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A Drug to Prevent Alzheimer's

Could a drug actually save your memory?

Everyone, no matter if you are a man or woman, family history or not, everyone with a brain is at risk for Alzheimer’s disease. Age is the biggest risk factor and America is aging. 
Right now, dozens of research sites across the country are testing an experimental drug to see if it might prevent memory loss associated with this terrible disease.
Veterinarian James Block has dedicated his life to helping his four-legged patients.
Now he’s going to focus on helping himself and his family.  His mother died of Alzheimer’s disease and he wants to know if he or his little boy is at risk.  That’s why he is planning to sign up for a prevention study investigating a new drug that targets a major risk factor for Alzheimer’s.
“I would be very willing and eager to participate to see if I have predisposition through genetic influence or evidence of early Alzheimer’s, or the lesions.” Block told Ivanhoe.
This summer, the A4 study will enroll 1000 people between the ages of 65 and 85 with normal thinking and memory function who have evidence of amyloid plaque build-up in the brain. 
Dr. Ranjan Duara, MD, Neurologist at Mount Sinai Medical Center pointed out the importance of studying the amyloid protein.
“We know that the amyloid starts being deposited in the brain typically at least15 years before the onset of the disease and as much as 30 years before the onset of the disease.” Duara explained. “The greater the amount of amyloid there is the redder the image tends to be.”
Volunteers must undergo a PET scan where they’re injected with a special tracer that highlights amyloid in the brain.
The investigational drug, solanezumab, is designed to target and remove amyloid from the brain. The study participants will get a monthly infusion of the drug or a placebo for 3 years. Researchers are hoping to learn two things.
“Do we have a way of treating the disease before it starts and secondly is amyloid really the cause of the disease.” Dr. Daura told Ivanhoe.
Finding those answers could change the future for Block and the rest of us.
The Wein center for clinical research is one of more than 50 A4 study sites in the U.S.  The principal investigators are Dr. Reisa Sperling at Harvard and Dr. Paul Aisen at UCSD. To enroll, call 1-800-272-3700 to ask about trial match.


BACKGROUND: Alzheimer’s disease is the most common form of dementia (accounts for 50-80% of dementia cases) that causes problems with thinking, memory and behavior. Alzheimer’s disease slowly breaks down brain cells. As it spreads, more cells lose their ability to function and eventually die, causing significant damage to the brain. President Barack Obama signed a bill into law containing $122 million for Alzheimer’s research, education, outreach and support in January of 2014.  This staggering amount includes an increase of $100 million for Alzheimer’s research at the National Institute on Aging, adding to nearly $484 million in funding across the National Institutes of Health in 2013. This increase translates into an additional $1 billion in research funds over the next decade. (Source: www.alz.org)
TREATMENT: There is no current cure for Alzheimer’s but researchers are continuing to search for new treatments that can alter the course of the disease. Common medications for cognitive symptoms of Alzheimer’s include cholinesterase inhibitors (Aricept, Exelon, Razadyne, Cognex) and memantine (Namenda). (Source: www.alz.org)
NEW TECHNOLOGY: The A4 Study (Anti-Amyloid Treatment in Asymptomatic Alzheimer’s study) is a clinical study using the drug, solanezumab, which targets the amyloid beta-protein and keeps it from building up in the brain as amyloid. The co-principal investigators of the A4 study are Reisa Sperling, M.D., professor of neurology at Harvard Medical School and Paul S. Aisen, M.D., professor of neurosciences at the University of California San Diego. Scientists believe that accumulation of a protein known as amyloid in the brain could play a vital role in the development of Alzheimer’s related memory loss. Enrollment for the study began in March of 2014. The test includes an expansion study known as the Longitudinal Evaluation of Amyloid Risk and Neurodegeneration (LEARN) which may provide scientists with an instrument to examine the accumulation of the tau protein into tangles in the brain. The start date for LEARN is scheduled for the fall of 2014. To find out more about the A4 study, go to a4study.org/locations. (Source: Dr. Ranjan Duara, M.D.)
FOR MORE INFORMATION ON THIS REPORT, PLEASE CONTACT:
Ranjan Duara, MD
Neurologist, Medical Director of the Wien Center for Alzheimer's Disease and
Memory Disorders at Mount Sinai Medical Center
Mount Sinai Medical Center
Phone:  305-674-2543
E-mail:  Ranjan.Duara@msmc.com
If this story or any other Ivanhoe story has impacted your life or prompted you or someone you know to seek or change treatments, please let us know by contacting Marjorie Bekaert Thomas at mthomas@ivanhoe.com


Ranjan Duara, MD, Neurologist at Mount Sinai Medical Center talks about an experimental drug that might prevent memory loss associated with Alzheimer’s.

