Biological Psychology Links

The immune system may have a key role in the development of Parkinson's disease, say US researchers. In a 20-year study of 4,000 people, half with Parkinson's disease, the team found an association between genes controlling immunity and the condition. The results raise the possibility of new targets for drug development, Nature Genetics reports. Parkinson's UK said the study strengthened the idea that immunity is an important driver of the disease. The team were not just looking for a genetic cause of the disease, but also considered clinical and environmental factors. During their search, they discovered that groups of genes collectively known as HLA genes are associated with the condition. These genes are key for the immune system to differentiate between foreign invaders and the body's own tissues. In theory, that enables the immune system to attack infectious organisms without turning on itself - but it is not always an infallible system. The genes vary considerably between individuals. Some versions of the genes are associated with increased risk or protection against infectious disease, while others can induce autoimmune disorders in which the immune system attacks the body's own tissues. Inflammation Multiple sclerosis has already been shown to be associated with the same HLA genetic variant seen in the latest study in Parkinson's disease, the researchers said. (C)BBC

By DENISE GRADY For her first appointment with Dr. Daniel Simon, Neelima Raval showed up with a rolling file cabinet full of documents. She had downloaded every word written by or about Dr. Paolo Zamboni, a vascular surgeon from Italy with a most unorthodox theory about multiple sclerosis. Dr. Zamboni believes that the disease, which damages the nervous system, may be caused by narrowed veins in the neck and chest that block the drainage of blood from the brain. He has reported in medical journals that opening those veins with the kind of balloons used to treat blocked heart arteries—an experimental treatment he calls the “liberation procedure”— can relieve symptoms. The idea is a radical departure from the conventional belief that multiple sclerosis is caused by a malfunctioning immune system and inflammation. The new theory has taken off on the Internet, inspiring hope among patients, interest from some researchers and scorn from others. Supporters consider it an outside-the-box idea that could transform the treatment of the disease. Critics call it an outlandish notion that will probably waste time and money, and may harm patients. These critics warn that multiple sclerosis has unpredictable attacks and remissions that make it devilishly hard to know whether treatments are working — leaving patients vulnerable to purported “cures” that do not work. Copyright 2010 The New York Times Company

CHAPEL HILL -- Taking care of chronically ill loved ones over long periods stresses caregivers, as everyone knows, but a new study provides strong new evidence that such continuing stress boosts the risk of age-related diseases by prematurely aging caregivers' immune systems. Levels of a damaging compound known as a proinflammatory cytokine not only increased considerably faster among those taking care of ailing spouses but also continued to increase faster for years after the spouses died. A report on the research, conducted by scientists at Ohio State University and the University of North Carolina at Chapel Hill, will appear online Monday afternoon (June 30) in the Proceedings of the National Academy of Sciences.

Mothers who suffer from major depression or anxiety disorders are more likely to have children with asthma and other allergy-based conditions, according to a US study. The association was only found for biological children, supporting a “shared genetic liability” theory. Ramin Mojtabai, a psychiatrist from Columbia University in New York, US, assessed the relationship between parental psychopathology and childhood allergy in more than 9000 parent-child pairs from the 1999 US National Health Interview Survey. Most of the parents were biologically related to their children, but 554 of the pairs were non-biological. The survey found that 6% of the parents had major depression, 3% had panic attacks and 3% had generalised anxiety disorder. In total, 31% of the children had allergic disorders including hay fever, eczema, wheezing, asthma and food allergies. Mojtabai’s analysis revealed that mothers who had major depression were 67% more likely to have biological children with allergic disorders, and the increased risk was 46% for mothers who had panic attacks. His study showed no statistically significant link between the psychopathology of parents and allergy in their non-biological children, or between fathers and their biological children. “The fact that adoptive parents with depression didn’t show a higher level of asthma in their children provides good evidence for the possibility of common genes for depression and panic disorder on the one hand, and allergic disorders on the other hand,” Mojtabai told New Scientist. He points out that previous studies had shown an increased risk of depression in children of parents with allergic disorders. © Copyright Reed Business Information Ltd.

