Alzheimer's Disease

She also earned an MS from Indiana State University in Agency Counseling. Sue Friedman became President and CEO of the Alzheimer’s Association in 2007 where, among her many duties, she is spokesperson for the cause overseeing development and educational programming, Helpline, public awareness, community and donor relations and management concerns. Among her awards she garnered the influential Women of Virginia 2011 Award from Virginia Lawyers Weekly and the Leaders Leader Annual Award in 2009 from the Leadership Charlottesville Alumni Association. She was also elected member National Planning Team for leadership meetings for the Alzheimer’s Association in 2009 on which she now serves. In our last conversation with Sue Friedman, amazingly two years ago now in 2013, we discussed among other things the history of Alzheimer’s Disease research, the warning signs and risk factors, the effects on family and caretakers. We also looked at a number of remarkable organizations that aid in management and support. We explored some lifestyle changes which may contribute to keeping our brains healthy as we age. I encourage all of you watching today to go to our website at politicsmatters.org and view this important two part conversation with Sue Friedman. Since our last meeting, a great deal of promising and quite exciting progress is being made nationally and internationally in forming a more thorough understanding of the underlying causes of Alzheimer’s Disease, looking at new imaging technologies as aids in research for slowing, arresting and ultimately finding a cure for this devastating disease. I also thought that it would prove useful today to look at some new directions being considered in drug treatment as well and at some of the more promising studies underway worldwide. We will conclude by looking at recent nonprofit foundation efforts and as always looking politically at legislation enacted or being considered in order to significantly increase funding streams and prioritize the vital quest for cure. Welcome again, Ms. Friedman.

Sue Friedman: Thank you so much, Jan.

Jan Paynter: As usual, Sue, there’s so much to look at and we’ll touch on as many points as possible in the brief time we have together. So first let’s tackle some of the new diagnostic tools available for diagnosis. In April a four year research study budgeted at $100 million was put in place by the Alzheimer’s Association as you know in conjunction with the American College of Radiology entitled “The Idea Study”. What is the purpose of this study and tell us briefly, if you would sue, a little about PET amyloid scanning and how such scans will advance our understanding of the disease.

Sue Friedman: Well, a few years ago, probably four years ago now through the University of Pittsburgh, the PET scan, the PIB-PET scan was developed and the very important part about that for now is that it is a huge part of research. Before, we might have an intervention, a treatment if you will, a drug but we couldn’t really prove that it was making any difference or doing anything to help cure or prevent or delay the disease. We had no way to demonstrate that. But now that we have the PET scan, we can, if you will, look into the brain without having to crack the brain open. Researchers have said to me for a long time, ‘The brain is the one part of the body you can’t just routinely open up and look at.’ And so we really need this PET scan to be our tunnel, our way into looking at the brain. And so this huge $100 million study with the radiologists allows us to perfect and demonstrate the efficacy of the PET scan. And our goal of course would be that the PET scan can move from research into every day medical and health practice.

Jan Paynter: Sue, what are biomarkers and which ones are being most closely studied at present and why is understanding of them so important?

Sue Friedman: A biomarker is something that would be a hallmark, if you will, of a disease. And so when looking at Alzheimer’s, we have for decades now looked at beta amyloid and the beta amyloid becoming a negative version, a plaque if you will, clogging and killing cells and when you kill neurons, you kill memory pathways, you kill judgment pathways. An additional biomarker we’ve been looking at for over the past decade is the tau protein and again, the tau is, if you will, the railroad system of messages in the brain. And what happens with tau, it’s like if the rails of the railroad fell off and started getting tangled. And so tau gets tangled in the brain and again, what does that do, it kills that neuron and that memory pathway. So these are two of the major biomarkers we’ve been looking at over the past 20 years in terms of how do you identify and therefore how might we address the problem of Alzheimer’s. More and more biomarkers are becoming known to us though. The correlation with diabetes may well be an indication. The growing correlation between inflammation and Alzheimer’s Disease is another area we’re looking at. So what we need to do is to continue to refine and, if you will, enhance the number of biomarkers that are out there and then figure a way that we can easily in your family practitioner’s office test for these particular biomarkers. And the one analogy I make that everyone seems to be able to understand is, we test for cholesterol and we know how to do that with the blood test. A blood test is a biomarker for potential heart problems; ie cholesterol being high gives us a red flag there might be a heart issue there, let’s deal with the cholesterol. So we’re looking at beta amyloid and tau as our primary biomarker focus but inflammation, diabetes and some others are also beginning to crop up as potentially important.