Let me ask you about the blood test that they’ve developed at Georgetown. Is that something that is not being used yet?
Dr. Duara: No, it is not being used. It has to be validated and we really need another longitudinal study to find out the relationship between people who have the Alzheimer profile on the test and the development of the disease and the development of the disease and the genetic factors which may modify that relationship. It’s not something that’s going to be immediately put into use because we need a lot more information for it to be validated.
Let’s start with the A-4 study. Why is this important, what’s the significance of this?
Dr. Duara: The A4 study provides us the opportunity to address two major, but closely related questions about Alzheimer’s disease. One is we feel that the treatment for Alzheimer’s disease should begin as early as possible, before the symptoms actually start. It may be too late once the disease itself begins. Amyloid beta protein, which is widely believed to initiate the disease process, is deposited in the brain at least 10 to 15 years before the clinical symptoms start. That might be the opportunity for intervention since we can now detect amyloid using PET scans and detect people who are amyloid positive, but are not showing any symptoms at all. The only way we can do that is to evaluate people who are in the age group that are at risk for developing amyloid deposition in the brain and doing PET scans and determining who’s positive and who’s negative. We’re trying to understand whether amyloid is in fact the cause of the disease and how it’s related to the disease. Is it protein that is just being deposited in the brain as part of something else like a waste product, or some other process that’s going on and this is just the manifestation of that other process?
 In the A4 study we will be infusing a drug that we believe can take amyloid out of the brain. The first question we will be able to address in the A4 study is whether we can prevent the disease from occurring, among people who are amyloid positive, by successfully removing the protein for the brain. If we are able to prove that we will have a way of treating Alzheimer’s disease very early in the disease process, well before the symptoms actually start. We believe that the reason why treatments have not been successful so far is that it may be too late to start treatment once the symptoms begin...
The other question we are trying to address is whether amyloid is in fact the cause of the disease, and, if not, how it’s related to the disease. If in the A4 study we show we can delay or prevent the onset of the disease, it will basically prove the hypothesis that amyloid is the cause or closely related to the cause of the disease. If it does not delay the onset of the disease, it will suggest that amyloid beta protein is not the cause, but may be closely related to some process that is the cause of Alzheimer’s disease.
So is it a cause at the very least that makes you think it might be a precursor?
Dr. Duara: Amyloid protein could be a major risk factor for the disease. That is you may need amyloid deposition plus something else. It could be that amyloid protein by itself may be the cause of the disease but we don’t know how long it will take. It may be that some people that never develop the disease just don’t live long enough to actually develop the disease or for us to know that they developed the disease.
Because you know for a fact that there are people who die with amyloid plaques in their brains and they don’t have Alzheimer’s.
Dr. Duara: Yes, the amyloid plaques may be present without the clinical disease. For Alzheimer’s disease to develop you also need tangles in the nerve cells in addition to amyloid plaques.
So that’s the big question mark.
Dr. Duara: Right, we know that the amyloid starts being deposited in the brain typically at least 15 years before the onset of the disease and as much as 30 years before the onset of the disease. So there is amyloid being deposited and it may be just part of a normal aging process. It certainly increases the risk for developing amyloid in the brain which increases with age. It increases with certain known genetic factors that we can test for, like the APOE gene. People who are E4 positive have much more amyloid in their brain than people who are E4 negative. That’s a genetic test that’s easily done and we think that’s why the E4 gene is a risk factor for Alzheimer’s disease, because it increases amyloid deposition in the brain.
So anyone who has died with Alzheimer’s has amyloid in their brain? A lot like not everyone who has amyloid has Alzheimer’s? Isn’t that the way it works?
Dr. Duara: That’s almost correct except that it depends on how you define Alzheimer’s disease. There is a small group of people who have the tangles, lots and lots of tangles in their brain and don’t have any amyloid in their brain. Do they have a different disease or do they have Alzheimer’s disease without amyloid? That’s a question that has not been answered yet.  This is a very small group of people, probably less than one percent, with no amyloid in the brain and yet has the other feature that is classical for Alzheimer’s and is actually associated with the clinical features of the disease. That’s the tau protein in the tangles that they are associated with.