By DAVID TULLER For decades, people suffering from chronic fatigue syndrome have struggled to convince doctors, employers, friends and even family members that they were not imagining their debilitating symptoms. Skeptics called the illness “yuppie flu” and “shirker syndrome.” But the syndrome is now finally gaining some official respect. The Centers for Disease Control and Prevention, which in 1999 acknowledged that it had diverted millions of dollars allocated by Congress for chronic fatigue syndrome research to other programs, has released studies that linked the condition to genetic mutations and abnormalities in gene expression involved in key physiological processes. The centers have also sponsored a $6 million public awareness campaign about the illness. And last month, the C.D.C. released survey data suggesting that the prevalence of the syndrome is far higher than previously thought, although these findings have stirred controversy among patients and scientists. Some scientists and many patients remain highly critical of the C.D.C.’s record on chronic fatigue syndrome, or C.F.S. But nearly everyone now agrees that the syndrome is real. “People with C.F.S. are as sick and as functionally impaired as someone with AIDS, with breast cancer, with chronic obstructive pulmonary disease,” said Dr. William Reeves, the lead expert on the illness at the C.D.C., who helped expose the centers’ misuse of chronic fatigue financing. Copyright 2007 The New York Times Company

By GINA KOLATA For years, a prevailing theory has been that one of the chief villains in Alzheimer’s disease has no real function other than as a waste product that the brain never properly disposed of. The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognizing friends and family. But now researchers at Harvard suggest that the protein has a real and unexpected function — it may be part of the brain’s normal defenses against invading bacteria and other microbes. Other Alzheimer’s researchers say the findings, reported in the current issue of the journal PLoS One, are intriguing, though it is not clear whether they will lead to new ways of preventing or treating the disease. The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph E. Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimer’s disease. Copyright 2010 The New York Times Company

ATLANTA - Tests of the first two oral drugs developed for treating multiple sclerosis show that both cut the frequency of relapses and may slow progression of the disease, but with side effects that could pose a tough decision for patients. Two experts not involved in the studies said the drugs appear effective but with potentially dangerous side effects. It’s too soon to know if the pills will be approved by the government or widely adopted by physicians, they said. About 2.5 million people around the world have multiple sclerosis, a neurological disease that can cause muscle tremors, paralysis and problems with speech, memory and concentration. The studies involve the most common form of the disease, in which people are well for a while and then suffer periodic relapses. Current treatments can reduce the duration and severity of symptoms but require daily or regular shots or infusions. The new studies tested two types of pills. Cladribine, made by Merck Serono, is already sold to treat a rare blood cancer. For MS, it would be taken eight to 10 days a year. Fingolimod is a daily MS pill being developed by Novartis. The research found that patients on the pills were about half as likely to suffer relapses of symptoms as those who took dummy pills or a commonly prescribed shot for MS. © 2010 The Associated Press.

Depression, coordination and speech problems, muscle weakness and disability are just a few of the symptoms of Multiple Sclerosis (MS). Researchers from the Mouse Biology Unit of the European Molecular Biology Laboratory (EMBL) in Italy and the Department of Neuropathology at the Faculty of Medicine, University of Göttingen, Germany, have now discovered that these symptoms are aggravated by a specific signal in cells in the nervous system. The study, which will appear in this week's online issue of Nature Immunology, suggests that blocking the proteins that regulate the signal might be an efficient strategy for new therapies against MS. Nerve cells in our brain and spinal cord communicate with each other using electrical signals. This communication is fast and efficient because - just like wires in an electrical circuit - the axons of our nerves are surrounded by an insulating layer. In MS this protective sheath, made up of a mixture of lipids and proteins called myelin, gets destroyed by cells of our own immune system, and the communication between nerve cells gets disrupted. A central player in the molecular mechanisms behind MS is a signaling molecule called NF-kB. "We have known for a long time that NF-kB is crucially involved in MS," says Manolis Pasparakis, a former Group Leader at EMBL's Mouse Biology Unit who now works as a Professor at the Institute for Genetics at the University of Cologne, "but until now it was not clear if it was friend or foe. We were not sure whether it protects the brain cells against the consequences of the disease or actually aggravates the damage."

DALLAS – A common drug given to multiple sclerosis patients appears to stimulate weakened immune system cells, according to a study published by researchers at UT Southwestern Medical Center at Dallas. While Copaxone, or glatiramer acetate, has long been known to slow or stop the progression of attacks in MS patients, researchers have not known exactly how the drug treated the disease. In the March issue of the Journal of Clinical Investigation, lead author Dr. Nitin Karandikar, UT Southwestern assistant professor of pathology and neurology, and colleagues report that Copaxone appears to stimulate a certain type of T cell in MS patients. Produced by the thymus gland, T cells are white blood cells that fight infection and, in healthy people, coordinate the body’s immune response. There are two types of T cells, CD4 and CD8 cells. Both are involved in the immune process that underlies MS and, in MS patients, the cells function abnormally to give rise to this disease. The researchers used flow cytometry to analyze cells taken from MS patients and were able to see the T cells rallying under the effect of Copaxone.