Jan Paynter: I see. I see. Discuss if you would, Sue, the importance of diagnosing mild cognitive impairment. What is it and what kinds of changes associated with it occur.

Sue Friedman: Mild cognitive impairment is now an actual clinical diagnosis—only been in existence for three years and what we’re saying when you have mild cognitive impairment is that there are noticeable memory or judgment or communication problems but they’re not yet to the level that I have to quit my job or that I have to discontinue driving or that I really need to change my life other than being aware that I’m having these challenges and developing, if you will, my crutches, my strategies to work around these challenges. And what’s critically important about knowing if MCI is something that is impacting you is about half of those with MCI will move into Alzheimer’s but about half won’t. So it gives us the opportunity to look at am I taking advantage of those 10 healthy brain habits now and if I’m not, let me do that, let me discontinue smoking, let me make sure I am exercising, let me pay attention to Mediterranean Diet, let me pay attention to my sleep—the amount of sleep and the quality of sleep, etc. So it gives us a great opportunity to have a little more control and absolutely make different choices because mild cognitive impairment doesn’t mean you will have Alzheimer’s. It means you are at greater risk of developing Alzheimer’s.

Jan Paynter: It’s fascinating. I wanted to look now going from the…also the markers…the biomarkers and the technology used to explore the brain and talk about drug treatments. We know that between 2002-2012 for example according to the stats, 99.6% of drug studies whose goal is preventing, curing or improving symptoms have either been halted or discontinued. But, I know there are very important and positive developments in the work. What existing drugs, Sue, already approved for other uses have recently come to light and have been shown to be effective against Alzheimer’s Disease?

Sue Friedman: Well, there are some drugs that are certainly being tested. The statins, the high blood pressure medicine is being looked at as potentially a protector against Alzheimer’s Disease or certainly maybe a delayer against Alzheimer’s Disease. I know for a while we were looking at that Russian antihistamine drug. Really had great, great hopes for that. That did not reach the level of effectiveness through drug trials but again, one of the quickest ways that we can have a drug that really modifies the disease, which as you know we do not have now, is to find something that is already on the market and how it might be repurposed. There’s been some discussion about various cancer drugs that may actually…

Jan Paynter: Well, I know Bexarotene has…was approved in ’99.

Sue Friedman: Yes.

Jan Paynter: I didn’t mean to cut you off there. But I thought it was interesting because it was used for T-cell lymphomas.

Sue Friedman: Yes.

Jan Paynter: And what is fascinating to me about what you’re talking about is that the lag time for testing and approval is so long.

Sue Friedman: It is.

Jan Paynter: And in the meantime people are suffering and passing from this disease. So it seems very exciting to me if there are existing drugs that we could take advantage of. Now the other side of that is in a way the drug industry might not be wildly excited about that because some of the stuff might be off market. So it’s…the politics of cure come into play.

Sue Friedman: Oh, always the politics. But there are enough… There’s enough balance I think between looking at existing drugs and repurposing them and the potential for the new drugs. I know one of the things, you mentioned 2012. One of the things we learned through an Eli Lily drug study, the drug in clinical studies is called Solanezumab. We will not call it that when it reaches the market but Solanezumab failed dismally in its clinical trial of looking at those who were in mid to late stage Alzheimer’s. But there was a subgroup there of individuals who were in the very early stages of Alzheimer’s Disease and showed a 34 percent reduction in beta amyloid plaque.

Jan Paynter: It’s great that you bring that up because I was going to ask you about that as I struggled with the pronunciation, which you did beautifully. Okay, so now let’s look at some new drugs evolving which appear to slow the process. In July The Guardian reports that again, this drug that you mentioned, Solanezumab?

Sue Friedman: Yes.

Jan Paynter: Shows great promise and that 30 percent decline in memory loss on cognitive tests is really impressive. Why is making progress and slowing the disease so significant in moving toward an eventual cure?

Sue Friedman: What we have discovered is this disease is very complex because the brain is very complex and we still do not know all there is to know about the brain. So rather than say, ‘We must know everything there is to know about the brain and how it works and how it interacts with the rest of the body’, we now say, ‘What we need to do is to work on all fronts things that can have a delaying impact now while still working on prevention and still working on cure of course. But to delay would be phenomenal.’ If we could delay the onset of the disease by five years, the impact on Medicare, Social Security and private health insurance would be billions and billions of dollars. So straight economic political point of view, there’s benefit there. But there’s also huge personal benefit if I have five more years of economic productivity and five more years of fully being engaged with my family and my community. And so I would venture to say that our greatest priority and opportunity now is that delay, is being able to delay the disease coupled with slowing down the disease. Those are the two greatest opportunities we’re seeing now.

