Experimental drug to prevent Alzheimer's tested - 8 News NOW

Experimental drug to prevent Alzheimer's tested

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MIAMI (Ivanhoe Newswire) — 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 least 15 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?Dr. Duara:

Dr. Duara: 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.

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