March 11, 2011
NIH Podcast Episode #0129
Balintfy: Welcome to episode 129 of NIH Research Radio with news about the ongoing medical research at the National Institutes of Health – the nation's medical research agency. I'm your host Joe Balintfy. Coming up in this episode how a rare genetic glitch may hold clues for treating schizophrenia, two pesticides are associated with Parkinson’s disease, identifying and understanding Transient Ischemic Attacks, and the conclusion of our conversation covering a decade of Alzheimer’s disease research—what we know today. But first, this news update. Here’s Craig Fritz.
Fritz: The National Institute of Environmental Health Sciences has started a new study to examine the impact of the Deepwater Horizon oil spill in the Gulf of Mexico. The GuLF study will follow 55,000 clean up workers and volunteers for up to 10 years to monitor possible health effects from the spill. This effort is the largest ever to examine the aftermath of a major oil spill. Over time, the gulf study will generate important data that may help inform policy decisions on health care and health services in the region. Findings may also influence responses to other oil spills in the future. Researchers note that they are enrolling workers and volunteers because they were closest to the disaster and had the highest potential for being exposed to oil and dispersants. Potential participants will be contacted by mail to enroll. A second phase of the study will follow approximately 20,000 people and include an at home visit and follow-up telephone interviews in subsequent years.
Researchers funded by the Eunice Kennedy Shriver National Institute of Child Health And Human Development have found that a new drug regimen can help cut the spread of HIV from a mother to her baby. Pregnant women who are unaware that they have HIV miss the chance for drug treatment that can benefit not only their own health, but could also prevent them from transmitting the virus to their infants. When HIV is not diagnosed until women go into labor, their infants are usually treated soon after birth with a single anti hiv drug to prevent the infants from becoming infected with the virus. The new study has found that adding one or two drugs to the standard treatment can reduce the chances that an infant will develop an HIV infection by more than 50 percent.
March is National Kidney Month and the National Institute of Diabetes And Digestive And Kidney Diseases is raising awareness about what you can do to take care of your kidneys. Topping their list of preventative measures is getting tested for kidney disease if you have diabetes, high blood pressure or a family history of kidney failure. An estimated 20 million Americans have chronic kidney disease, which can also lead to heart disease.
For this NIH News Update – I’m Craig Fritz
Balintfy: News updates are compiled from information at www.nih.gov/news. Coming up later in the program, Alzheimer’s disease, Parkinson’s disease and TIAs; but first, a genetic glitch that may hold clues for schizophrenia. That’s next.
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Rare gene glitch may hold clues for schizophrenia
Balintfy: Schizophrenia is a chronic, severe, and disabling brain disorder that affects about 1 percent of Americans. Current treatments may help relieve many symptoms of schizophrenia, but most people who have the disorder cope with symptoms throughout their lives. Now scientists have identified a rare genetic glitch that could help improve treatments for the disorder. Britt Ehrhardt files this report.
Ehrhardt: New research has linked a rare genetic mutation to the mental illness schizophrenia. The mutation has been found in a very small percentage of people, but the finding could help to improve treatment for many with the disorder.
Sebat: This has immediate implications for diagnosis and treatment.
Ehrhardt: Dr. Jonathan Sebat works for the University of California San Diego. He led the study team, and he explains that discovery of this shared genetic abnormality is an important advance.
Sebat: Schizophrenia is a genetic disorder. We can find these genes, and these genes identify new pathways that are potential avenues for drug development.
Ehrhardt: Dr. Sebat says that schizophrenia is known to have a strong genetic componen—having a parent or sibling with the disorder increases one's risk tenfold. However, genetic studies have so far explained relatively few cases of the illness. Dr. Sebat and his colleagues found mutations in a gene that controls part of the system for a brain chemical called a neuropeptide.
Sebat: Neuropeptides are interesting because they affect neurons in other ways. Neuropeptides help to regulate gene expression, blood flow, and the formation of synapses, for example.
Ehrhardt: A neuropeptide acts as a chemical messenger in the brain. Scientists focused on the gene for V-I-P-R-2, pronounced “viper two,” a receptor for one of these neuropeptide chemical messengers.
Sebat: Our findings established a link between the neuropeptide receptor VIPR2 and schizophrenia.
Ehrhardt: This neuropeptide and its receptor are known to play a role in brain development. However, the discovery of a link to schizophrenia was a surprise to scientists.
Sebat: The VIPR2 gene helps to regulate learning and behavior. However, this gene was certainly not on anybody’s top ten list.
Ehrhardt: Dr. Sebat explains that schizophrenia patients were 14 times more likely to have multiple copies of the gene for VIPR2.
Sebat: There were duplications that occurred 14 times more frequently in patients than in controls.
Ehrhardt: VIPR2 triggers a signaling system in the cell. Dr. Sebat and other scientists now believe other schizophrenia patients could also have disturbances of this signaling system, even if they lack this particular genetic mutation. He says many people could benefit.
Sebat: Genetic tests for mutations in VIPR2 could help to identify people at risk for schizophrenia, and it could help to identify patients with schizophrenia that were most likely to benefit from a treatment that targets this gene.