Jan Paynter: And also from what I had read it appeared that also if you learn about how to slow the disease, you have a foot in the door toward potentially a cure.

Sue Friedman: Most definitely. Absolutely.

Jan Paynter: I wanted to talk about some intriguing studies in mice and of course many people…

Sue Friedman: Don’t we love those mice?

Jan Paynter: We love these…these poor mice but they do great service to humanity. In June at an Alzheimer’s conference in Manchester, England…

Sue Friedman: Yes.

Jan Paynter: One of the speakers, Professor Giovanna Mallucci from the University of Cambridge discussed drugs used in mice for Prion’s Disease, which as you know is similar but not identical to Alzheimer’s, and that this was effective in reversing some of the effects of dementia. The drug inhibits an enzyme called PERK, thus restoring protein production and arresting brain cell death and memory loss. And, the mice appeared to be able to complete tasks, run mazes, etc. And then at Duke University in North Carolina, Professor Carol Colton’s research team found that by blocking the formation of plaque, they prevent the immune system, as we talked about before the program, from going rogue and consuming important nutrients such as arginine. So, this is a very exciting possibility. Does this new study in particular that I’ve been referring to suggest a shift away from targeting the amyloid plaques as the root cause of the disease and then viewing them instead as a symptom of neurodegeneration?

Sue Friedman: I think we have been there for a few years now in the research community. I had a researcher put it very graphically but I think very accurately. We know the bullets, beta amyloid plaque and tau tangles, inflammation, diabetes, etc. We don’t know the trigger. So we don’t know the basic reason that beta amyloid starts creating plaque. We don’t know the reason that tau starts tangling. We know the result is neuro death and loss of memory and judgment function. So I think for a while we have said we may not know the trigger but we can still have some major disease modifying discoveries knowing that it is beta amyloid that creates the plaque that clogs up the memories in the neuro pathways. So I think we are… Again, because there is still much to know about the brain, we’re seeing Alzheimer’s research look at several fronts now. I think the beta amyloid hypothesis is still a primary hypothesis. I don’t know that we believe it is the only one or the most important one but it is one that we’re getting closer and closer to having some real impact on.

Jan Paynter: I think those of us that have had relatives who’ve suffered from Alzheimer’s know that there are also big side effects with the medication. One of the things in reading for this today that I found exciting was the non-invasive ultrasound treatments which people are starting to use. Do you feel that these treatments have promise going forward?

Sue Friedman: I think… One of the things we try to do at the Alzheimer’s Association is to help all of our constituents become savvy consumers of research. And what we say is, ‘Every single piece of research is helpful.’ So the focused ultrasound component—and I understand that there may be a human trial that will happen in Canada–

Jan Paynter: 2017 possibly. Yeah.

Sue Friedman: Yes. Using the focused ultrasound in terms of eradicating/repairing the negative impacts of Alzheimer’s Disease. Every single one of these studies has great, great benefit. I heard yesterday morning on the news again about sleep and about now…sleeping on your side may be the best way to be brain healthy. That sleeping on your side as opposed to your back or your stomach may actually help the brain do its cleanup much better.

Jan Paynter: That is really intriguing.

Sue Friedman: Very intriguing. So see, there’s so many different moving parts here that focused ultrasound may become something that is the answer or an answer for some people or we may discover that it doesn’t sustain. That’s one of the things that we need to find with all of our research is something may work—and I’ll give you Solanezumab. It’s been in study two years and it’s showing great promise at year one and year two but it needs to sustain through year three in order for us to feel that it is absolutely going to be that disease modifying treatment.

Jan Paynter: Sue, I wanted to discuss at greater length with you today the role genetics play in Alzheimer’s Disease. In February of this year, The New York Times had an intriguing article by Carl Zimmer concerning the so-called super agers, people who in their 80s were able to perform cognitive tests typically achieved by people in their 50s. What is the significance in this connection of the von Economo neuron in the brains of this particular group studied and why is it significant?

Sue Friedman: That’s…we don’t know exactly why it’s significant but the fact that these people who are doing so well seem to exhibit additional capacity. It may be due to that. So there’s another research strategy, another research study that we need to look at. One of the things we already know is that the concept of cognitive reserve absolutely allows people to be in their 80s and 90s or even 100 and maintain their cognitive capacity. And what cognitive reserve is that the more memory pathways you have to Fact A or Memory B, the more you can maintain your level of functioning even as some of those pathways are diminished by the disease process. So one of the 10 tenets of having a healthy brain is to continue to learn new things. So the more education one has—and we’re not saying the more degrees or the more classes but those certainly count. The more education and learning one has, the greater your cognitive reserve.

