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August 7, 2009
NIH Podcast Episode #0090
Balintfy: Welcome to the 90th episode 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: A couple stories from the National Institute on Drug Abuse: one on preventing risky behavior in teens, the other on how smokers see anti-smoking campaigns. Also, we’ll hear how middle-aged mice surprised researchers with their ability to regenerate tissue. But first: news on how schizophrenia and bipolar disorder may share the same genetic roots. That's next on NIH Research Radio.
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Schizophrenia and Bipolar Disorder Share Genetic Roots
Balintfy: A trio of genome-wide studies — collectively the largest to date — have pinpointed a vast array of genetic variation that together may account for at least one-third of the genetic risk for schizophrenia, a brain disorder that’s symptoms can include hallucinations, delusions and disordered thinking. One of the three genetic research studies, which are appearing on-line in the journal Nature, is showing that schizophrenia may share the same genetic roots as bipolar disorder, an illness that causes shifts in a person's mood, energy and ability to function.
Insel: This new set of studies builds on a hint that we had before that the genetic risk for schizophrenia may overlap the genetic risk for bipolar.
Balintfy: Dr. Thomas Insel is the director of the National Institute of Mental Health.
Insel: We don’t have a smoking gun here, and I think the one thing you can say from these three studies is there isn’t going to be a smoking gun. And it’s only in very rare cases that you’re going to find a large-effect gene that actually could be considered to be a cause rather than just a risk factor.
Balintfy: Though all three studies implicate an area of Chromosome 6, most of the genetic makeup of schizophrenia, which is estimated to be at least 70 percent heritable, remains unknown. Dr. Insel says that the short arm of Chromosome 6 is a very interesting area.
Insel: In some ways it’s like the Bermuda Triangle of the human genome sequence because it’s an area with a tremendous amount of variability
Balintfy: He adds that this is an area of great complexity in the genome, previously associated with a number of autoimmune diseases, including type-1 diabetes, rheumatoid arthritis, and Crohn’s disease. And now it may be significant for schizophrenia.
Insel: We didn’t know that before, and so this is news, and it’s something that will be an important area for further study as we try to understand how there could be an autoimmune aspect to schizophrenia that at least plays out in terms of genetic risk.
Balintfy: Dr. Insel says the studies also remind that these disorders, that both cause psychosis, may have more in common, changing the thinking of the past century.
Insel: We’ve really been essentially dividing up psychotic illnesses into those, like schizophrenia, that are mostly about thought disorder, hallucinations and delusions, and those that are more about mood regulation like bipolar illness, which in an earlier form was called manic-depressive illness. It’s never been the case that it’s a perfect line for every subject. You do see people who seem to have elements of both. And these kinds of studies, looking at the genetic underpinnings, suggest that yes, you know, that even at the genetic level there may be more overlap than what we’ve thought.
Balintfy: The new findings could eventually lead to multi-gene signatures or biomarkers for severe mental disorders. Dr. Insel emphasizes that as more is learned about the implicated gene pathways, it may be possible to sort out what’s shared by, or unique to, schizophrenia and bipolar disorder. For more information on these studies and diseases, visit www.nimh.nih.gov.
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Prevention Program Helps Teens Prevail Over a Gene Linked to Risky Behavior
Balintfy: Speaking of genes, DNA test results show some youths carried a gene found to increase the risk of substance use. So researchers developed a program called "Strong African American Families" to help rural African American 11-year-olds avoid such risky behaviors as drinking, smoking marijuana, and sexual activity. A study found that the teens who had the gene but didn’t participate in the program were almost twice as likely to have engaged in the risky behaviors as teens who had the gene and did take part in the program. Wally Akinso brings us the details.
Akinso: A family-based prevention program helps teens override a gene linked to risky behavior.
Brody: We worked with families because the families are the most powerful factors in young adolescence lives.
Akinso: Dr. Gene Brody is the Director of the Center for Family Research at the University of Georgia and the lead author of the study.
Brody: We try to enhance parenting skills that are protective, and we try to arm the adolescents with a set of skills and ideas about the future that also protect them from initiating alcohol and marijuana use.