So usually first there is amyloid and then in some cases there are the tangles and the tau?
Dr. Duara: Right and there are always tangles in people with the symptoms and signs of Alzheimer’s disease during life. They don’t actually have the clinical symptoms of the disease unless they have tangles. If they just have amyloid in the brain and no tangles then they don’t have Alzheimer’s disease but, that’s the population that has a major risk factor for the disease.
So the disease is amyloid plus tangles?
Dr. Duara: Yes and presumably you can have amyloid in your brain for many years and never develop the tangles or manifest the features of Alzheimer’s disease. If they have amyloid and tangles then they have the pathology of the disease, but they do not necessarily have the symptoms and signs of the disease.
So if you cut off the amyloid early on you’re hoping that perhaps you can prevent the tangles from forming?
Dr. Duara: Exactly, yes. Amyloid is either a major risk factor or it’s the actual cause of the disease. We don’t know which one it is. But either way, by removing the amyloid we’ll get an answer as to the importance of amyloid in initiating the disease. It may be that there’s some other process underlying the amyloid that causes the disease itself and then requires amyloid in addition to make the disease produce the changes in the brain, the neurofibrillary tangles that are required for the clinical syndrome of Alzheimer’s disease.
Is this the first trial where you’re looking at an actual agent that might be preventative?
Dr. Duara: Yes, it is the first such trial for the common older onset form of the disease.
So this is a pretty big deal.
Dr. Duara: This is a big deal, everybody is watching this whole process and the findings here are going to be crucial in understanding the disease and knowing how we may go forward in trying to treat the disease effectively.
One thing that Dr. Block mentioned today, he was wondering about what the side effects are. I know that usually with a monoclonal antibody it’s so targeted that usually there aren’t that many side effects. What are some of the things you will talk to your patients about concerning side effects?
Dr. Duara: Every drug has some side effects and there are people who may have allergic symptoms to the drug. The usual type of gastrointestinal and skin problems, dizziness and headaches can occur. These are all basically manifestations of some kind of an allergic reaction to the drug itself. We are infusing a protein into individuals that’s a monoclonal antibody, but it’s basically a protein and any protein can produce some sort of an allergic reaction. The drug itself has been used in several thousand patients with Alzheimer’s disease in clinical trials.  The results so far have been that the drug does not work in people with clinical Alzheimer’s disease, or at best it may have had a positive effect among a group of very mild cases of Alzheimer’s disease. The side effects were very small, so that’s positive.
So you know this drug doesn’t really work once you have Alzheimer’s and you’re hoping this works before you get the actual symptoms?
Dr. Duara: Right, exactly.
Anything else you want to say? So at the end, half will get placebo and half will get the drug and if it’s found to work, all will get the drug?
Dr. Duara: Well there are other things we can discuss if you want to.
About the trial.
Dr. Duara: The protocol requires the person to have a cognitive evaluation, and they have to be shown to be cognitively normal to enter into the study. Then they have an MRI scan to make sure that there’s no abnormalities in the brain that could be ultimately causing memory problems. Once they’ve passed through those two tests then they go on to get the amyloid PET scan. Before they get the PET scan the individual has to understand that we will be telling them the results of the scan. In fact, this is one of the few research studies using amyloid PET scans in which the results are revealed to the individual during the study. It’s like genetic counseling, it’s sort of similar. In this case it’s not genetic test results, but information about what their risk is of developing Alzheimer’s disease because they have been found to be amyloid positive or negative. It takes about an hour to counsel the individuals. Once the subject knows that they’re amyloid positive or negative, they may decide if they  want to continue to take part in the study or do a variety of other things to plan for the future because who knows whether this drug is going to work or not. These are issues that we’ll have to discuss in detail so they are fully informed about their decision to participate