Jan Paynter: Yeah, training your mind to be curious.

Sue Friedman: Curious and also to build up really the reserve because if I’ve got a wonderful memory of something when I’m 25 but I have eight ways that I can retrieve that and the disease process starts in my brain, I won’t realize that for several years because my brain is able to work around and compensate for that.

Jan Paynter: Well, we’re going to have to speed along here. I had more questions on this topic. However, we’re a political program. Let’s talk about legislation and governmental involvement. In June the U.S. House of Representatives passed the 21st Century Cures Act. What in your view will be the impact of this recent legislation, Sue, in facilitating potential treatments and possible cures for Alzheimer’s?

Sue Friedman: Well, we believe that Congress, we know that the White House has been for some time, but we believe that Congress now fully understands the critical importance of investing in research for Alzheimer’s Disease. And so with a national Alzheimer’s plan passed by Congress unanimously and signed by President Obama four years ago that says we will have a real treatment that modifies the disease, we will have a cure and we will have a prevention by 2025. This legislation is just the next step to make sure that we keep our feet to the grindstone and we keep monitoring to make sure that we are truly moving in that direction. We have but 10 years to reach those goals.

Jan Paynter: Now it’s very exciting then June the Senate Appropriations Committee approved a 60 percent increase which comes to roughly $350 million which is astonishing. What is the hope for Alzheimer’s Act and why is it significant, Sue?

Sue Friedman: The hope for Alzheimer’s Act is critically important for today and those who are diagnosed tomorrow. What it will do is it will combine community based resources with the diagnosis and the treatment. And I’ll give you an example and I know this personally. My niece had a beautiful baby girl who was diagnosed with Down Syndrome. Before she left the hospital, not only did they have their diagnosis, not only did they have their treatment plan if you will, she had social workers and physical therapists and counselors assigned to her and she had a community of resources. So what the Hope Act will do is make it a requirement that not only do you receive a diagnosis, you receive what treatment we have to offer but you also get these community based resources and referrals and so that you’re not simply going home to figure it out for yourself.

Jan Paynter: What I love too is that this is very bipartisan…

Sue Friedman: Yes.

Jan Paynter: And that’s very thrilling actually. Sue, what was the outcome of the 2013 G8 Summit in Northern Ireland?

Sue Friedman: Fascinatingly and very, very gratifying to us, for the first time ever they addressed an issue beyond the economic spectrum and that issue was Alzheimer’s. And so there is now a commitment amongst the G8, G7 countries to prioritize, research and focus around finding these solutions for Alzheimer’s Disease, around every country having their own national plan, although I will say the United States was by far not the first of these countries to have developed a national plan to address Alzheimer’s. We were a bit late coming to that party but we are there now.

Jan Paynter: Sue, for my last question, do you foresee a time when Alzheimer’s Disease might be treated as a chronic disease to be managed for instance much as AIDS and certain forms of cancer have come to be?

Sue Friedman: Yes. But beyond that, we really see a time where we can prevent Alzheimer’s. We believe that is absolutely on the horizon and it will be a combination of treatments and lifestyle. But that is still very much…our vision is a world without Alzheimer’s, not a world where you live with Alzheimer’s, and we think that that is definitely doable and still very much the research shows that’s possible. But along the way, there will be the delaying and then the living with and then the potential for the cure which is…when you think about those mice, something they no longer were able to do is now returned to them. Wouldn’t that be an amazing thing?

Jan Paynter: All right, Sue. Thank you very much for doing this program today. This is going to be very valuable learning for everybody watching and I appreciate you taking the time.

Sue Friedman: Thank you again for having me.

Jan Paynter: Thank you at home for joining our conversation. If you would like more information concerning the topic under discussion today we invite you to take a look at our website at politicsmatters.org. We will be posting a number of books, articles and relevant links on many of the issues under discussion today there for you. You will also find there a complete archive of all prior Politics Matters programs which you may watch anytime. We will be posting extended versions of the interviews online on our site as well and will continue to add more content. As always, we are very interested in hearing from you with any ideas, questions and concerns for future programs. We encourage you to email us at jan@politicsmatters.org. We are on PBS WVPT on the second and last Sunday of every month at 11:30 am. Thank you again and until next we meet, I’m Jan Paynter and this is Politics Matters.