, I know that some of this is simple aging, but my medical doctor has ruled out all the things medically that might cause that problem -- cause problems. So I'd love to be in their studies.
REHMDr. Bateman, can you talk about that?
BATEMANYes. So it's a common concern that when people come in to their physician's office or we -- memory specialty clinic, concern about changes in a person's memory and -- especially in people who are familiar with Alzheimer's disease because the natural association as well, if I'm losing my memory, then maybe it's because I'm now starting to have the first signs of Alzheimer's disease, and that's obviously a very scary thing.
BATEMANAnd so people want that fully evaluated. And there's a process that we go through to check a person out to determine what's causing the memory impairment and if it might -- may be associated with Alzheimer's disease. And I think the first place to do that is at a physician's office to have that evaluated. And sometimes it is, in fact, the beginning signs of Alzheimer's disease, but often, it may not be.
BATEMANAnd there are some subtle changes there with aging, but, typically, those don't interfere with activities of daily living and having people do what they want to do if they're normal. It becomes a problem when it interferes with those activities of daily living.
REHMA number of our listeners are asking, what's the difference between dementia and Alzheimer's disease? Brigid.
REYNOLDSSo that's a question that I hear frequently, and Alzheimer's disease is one form of dementia and, in fact, the most common form of dementia. There are other types of dementia. You can have Parkinson's with dementia, Lewy body dementia. So Alzheimer's is the most common form of dementia.
REHMAnd another question we've had: is anyone at the conference looking at caregivers and the role they play in Alzheimer's? George Vradenburg.
VRADENBURGWell, caregivers are really the frontline troops in caring for those who have the disease early or late. They are our frontline troops, and they need a good deal of support. The answer is, yes, we are looking at ways that we can support family caregivers and non-family caregivers. The enormous challenge here is that two-thirds of the caregivers are women. Most of those women work but are beginning to have either to back out of their careers or jobs or diminish their progress in those positions or careers because of the caregiving burden.
VRADENBURGSo there is a good deal of discussion about how to deal with the social impacts, particularly the social impacts on women of caregiving. Strikingly, two-thirds of the victims, so twice the incidents of Alzheimer's in African-Americans as in Caucasians, for reasons that I don't know, that I've heard a good explanation.
VRADENBURGAnd so if you look at the combination of impact on women or impact upon low-income families of this disease, of caring for this disease, it is going to -- already has, but will in the future -- enormously impact our family structures and our ability to keep women in the workforce. And the lower-income populations who are already struggling will continue to struggle with the families that are affected by this disease.
REHMDr. Sperling, is there any indication as to why African-Americans suffer from Alzheimer's at greater numbers?
SPERLINGYes. There is some research into this, and we believe that more research is desperately needed so that we can stop confounding ethnicity and racial effects from other effects such as education and socioeconomic status because, unfortunately, the generation that's now developing Alzheimer's disease dementia, there were clear disparities in economics and education for some of these families. However, there are some medical reasons and genetic reasons that differ among African-American populations, Latino populations and Caucasians.
SPERLINGSo one of these genes that can influence the likelihood of late-onset Alzheimer's disease is a bit more frequent in the African-American and Latino populations, and, again, there is an interaction between this gene and gender so that women with this gene, apolipoprotein E4, this allele of a gene, are more likely to develop Alzheimer's disease. And then there are what we call co-morbidities. So, unfortunately, hypertension and diabetes are also a bit more common in the African-American and Latino populations.
SPERLINGAnd this, we know, can interact with Alzheimer's disease pathology to worsen dementia. But we need a lot more research. And I hope that we will do research that includes more African-American older individuals, more Latino older individuals in our prevention trials. And the Alzheimer's Association trial match and the National Institutes of Health are really putting great efforts into having a much more diverse research population because this is critical.
REHMI have a number that people can call if they'd like to be part of those clinical trials at NIH. That number is 1-800-438-4380. And we'll repeat that number again at the end of the program. Please have your pencils ready. Another email, "Is Alzheimer's becoming more prevalent in our aging population? Or was it always there, and we simply had no name or insight into the disease?" Dr. Bateman.
BATEMANAlzheimer's is much more common now than it used to be, and the main factor for that is the fact that we're living longer. We're doing better at living past our 60s, into our 70s, 80s and beyond, and the number one risk factor for Alzheimer's disease is age. It far outweighs almost all of the risk factors with the exception of the very rare mutations. And as we get older, the risk of Alzheimer's disease doubles every five years. So past the age of 60 or 65, every five years, a person's chance of getting Alzheimer's disease doubles every five years.
BATEMANAnd what this means is that in the 60s, a few percent of people will have Alzheimer's disease. But in the 70s, that rises to about one out of 10 people in their 70s will have Alzheimer's disease and have to deal with its consequences. And by the time a person reaches their 80s, the numbers of people -- from 30 to 50 percent of people will have Alzheimer's disease in the 80s and beyond. And so it's really the aging of the population which has led to the explosion and the epidemic of Alzheimer's disease that we are now facing.
REHMGeorge Vradenburg, this sounds like an horrific explosion in the numbers of people who will somehow attain Alzheimer's. And how in the world is the U.S. going to deal with that?