Ehrhardt: This research was funded in part by the National Institutes of Health. For more information on schizophrenia and this study, visit www.nimh.nih.gov. This is Britt Ehrhardt at the National Institutes of Health, Bethesda, Maryland.
NIH study finds two pesticides associated with Parkinson's disease
Balintfy: A recent study is showing a link between use of two common pesticides and Parkinson's disease. Parkinson's disease, as you may know, is a disorder that affects nerve cells, or neurons, in a part of the brain that controls muscle movement. There is no cure for Parkinson’s disease so researchers hope these new study findings will have implications for new treatment and prevention options. Wally Akinso has the details.
Akinso: New research shows a link between the use of two pesticides and Parkinson’s disease.
Kamel: Both of these pesticides have been connected to Parkinson’s disease.
Akinso: Dr. Freya Kamel is a staff Scientist for the Epidemiology Branch at the National Institute of Environmental Health Science.
Kamel: Rotenone is an insecticide that was used in the past and home gardens and on pests. It was considered to be a safe chemical because it’s synthesized by plants, in other words it could be considered to be organic. The other pesticide that we looked at in our study is called paraquat and that’s an herbicide, which is used to kill weeds.
Akinso: The study was a joint effort conducted by researchers at the NIEHS, and the Parkinson’s Institute and Clinical Center in Sunnyvale, California. The researchers studied 110 people with Parkinson’s disease and over 300 controls matched by age, gender and state to investigate the relationship between Parkinson’s disease and exposure to pesticides or other agents that are toxic to nervous tissue. Dr. Kamel says people that used these pesticides were more likely to develop Parkinson's disease.
Kamel: We found that both paraquat and rotenone were associated with Parkinson’s disease. Exposure to either of those chemicals caused about a two fold increase in the risk for Parkinson’s disease. We also looked at some other chemicals, other pesticides that have mechanisms that are very similar to either rotenone or paraquat. And these other chemicals considered as a group also increased the risk of Parkinson's disease.
Akinso: The Farming and Movement Evaluation study is a case-control study that is part of the larger Agricultural Health Study, which is a study of farming and health in approximately 90,000 pesticide applicators and their spouses. Dr. Kamel is optimistic that this study could lead to possible treatment or prevention for Parkinson's disease.
Kamel: So not only do we know something about risk factors for the disease but this study also increases our understanding of the mechanisms that are involved. And this finding is particularly important because it may help us develop treatment or even preventive measures for the disease.
Akinso: Dr. Kamel says these findings help researchers to understand the biologic changes underlying Parkinson’s disease. For more information on this study, visit www.niehs.nih.gov. More on Parkinson's disease can be found at www.ninds.nih.gov. This is Wally Akinso at the National Institutes of Health Bethesda, Maryland.
Transient Ischemic Attack - TIA
Balintfy: Transient Ischemic Attacks are often called “mini strokes.” Cherry Graziosi reports on how serious they can be.
Graziosi: Transient Ischemic Attacks or TIAs often come on suddenly and the symptoms can be dramatic.
Warach: Weakness on one side of the body, speech disturbances, aphasia.
Graziosi: And, according to Dr. Steven Warach of the National Institute of Neurological Disorders and Stroke, TIAs are warning signs that something more serious can be right around the corner.
Warach: We know that patients that have TIAs, particularly those that may cause a little brain injury, are much more likely to have the big one - big stroke - over the next days and weeks.
Graziosi: Dr. Warach says knowing your risk factors, such as high blood pressure and diabetes, can help prevent TIAs.
Warach: So to have a TIA is really like a wake-up call to say better check everything especially if you already have risk factors or are on medicines.
Graziosi: Dr. Warach says since TIAs normally don’t cause brain injuries, doctors must get a good clinical history on the patient to determine if the patient suffered a TIA or something more serious. For more information on TIAs visit www.ninds.nih.gov. This is Cherry Graziosi, National Institutes of Health, Bethesda, Maryland.
Balintfy: Coming up, we wrap up an in-depth interview on Alzheimer’s disease. That’s next on NIH Research Radio.
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A decade of Alzheimer’s disease research - Part 2
Balintfy: In our last episode we started a conversation with Dr. Marcelle Morrison-Bogorad, the former director of the Division of Neuroscience at the National Institute on Aging. After serving 14 years in that position, she is retiring. We talked to her about how Alzheimer’s disease research has changed. Now we look ahead. We pick up here with what we have learned in terms of identifying the risk factors for Alzheimer’s disease – are there things we can do, change diets or exercise that can help prevent the disease?
Morrison-Bogorad: Well obviously, one thing that people would like to do is take their future into their own hands and one of the awful things about Alzheimer's, I think, is its inevitability – that once you get it, once you're diagnosed, once it's started in your brain, really, there's no way to stop it right now. Wouldn't it be wonderful if you could exercise it away, you know, if you could eat it away? If you take enough olive oil, you know, the Mediterranean diet, to do your brain good and to stop it?