Akinso: For two-and-a-half years, investigators monitored the progress of 11-year-olds enrolled in a family-centered prevention program called Strong African American Families, and a comparison group. A DNA analysis showed some youths carried a common genetic variation known as 5-HTTLPR. This fairly common gene, found in over 40 percent of people, is known from previous studies to be associated with impulsivity, low self-control, binge drinking and substance use. Dr. Brody explains the findings within the two groups.
Brody: Pre-adolescents who had this variant, who did not participate in the program over time were much more likely to engage in risk behaviors than pre-adolescents use who were like them in all ways except that they didn’t participate in the program.
Akinso: The parents and children participated in seven consecutive weeks of two-hour prevention sessions. The parents learned about effective strategies that included monitoring, emotional support, family communication, and handling racial discrimination. The children were taught how to set and attain positive goals, deal with peer pressure and stress and avoid risky activities. Dr. Brody says the prevention program proved especially beneficial for children with a genetic risk factor tied to risky behaviors.
Brody: The program provided them with an inoculation, just like a flu shot provides an inoculation against getting the flu, the strength that the program brought out in families was able to provide the use within an inoculation that was able to prevent them from becoming involved in these risk behaviors.
Akinso: This study was supported by the National Institute on Alcohol Abuse and Alcoholism, and the National Institute on Drug Abuse. For information on this topic, visit www.niaaa.nih.gov or visit www.drugabuse.gov. This is Wally Akinso at the National Institutes of Health, Bethesda, Maryland.
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Low-Key Anti Smoking PSAs are More Likely to be Remembered than Attention-Grabbing PSAs
Balintfy: In this program, you can usually hear a couple public service announcements. PSAs are also used in print and TV. In this next story, we learn about how a study reveals that low-key and attention-grabbing anti-smoking PSAs stimulate different patterns of activity in smokers’ brains; and that smokers are more likely to remember the low-key PSAs than the attention-grabbing ones. Again, Wally Akinso has the story.
Akinso: Low key anti-smoking public service announcements, or PSAs, are more likely to be remembered than attention-grabbing PSAs. This according to a National Institute on Drug Abuse study.
Grant: This study was a study of how the brain processes information in smoking prevention ads.
Akinso: Dr. Steven Grant is NIDA’s chief of the Neuroscience Branch in the division of Clinical Neuroscience and Behavioral Research.
Grant: The question is, that there are two competing theories about how smoking prevention ads should be constructed.
Akinso: For the first time, preliminary research using brain-imaging technology has shown that low-key and attention-grabbing anti-smoking PSAs stimulate different patterns of activity in smokers’ brains and that smokers are more likely to remember seeing the low-key PSAs. Dr. Steven Grant explains the findings.
Grant: What they found was that the high message sensation value ads activated the back of the brain, the visual sensory parts of the brain, which makes sense when you think about it. Because these ads are full of sounds and fury and they have a lot of visual content that’s changing very rapidly. So it primarily activated the visual areas of the brain as well as auditory sensory areas of the brain because they’re a lot of rapidly changing information.
Akinso: Dr. Grant adds that high message sensation value PSAs compare differently to low key PSAs.
Grant: The low message sensation value ads which have higher informational content or actual message value, those activated by contrast the front parts of the brain. Where it is thought that there is more rational decision making and evaluation of stimuli goes on.
Akinso: Dr. Grant says the finding suggest that the attention-grabbing PSA format may impede the retention of a PSA.
Grant: The high message sensation value ads were processed in a shallow manner, they never got out of the early stages of sensory processing. The low message sensation value ads were deeply processed and were activated areas in the frontal lobe that are involved in deep processing. So, the meaning of the ads were being processed. And this was consistent then with their second phase of the study—where they asked people which ads did they remembered better and they. And they remembered the low message sensation value ads better.
Akinso: Dr. Grant emphasizes that the findings are new in that they offer a general approach for objectively evaluating PSAs before they are released. For more information, visit www.drugabuse.gov. This is Wally Akinso at the National Institutes of Health Bethesda, Maryland.
Balintfy: Coming up, after this PSA, news about scarring: new research on regenerating old tissue.