For at least one of North America’s most common birds, mating songs are more than just empty amorous enticement, according to a new study from The Johns Hopkins University. Scientists have found that male starlings’ singing ability is strong evidence of the health of their immune systems and, thus, their suitability as breeding partners. The new finding may explain why female starlings take singing talent into account when choosing their mates and is an important first step towards proving a decade-old theory that suggests evolution has found a way to stop male birds from engaging in false sexual advertising. “The theory, which is known as the Immunocompetence Handicap Hypothesis, or ICHH, proposes that males of lesser reproductive quality are prevented from cheating – producing a signal that falsely indicates high reproductive quality – by some cost associated with producing that signal,” explains Deborah Duffy, lead author on the new paper. Duffy, a recent Ph.D. graduate of Johns Hopkins, is now a postdoctoral fellow at Indiana University. She is co-author with Greg Ball , professor of psychological and brain sciences in the Krieger School of Arts and Sciences at Johns Hopkins, of a paper published in the April 22 issue of The Proceedings of the Royal Society of London.

In multiple sclerosis, new drugs and new insights are giving rise to new hopes BY KATHERINE HOBSON Lawrence Vail knew something was terribly wrong. More than a year ago, he was walking across a busy street in Boston when his leg went numb. Then came double vision and a mental fog that was so bad the 44-year-old thought he'd have to quit his job. But almost as quickly as he was diagnosed with multiple sclerosis, his doctor at Boston's Brigham and Women's Hospital put him on Avonex, one of several MS drugs approved over the past decade. After the disease changed his life, the medicine has changed it back. He can talk and express himself again. "The drug meant you go from the edge of the cliff to about 30 feet before the edge," he says. Tanya Pugliano, another MS patient at Brigham, also tried Avonex. But it didn't stop her legs from giving out or her hands from going numb. Neither did another MS drug, Copaxone. Now the 29-year-old is undergoing monthly chemotherapy treatments, like a cancer patient, trying yet another way of fighting back against the disease. Had either patient developed MS 15 years ago, even doctors at renowned medical centers like Brigham would have had little to offer them. They would have been powerless to stop the basic disaster of MS: a patient's immune system that savagely assaults the nerves in the brain and spinal cord. Now, thanks to a handful of recently developed drugs–one just approved a few months ago–physicians can blunt this attack. "It's not a cure, but it's a far cry from what we had before," says neurologist Fred Lublin, director of the Corinne Goldsmith Dickinson Center for Multiple Sclerosis at Mount Sinai Hospital in New York. Copyright © 2002 U.S. News & World Report, L.P.

Clear patterns emerge outlining greater damage from chronic stress WASHINGTON — Psychologists have long known that stress affects our ability to fight infection, but a major new “meta-analysis” – a study of studies – has elucidated intriguing patterns of how stress affects human immunity, strengthening it in the short term but wearing it down over time. The report appears in the July issue of Psychological Bulletin, which is published by the American Psychological Association. Major findings are three-fold. First, the overlapping findings of 293 independent studies reported in peer-reviewed scientific journals between 1960 and 2001 – with some 18,941 individuals taking part in all -- powerfully confirm the core fact that stress alters immunity. Second, the authors of the meta-analysis observed a distinctive pattern: Short-term stress actually “revs up” the immune system, an adaptive response preparing for injury or infection, but long-term or chronic stress causes too much wear and tear, and the system breaks down. Third, the immune systems of people who are older or already sick are more prone to stress-related change. Psychologists Suzanne Segerstrom, PhD, of the University of Kentucky, and Gregory Miller, PhD, of the University of British Columbia, analyzed the results of the nearly 300 studies by sorting them into different categories and statistically evaluating relationships. For example, the five stressor categories included: © 2004 American Psychological Association

COLUMBUS, Ohio – A new study suggests that wounds on mice that prefer multiple mates heal at the same rate, whether the mice are housed with a mate or live in isolation. But the same doesn't ring true for monogamous mice, said Courtney DeVries, an assistant professor of psychology and neuroscience at Ohio State University. She and Erica Glasper, a doctoral student in psychology at Ohio State, took a closer look at the effects social bonding had on wound healing in monogamous and non-monogamous deer mice. Non-monogamous males mate with more than one female during a breeding season. The researchers especially wanted to see if social interaction, or the lack of it, made a difference in the rate of wound healing in the non-monogamous mice. It didn't. In fact, levels of corticosterone – a stress hormone that rodents secrete – in the non-monogamous mice were the same whether they were paired or alone, and were also significantly lower than the corticosterone levels of paired, monogamous mice.