Now there was a Consensus Conference at NIH last year, which I think rightly so said that there is no definitive evidence at the moment that diet or exercise or being in the company of other people, being interactive socially, going to church, any of these things—getting married—can stave off Alzheimer's, but we've got a big investment in clinical trials to see whether some of these things might work. And that's what's important. Going from the realm of fantasy and we wish it were so, to actually proving in a clinical trial that it is or isn't so. It costs a huge amount of money. We're putting money into a trial called “Life” right now, which is a big exercise trial that has a big cognitive component in it. And that's the only way—with a lot of money invested—that we're going to find out, once and for all, whether the potential of exercise is actually there or not.
Balintfy: I hear the clinical trial called the gold standard for research.
Morrison-Bogorad: Well, we think it is. The clinical trial has to be compared to what's called epidemiology, where you compare groups of people who are as alike as you can make them, apart from whether they have a disease or not. And from the epidemiology studies, many of them do suggest that exercise is beneficial. There are a number of epidemiology studies which have compared people with Alzheimer's and people with not, and they have often shown that people who don't get Alzheimer's have exercised more regularly than the people who do. But there are just so many caveats to that sort of study and that's why the consensus conference decided that the evidence just wasn't good enough. A lot of it was based on epidemiology. You need a clinical trial to actually see whether it's going to be effective or not.
Not that exercise isn't good anyway. Exercise is good for the heart and for the rest of the body, as well as the brain. So, you should exercise anyway. But it might just help your head as well as your body.
Balintfy: Are there some successes you would highlight regarding Alzheimer’s disease research?
Morrison-Bogorad: Yeah, the Alzheimer's Disease Neuroimaging Initiative, ADNI, which I think has been one of the most successful private-public partnerships that the NIH and the NIH Foundation and the scientists and the NIA have -- or any of the institutes have actually done. And there, what they're trying to do is really identify the first signs of Alzheimer's disease that occur in the brain by using imaging or even using biological analysis of things like cerebrospinal fluid, not only to identify the very early stages of the disease, but also to determine more accurately and more readily whether people who are getting a drug in a particular clinical trial are getting better or not. So, ADNI has been extraordinarily successful.
And, I think one thing has come up in the past year or two, which has really I think shown yet again, that we don't understand what's going on in the brain as much as we think we should. And that has come about through ADNI, through imaging studies looking now at amyloid in the brain of people who are still alive; so you can look into the brain, you can give a radio label tracer that sticks to the amyloid in the brain, and then you can visualize it. And the really surprising result that has come out of that, which had been—there were—there was research on people who had died that sort of suggested this, but the results of living people were so extraordinary. And the results were that you could have a person who seems quite okay mentally and they sometimes have as much amyloid in their brain as a person who has Alzheimer's disease.
So, of course, how can this be? You know, we thought that the amount of amyloid in the brain would be much higher in people with Alzheimer's disease and we thought the people who were cognitively normal wouldn't have much of it. This really turned us upside-down and there have been so many instances of cases like this in the research on Alzheimer's disease. Those are just the latest twirl that nature has given us.
So why—how can these people withstand this amount of amyloid in their brain and still function quite normally? Are they in the early stages of Alzheimer's disease? So, on the first hand, it might give us a clue about how to withstand Alzheimer's. How do these brains withstand such a large amount of amyloid? The other things, are the people with amyloid in their brains, no matter how normal they seem to be now, actually on that slippery slope towards Alzheimer's disease?
Balintfy: So what do you see looking ahead?
Morrison-Bogorad: Eventually, when we have an intervention that works, what we want to do is to use it in people who are minimally damaged so far. And so, you know, a lot of work at ADNI and other labs around the world has been what are the earliest signs? And I've talked about one now, the fact that some people have larger amounts of amyloid in their brain. And so many people think that's one of the first things that happens and that it leads to loss of connections between neurons and neuron death and loss of the size of different brain regions, like the hippocampus. So, a lot of our work has been on identifying these earliest stages biologically and that not only give us hope for being able to diagnose Alzheimer's earlier, but also gives us major clues just like the genetics does of what happens first and what do we have to concentrate on at these early stages that will stop the disease in its tracks?
A lot of people think that the clinical trials that haven't worked so far, many of which have been against amyloid itself, haven't worked because the disease is too advanced by the time the drugs have been tried. And so, perhaps we're going to have to go back to clinical trials and test much earlier stages, people with amyloid in their brains, but no cognitive symptoms, for example. And the trouble with these trials is that the earlier you go, the more people you need, the more expensive they are, the more time they take. We're hoping that ADNI will give us the results that will allow us to make the trials shorter and smaller, but we've got a little bit of a way to go before that can happen. So, it's a time, unfortunately, where we need a lot of money to do the sort of research that's needed to really advance the field and find a cure. And yet, as you all know, money is very lacking right now and that is a huge, huge problem for the field.
Balintfy: Thank you very much Dr. Marcelle Morrison-Bogorad. For more information on Alzheimer’s disease visit www.nia.nih.gov. And that’s it for this episode of NIH Research Radio. Please join us again on Friday, March 25th – our next edition will feature a diabetes interview. If you have any story suggestions for a future episode or questions or comments about this program, please let me know. Best to reach me by email—my address is email@example.com. I'm your host, Joe Balintfy. Thanks for listening.
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