VRADENBURGWhat you -- if we were sitting here in 1900 and the average life expectancy were 47 years old and a person in their 40s was regarded as old age and lucky and then we look at the same situation in 2000 and said the average life expectancy was 78, we have had what is an extraordinary run in public health and in research, which has lengthened our lives. It has not only reduced, in some sense of the word, certainly the costs of care for those in their 40s and 50s and 60s, but it shifted it to an older age. But it's also contributed to the growth of the American economy.
VRADENBURGSo if you really think that we are sort of in the 20th century, we conquered any number of diseases through public health improvements through a variety of cures. And we grew the American economy as we did. And we look at it today -- we should be saying we should be turning the kind of attention to chronic diseases of the elderly that we paid to other diseases in the 20th century. And as a consequence of doing that, we can continue to extend life, continue to extend healthy aging in a way that would make our economy more productive.
VRADENBURGIt goes back to how it is that we decide as a nation to allocate our research expenditures. Whether we look at the situation as it existed in the mid-'90s and say that's the way we're going to freeze our strategy for how we invest toward disease or whether we look forward and say the chronic diseases of the aging -- particularly Alzheimer's but not limited to Alzheimer's -- should be a major focus of our research investments.
VRADENBURGBecause not only will it make -- alleviate the social and health burden of our population, but it will continue to grow the American economy and turn our elderly populations into productive workers, who are paying taxes, rather than disabled workers who are drawing down on Medicare and Medicaid and other social programs.
REHMAll right. Let's take a caller in Fort Lauderdale, Fla. Good morning, John.
JOHNI have a question relating to sleep apnea. It seems to be quite common in Alzheimer's patients. And one drug, I think -- I don't know how to say it -- Donepezil or something like that improves sleep apnea and Alzheimer's symptoms. My question is, has a study been done to determine how much of effect your sleep apnea is in onset of Alzheimer's?
SPERLINGWell, I think, actually, there's a quite a bit of research going on in sleep and Alzheimer's disease. And you're correct that sleep apnea is not necessarily a cause of Alzheimer's disease, but doctors do believe that sleep apnea can make thinking and memory impaired. And so this certainly would worsen Alzheimer's disease symptoms. But we do believe that there's an interesting link between sleep and some of the abnormal proteins that accumulate in Alzheimer's disease, such as amyloid and memory problems.
SPERLINGAnd I actually believe this is going to be an area of increased research over the next few years because sleep also changes with aging, not just sleep apnea, but the ability to get a good night's sleep. And this is an area of critical research that we can all sleep better and have better memories.
REHMAll right. And to West Tisbury, Mass. Good morning, Cindy. You're on the air.
CINDYGood morning. Thank you so much for taking my call.
CINDYYes. I was listening and heard that exercise is very crucial to stopping the progression of Alzheimer's. And I'm curious to know about diet because I have been studying and reading Dr. Natasha Campbell-McBride. She's a neurologist and a nutritionist, and she cured her son from autism, healing the lining of the gut and really talking about how important nutrition and diet is in healing the lining of the gut to heal brain disorders.
REHMWhat about that, Dr. Bateman? Dr. Bateman.
BATEMANYes. The treatments that are being explored now and the recommendations for lifestyle are things that could have a relatively large public health impact. And so, for example, the recommendation of regular exercise and aerobic exercise is estimated that, based on its effect across the population of large numbers of people who do that, that it can have an impact on the numbers of -- potentially the numbers of people who get Alzheimer's but also the rate at which the disease advances. But these effects are relatively mild.
BATEMANAnd I think that it's something we -- it's what we have now, and it's what we recommend to our patients. And as prevention efforts, for people who are concerned about the risk of Alzheimer's disease, we give that as a recommendation, but it doesn't stop the disease from coming on, that the disease will occur and in great numbers in people whether we lower that risk by exercise or not. And so we really need better strategies. And so people are looking into a multitude of approaches.
BATEMANAnd these includes others things such as cognitive and social stimulation and diet. And diet, we know, is an important thing for healthy living. And we know that it has effects on heart health, as well as the risk of vascular risk factors, such as strokes in the brain. And these things may and likely do interact with Alzheimer's disease. And so by eating a healthy diet and having a good healthy exercise program, one can reduce the risk.
BATEMANBut I want to be clear that I think it's -- it potentially could be a false sense of security that these kind of general prevention approaches that we're trying will not spare us the epidemic of Alzheimer's disease and that we really do need to focus on highly effective therapies, which can have a large impact on this disease.
REHMHow far away do you think we are from a cure for Alzheimer's, Dr. Sperling?
SPERLINGSo I'm one of the optimistic individuals. I do believe that these trials that will come out over the next few months will help us know how close we are. But if those trials show us evidence that we are able to affect the biology of the disease even if we don't fully treat at the stage of dementia, the next step will be taking these treatments earlier.
SPERLINGAnd if those trials will succeed both in the genetic population and in the older population with early biomarker evidence of Alzheimer's disease, I hope in a decade from now, we're talking about how we can treat Alzheimer's disease in 50- and 60-year-olds and prevent dementia altogether.
REHMFingers crossed. And that telephone number again at NIH, if you'd like to volunteer for clinical trials, 1-800-438-4380. Thanks to Reisa Sperling, George Vradenburg, Randall Bateman and Brigid Reynolds for your very important work. Thanks for listening, all. I'm Diane Rehm.
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