If they are amyloid positive they will be invited to participate in the treatment part of the study. This is a double blind study lasting three and a half years and includes monthly intravenous infusions of the active antibody or a placebo (it’s double blind because neither the participant nor the investigator will know what is being infused).
But at least you’re offering a drug that potentially could do something about it which I think is the good news. So let’s talk about the tangles on the taus. A big question is exactly what is the role of amyloid in this whole process?
Dr. Duara: We know that amyloid is deposited in the brain and that at some point in people who start developing the disease, the tangles start accumulating in a very specific part of the brain called the medial temporal lobe, then spreading to other parts of the brain, but first involving the hippocampus which is intimately involved with memory function. The patients manifest symptoms of memory impairment and that is why memory is such an early feature of Alzheimer’s disease. Once the tangles develop in other parts of the brain, the patient starts manifesting all the other symptoms of Alzheimer’s disease , which could be language impairment(the ability to express oneself verbally or to comprehend) , or visual spatial function (such as the ability to find one’s way around in space or knowing where things are located), or to perform skill movements (such as knowing how to use a microwave oven or a remote control of a television).It can also involve vision, the ability to read and comprehend what one is reading.
And that is specifically related to the tangles?
Dr. Duara: Yes, the location of where the tangles develop is related to what symptoms develop. If the left side of the brain is involved early with the tangles then language function will start getting impaired early in the disease course. If it’s the right side of the brain it’s more likely that visual spatial impairment occurs early. If it’s more the frontal lobes you’ll get changes in behavior that are very frequent in those patients, lack of inhabitation and inappropriate behavior and so forth may occur early in the disease.
You’re saying that now the next phase of study that needs to be done or is being done is tau, the deposit of that in the brain.
Dr. Duara: To understand the disease better, it’s important for us to be able to determine where the tau is being deposited and its relationship to amyloid. In the last year or two we have started being able to image the presence of the tau protein in the brain. That is going to give us another perspective of how amyloid is related to tau and how tau protein is related to the disease. Ultimately, it will also help us determine whether we are successful at a very early stage in preventing the onset of the disease. For example, this particular drug that we are planning to test, solanezumab, if it removes amyloid, does it also prevent the onset of tau deposition as well? We might be in the future doing studies where we’re doing both amyloid scans as well as tau PET scans.
So you think it’s likely that the two work in combination?
Dr. Duara: Right and it will be an early marker of the success of the treatment. For instance, if you removed amyloid in the brain but the deposition of tau continues or stops occurring, then you’re not going to be very effective in treating the disease. So in that case. you’ve successfully removed amyloid but you haven’t actually changed the course of the disease because tau is what is going to determine what course the disease is going to take, whether the disease is going to begin clinically and how rapidly it’s going to progress.
So in a way you’re kind of testing indirectly if this has an effect on tau?
Dr. Duara: Yes, if we do both the scans together. Right now in place of the tau scan what we are doing is we’re looking at how cognitive function changes in these individuals. We’re using the tests of memory and other cognitive functions to determine whether they stay stable throughout the four year duration of the clinical trial.
Is there anything in the works in terms of drug trials in the future to specifically target tau?
Dr. Duara: There have been attempts to develop drugs but nothing has been successfully developed. That is a major interest for a lot of pharmaceutical companies and for the people in the field in general. Without the tau, you don’t get the disease so that would be the most important way in which we could treat the disease. Not only before the disease starts but for those people who already have the disease. So it’s going to be important for all phases of the disease.
This information is intended for additional research purposes only. It is not to be used as a prescription or advice from Ivanhoe Broadcast News, Inc. or any medical professional interviewed. Ivanhoe Broadcast News, Inc. assumes no responsibility for the depth or accuracy of physician statements. Procedures or medicines apply to different people and medical factors; always consult your physician on medical matters.