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Tissue Regeneration in Middle-Aged Mice
Balintfy: Wouldn’t it be great to be able to grow back — or regenerate — skin, muscle, maybe even limbs — like a salamander can grow back its tail? Many would say that’s science fiction, but an unexpected discovery may hold future promise for tissue regeneration. Dr. Brandon Reines, a recent post-doctoral fellow in the laboratory of cellular and molecular biology at the National Institute of Allergy and Infectious Diseases explains the view on tissue regeneration may be changing.
Reines: The thinking for about 150 years has been that adult mammals can’t regenerate, and that only certain very unusual species or strains have the capability of complete regeneration, and when I say complete regeneration I mean it doesn’t scar at all, all of the original tissues come back.
Balintfy: Dr. Reines says that one of those unusual mammals is a rabbit — it’s been known for a while that if a rabbit gets a hole in its ear the ear tissue grows back, filling the hole:
Reines: All of the original tissues come back, the cartilage comes back, the fat comes back, the blood vessels come back, everything comes back and it looks totally normal again. In mice, it was thought that there was only one strain — a very large white mouse called the Murphy Roths Large strain or MRL strain was thought to be the only strain that could completely regenerate.
Balintfy: Dr. Reines and coauthors have written about an ear tissue regeneration study in a recent issue of the journal Rejuvenation Research. The discovery may have broader implications.
Reines: What I found is that, contrary to long-standing belief actually, average mice of common strains of mice can regenerate all of the original tissues, as rabbits and this one strain of white mouse can do.
Balintfy: He adds that what’s especially surprising is that middle-aged common mice regenerate ear tissue better than younger mice. He says it was at the age of five to 11 months when mice have the capacity to regenerate ear tissue, complete with new cartilage, fat and blood vessels – all of the original tissues that were there before. The younger mice, those about four weeks old, have an extremely hard time regenerating ear tissue.
Reines: So I was thinking that, since I’m a veterinarian, I noticed that older animals can do some remarkable things sometimes, so I decided I wanted to take a look at older mice and see what they could do. And it turned out that actually they have some really remarkable regenerative capacities.
Balintfy: So much for that old saying, you can’t teach an old dog, or mouse, new tricks…
Reines: That’s true, that’s true. Yeah, it looks like older animals, and maybe older people too, actually have better regenerative capacity than a young adult. It looks like, from the studies that have been done in humans, that older people actually scar less than younger people do. Young adults just scar terribly, and think of a child who falls off a bicycle and they hit their chin, they just get these massive scars. When you get older, if something like that happens to you, actually you don’t scar quite as badly, and that’s been studied a bit. So my findings show that not only can you regenerate the dermis or the skin, you can actually regenerate cartilage better as you get older, you can regenerate blood vessels better as you get older, fat tissues; all the different tissues that you need can come back again. So it’s been really surprising that the average animal, the average adult mammal seems to be able to regenerate.
Balintfy: Dr. Reines says that there are future implications for this discovery.
Reines: There are a few possibilities in terms of practical implications. One has to do with just the — knowing that — that we adult, average mammals do have the capacity to regenerate I think will help put a lot more enthusiasm into the field; that researchers really have every reason to hope that we can get things to re-grow, and particularly when we look at particular structures in the head and the face. Since I was studying ears, it’s not altogether clear I can extrapolate to every other part of the body, but I think there’s a certain part of the embryo called the neural crest, and ears and the face come from the neural crest. So it looks like the face, the ears, the paranasal sinuses, all the structures in the head that come from the neural crest probably have a remarkable regenerative capacity, a lot more than we ever thought. So if we look — if we look at those structures, I think we can figure out ways to get things to re-grow and not scar anymore.
Balintfy: Thank you very much, Dr. Brandon Reines. For more information on this study, look up the Laboratory of Cellular and Molecular Immunology at the National Institute of Allergy and Infectious Diseases-website: www.niaid.nih.gov.
That’s it for this episode of NIH Research Radio. Please join us again on Friday, August 21 when our next edition will be available for download. I’m your host, Joe Balintfy. Thanks for listening.
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NIH Research Radio is a presentation of the NIH Radio News Service, part of the News Media Branch, Office of Communications and Public Liaison in the Office of the Director at the National Institutes of Health in Bethesda, Maryland, an agency of the US Department of Health and Human Services.
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