If you would like more information, please contact:

Ranjan Duara, MD
Neurologist, Medical Director of the Wien Center for Alzheimer's Disease and
Memory Disorders at Mount Sinai Medical Center
Mount Sinai Medical Center
Phone:  305-674-2543
E-mail:  Ranjan.Duara@msmc.com

Sign up for a free weekly e-mail on Medical Breakthroughs called
First to Know by clicking here.




Ranjan Duara, MD, Neurologist at Mount Sinai Medical Center talks about an experimental drug that might prevent memory loss associated with Alzheimer’s.

Let me ask you about the blood test that they’ve developed at Georgetown. Is that something that is not being used yet?
Dr. Duara: No, it is not being used. It has to be validated and we really need another longitudinal study to find out the relationship between people who have the Alzheimer profile on the test and the development of the disease and the development of the disease and the genetic factors which may modify that relationship. It’s not something that’s going to be immediately put into use because we need a lot more information for it to be validated.
Let’s start with the A-4 study. Why is this important, what’s the significance of this?
Dr. Duara: The A4 study provides us the opportunity to address two major, but closely related questions about Alzheimer’s disease. One is we feel that the treatment for Alzheimer’s disease should begin as early as possible, before the symptoms actually start. It may be too late once the disease itself begins. Amyloid beta protein, which is widely believed to initiate the disease process, is deposited in the brain at least 10 to 15 years before the clinical symptoms start. That might be the opportunity for intervention since we can now detect amyloid using PET scans and detect people who are amyloid positive, but are not showing any symptoms at all. The only way we can do that is to evaluate people who are in the age group that are at risk for developing amyloid deposition in the brain and doing PET scans and determining who’s positive and who’s negative. We’re trying to understand whether amyloid is in fact the cause of the disease and how it’s related to the disease. Is it protein that is just being deposited in the brain as part of something else like a waste product, or some other process that’s going on and this is just the manifestation of that other process?
 In the A4 study we will be infusing a drug that we believe can take amyloid out of the brain. The first question we will be able to address in the A4 study is whether we can prevent the disease from occurring, among people who are amyloid positive, by successfully removing the protein for the brain. If we are able to prove that we will have a way of treating Alzheimer’s disease very early in the disease process, well before the symptoms actually start. We believe that the reason why treatments have not been successful so far is that it may be too late to start treatment once the symptoms begin...
The other question we are trying to address is whether amyloid is in fact the cause of the disease, and, if not, how it’s related to the disease. If in the A4 study we show we can delay or prevent the onset of the disease, it will basically prove the hypothesis that amyloid is the cause or closely related to the cause of the disease. If it does not delay the onset of the disease, it will suggest that amyloid beta protein is not the cause, but may be closely related to some process that is the cause of Alzheimer’s disease.
So is it a cause at the very least that makes you think it might be a precursor?
Dr. Duara: Amyloid protein could be a major risk factor for the disease. That is you may need amyloid deposition plus something else. It could be that amyloid protein by itself may be the cause of the disease but we don’t know how long it will take. It may be that some people that never develop the disease just don’t live long enough to actually develop the disease or for us to know that they developed the disease.
Because you know for a fact that there are people who die with amyloid plaques in their brains and they don’t have Alzheimer’s.
Dr. Duara: Yes, the amyloid plaques may be present without the clinical disease. For Alzheimer’s disease to develop you also need tangles in the nerve cells in addition to amyloid plaques.
So that’s the big question mark.
Dr. Duara: Right, we know that the amyloid starts being deposited in the brain typically at least 15 years before the onset of the disease and as much as 30 years before the onset of the disease. So there is amyloid being deposited and it may be just part of a normal aging process. It certainly increases the risk for developing amyloid in the brain which increases with age. It increases with certain known genetic factors that we can test for, like the APOE gene. People who are E4 positive have much more amyloid in their brain than people who are E4 negative. That’s a genetic test that’s easily done and we think that’s why the E4 gene is a risk factor for Alzheimer’s disease, because it increases amyloid deposition in the brain.
So anyone who has died with Alzheimer’s has amyloid in their brain? A lot like not everyone who has amyloid has Alzheimer’s? Isn’t that the way it works?
Dr. Duara: That’s almost correct except that it depends on how you define Alzheimer’s disease. There is a small group of people who have the tangles, lots and lots of tangles in their brain and don’t have any amyloid in their brain. Do they have a different disease or do they have Alzheimer’s disease without amyloid? That’s a question that has not been answered yet.  This is a very small group of people, probably less than one percent, with no amyloid in the brain and yet has the other feature that is classical for Alzheimer’s and is actually associated with the clinical features of the disease. That’s the tau protein in the tangles that they are associated with.
So usually first there is amyloid and then in some cases there are the tangles and the tau?
Dr. Duara: Right and there are always tangles in people with the symptoms and signs of Alzheimer’s disease during life. They don’t actually have the clinical symptoms of the disease unless they have tangles. If they just have amyloid in the brain and no tangles then they don’t have Alzheimer’s disease but, that’s the population that has a major risk factor for the disease.
So the disease is amyloid plus tangles?
Dr. Duara: Yes and presumably you can have amyloid in your brain for many years and never develop the tangles or manifest the features of Alzheimer’s disease. If they have amyloid and tangles then they have the pathology of the disease, but they do not necessarily have the symptoms and signs of the disease.
So if you cut off the amyloid early on you’re hoping that perhaps you can prevent the tangles from forming?
Dr. Duara: Exactly, yes. Amyloid is either a major risk factor or it’s the actual cause of the disease. We don’t know which one it is. But either way, by removing the amyloid we’ll get an answer as to the importance of amyloid in initiating the disease. It may be that there’s some other process underlying the amyloid that causes the disease itself and then requires amyloid in addition to make the disease produce the changes in the brain, the neurofibrillary tangles that are required for the clinical syndrome of Alzheimer’s disease.
Is this the first trial where you’re looking at an actual agent that might be preventative?
Dr. Duara: Yes, it is the first such trial for the common older onset form of the disease.
So this is a pretty big deal.
Dr. Duara: This is a big deal, everybody is watching this whole process and the findings here are going to be crucial in understanding the disease and knowing how we may go forward in trying to treat the disease effectively.
One thing that Dr. Block mentioned today, he was wondering about what the side effects are. I know that usually with a monoclonal antibody it’s so targeted that usually there aren’t that many side effects. What are some of the things you will talk to your patients about concerning side effects?
Dr. Duara: Every drug has some side effects and there are people who may have allergic symptoms to the drug. The usual type of gastrointestinal and skin problems, dizziness and headaches can occur. These are all basically manifestations of some kind of an allergic reaction to the drug itself. We are infusing a protein into individuals that’s a monoclonal antibody, but it’s basically a protein and any protein can produce some sort of an allergic reaction. The drug itself has been used in several thousand patients with Alzheimer’s disease in clinical trials.  The results so far have been that the drug does not work in people with clinical Alzheimer’s disease, or at best it may have had a positive effect among a group of very mild cases of Alzheimer’s disease. The side effects were very small, so that’s positive.
So you know this drug doesn’t really work once you have Alzheimer’s and you’re hoping this works before you get the actual symptoms?
Dr. Duara: Right, exactly.
Anything else you want to say? So at the end, half will get placebo and half will get the drug and if it’s found to work, all will get the drug?
Dr. Duara: Well there are other things we can discuss if you want to.
About the trial.
Dr. Duara: The protocol requires the person to have a cognitive evaluation, and they have to be shown to be cognitively normal to enter into the study. Then they have an MRI scan to make sure that there’s no abnormalities in the brain that could be ultimately causing memory problems. Once they’ve passed through those two tests then they go on to get the amyloid PET scan. Before they get the PET scan the individual has to understand that we will be telling them the results of the scan. In fact, this is one of the few research studies using amyloid PET scans in which the results are revealed to the individual during the study. It’s like genetic counseling, it’s sort of similar. In this case it’s not genetic test results, but information about what their risk is of developing Alzheimer’s disease because they have been found to be amyloid positive or negative. It takes about an hour to counsel the individuals. Once the subject knows that they’re amyloid positive or negative, they may decide if they  want to continue to take part in the study or do a variety of other things to plan for the future because who knows whether this drug is going to work or not. These are issues that we’ll have to discuss in detail so they are fully informed about their decision to participate
If they are amyloid positive they will be invited to participate in the treatment part of the study. This is a double blind study lasting three and a half years and includes monthly intravenous infusions of the active antibody or a placebo (it’s double blind because neither the participant nor the investigator will know what is being infused).
But at least you’re offering a drug that potentially could do something about it which I think is the good news. So let’s talk about the tangles on the taus. A big question is exactly what is the role of amyloid in this whole process?
Dr. Duara: We know that amyloid is deposited in the brain and that at some point in people who start developing the disease, the tangles start accumulating in a very specific part of the brain called the medial temporal lobe, then spreading to other parts of the brain, but first involving the hippocampus which is intimately involved with memory function. The patients manifest symptoms of memory impairment and that is why memory is such an early feature of Alzheimer’s disease. Once the tangles develop in other parts of the brain, the patient starts manifesting all the other symptoms of Alzheimer’s disease , which could be language impairment(the ability to express oneself verbally or to comprehend) , or visual spatial function (such as the ability to find one’s way around in space or knowing where things are located), or to perform skill movements (such as knowing how to use a microwave oven or a remote control of a television).It can also involve vision, the ability to read and comprehend what one is reading.
And that is specifically related to the tangles?
Dr. Duara: Yes, the location of where the tangles develop is related to what symptoms develop. If the left side of the brain is involved early with the tangles then language function will start getting impaired early in the disease course. If it’s the right side of the brain it’s more likely that visual spatial impairment occurs early. If it’s more the frontal lobes you’ll get changes in behavior that are very frequent in those patients, lack of inhabitation and inappropriate behavior and so forth may occur early in the disease.
You’re saying that now the next phase of study that needs to be done or is being done is tau, the deposit of that in the brain.
Dr. Duara: To understand the disease better, it’s important for us to be able to determine where the tau is being deposited and its relationship to amyloid. In the last year or two we have started being able to image the presence of the tau protein in the brain. That is going to give us another perspective of how amyloid is related to tau and how tau protein is related to the disease. Ultimately, it will also help us determine whether we are successful at a very early stage in preventing the onset of the disease. For example, this particular drug that we are planning to test, solanezumab, if it removes amyloid, does it also prevent the onset of tau deposition as well? We might be in the future doing studies where we’re doing both amyloid scans as well as tau PET scans.
So you think it’s likely that the two work in combination?
Dr. Duara: Right and it will be an early marker of the success of the treatment. For instance, if you removed amyloid in the brain but the deposition of tau continues or stops occurring, then you’re not going to be very effective in treating the disease. So in that case. you’ve successfully removed amyloid but you haven’t actually changed the course of the disease because tau is what is going to determine what course the disease is going to take, whether the disease is going to begin clinically and how rapidly it’s going to progress.
So in a way you’re kind of testing indirectly if this has an effect on tau?
Dr. Duara: Yes, if we do both the scans together. Right now in place of the tau scan what we are doing is we’re looking at how cognitive function changes in these individuals. We’re using the tests of memory and other cognitive functions to determine whether they stay stable throughout the four year duration of the clinical trial.
Is there anything in the works in terms of drug trials in the future to specifically target tau?
Dr. Duara: There have been attempts to develop drugs but nothing has been successfully developed. That is a major interest for a lot of pharmaceutical companies and for the people in the field in general. Without the tau, you don’t get the disease so that would be the most important way in which we could treat the disease. Not only before the disease starts but for those people who already have the disease. So it’s going to be important for all phases of the disease.
This information is intended for additional research purposes only. It is not to be used as a prescription or advice from Ivanhoe Broadcast News, Inc. or any medical professional interviewed. Ivanhoe Broadcast News, Inc. assumes no responsibility for the depth or accuracy of physician statements. Procedures or medicines apply to different people and medical factors; always consult your physician on medical matters.


If you would like more information, please contact:

Ranjan Duara, MD
Neurologist, Medical Director of the Wien Center for Alzheimer's Disease and
Memory Disorders at Mount Sinai Medical Center
Mount Sinai Medical Center
Phone:  305-674-2543
E-mail:  Ranjan.Duara@msmc.com

Sign up for a free weekly e-mail on Medical Breakthroughs called
First to Know by clicking here.




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