(Philadelphia, PA) – Later this fall, emergency-medicine physicians enter into what they call the "CO season" – a time when faulty furnaces and other mechanical mishaps lead to a spike in cases of carbon monoxide (CO) poisoning. CO poisoning is the leading cause of injury and death by poisoning worldwide, with about 40,000 people treated in the U.S. annually. Brain damage occurs – days to weeks later – in half of the patients with a serious case of CO poisoning. The physiological causes of this delayed decline were not well understood until now. A team led by Stephen R. Thom, MD, PhD, Professor of Emergency Medicine and Chief of Hyperbaric Medicine, at the University of Pennsylvania School of Medicine, report this week online in the Proceedings of the National Academies of Sciences, that CO causes profound changes in myelin basic protein (MBP) – a major protein constituent of myelin, the protective sheath surrounding neurons. Using an animal model, they showed that the CO-induced changes in MBP set into motion an autoimmune response in which lymphocytes, triggered to eliminate altered MBP, continue to attack normal MBP. Specifically, the researchers found that by-products of CO metabolism in the brain alter the charge and structure of MBP. "These changes in MBP have also been demonstrated in multiple sclerosis, which is why we paralleled the study along those lines," says Thom.

There is no association between two specific personality traits – neuroticism and extroversion – and cancer, according to a new study, one of the largest prospective twin studies to examine this issue. The study, published in the March 1, 2005 issue of CANCER (http://www.interscience.wiley.com/cancer-newsroom), a peer-reviewed journal of the American Cancer Society, also finds no evidence that personality traits indirectly lead to cancer through behavioral factors, such as smoking. Personality traits are popularly cited as risk factors for cancer. Some studies have gone so far as to suggest that two traits in particular, neuroticism and extroversion, may be such risk factors. Scientists have hypothesized that a high degree of extroversion and low degree of neuroticism are associated with an increased risk. Some studies further show that these personality traits influence known risk behaviors that would explain the increased cancer risk. However, other studies, some with larger study populations and better study designs, have found no such associations. Pernille Hansen, M.A. of the Department of Psychosocial Cancer Research at the Institute of Cancer Epidemiology in Copenhagen, Denmark led a team of investigators who reviewed cancer history, health behavior, and personality trait data collected from 29,595 Swedish twins enrolled in the Swedish Twin Registry. These patients were born between 1926-1958 and were followed an average 25 years

COLUMBUS, Ohio – A new study in mice suggests that, in certain cases, stress may enhance the body's ability to fight the flu. Short bouts of intense social stress improved the ability in the mice to recover from the flu. The stress apparently did so by substantially boosting the production of specialized immune cells that fought the virus. "Stressed mice had a stronger immune response and were able to fight off the infection faster," said Jacqueline Wiesehan, a study co-author and a graduate fellow in oral biology at Ohio State University. These special immune cells are called T cells and are part of the immune system's memory response. T cells "remember" specific infectious agents and can launch future attacks against these intruders. The researchers hope to learn more about the mechanisms behind the memory response, and to use this information to develop more effective flu vaccines in the future, said David Padgett, a study co-author and an associate professor of oral biology at Ohio State. Wiesehan, Padgett and John Sheridan, the study's lead author and a professor of oral biology at Ohio State, presented their findings on April 3 at the Experimental Biology 2005 conference in San Diego. The three also worked on this study with Michael Bailey, a postdoctoral fellow in oral biology at Ohio State.

PORTLAND, Ore. – Oregon Health & Science University researchers have measured genetic changes reflecting a drop in the body's ability to suppress inflammatory cells that attack nerve fibers and promote progression of multiple sclerosis. In a study published in the July issue of the Journal of Neuroscience Research, OHSU scientists, in collaboration with The Immune Response Corp. of Carlsbad, Calif., found that MS patients have lower expression of the FOXP3 gene found in a subset of T-cells that may regulate defense against MS and other autoimmune diseases, such as diabetes and arthritis. They say that when FOXP3 is reduced due to abnormalities in its expression, the suppressive activity of regulatory T-cells, or T-regs, also plummets. "This is an important marker," said Arthur Vandenbark, Ph.D., professor of neurology and molecular microbiology and immunology, OHSU School of Medicine, and senior research career scientist at the Portland Veterans Affairs Medical Center. "This is the first publication that links FOXP3 with reduced suppression in MS." But there may be a solution to the FOXP3 loss. NeuroVax, a T-cell receptor peptide vaccine co-discovered by Vandenbark and colleagues at The Immune Response Corp., was shown in a separate study to increase FOXP3 expression levels among MS patients receiving injections of the drug for a year.

Feeling depressed and fatigued does not increase a person's risk for cancer, according to a new study. Severely exhausted people, however, do engage in behavior that is associated with a higher cancer risk. The study, published in the September 15, 2005 issue of CANCER (http:/www.interscience.wiley.com/cancer-newsroom), a peer-reviewed journal of the American Cancer Society, is the first prospective study using the "vital exhaustion" questionnaire to investigate this link. The concept of vital exhaustion – described as feelings of excessive fatigue and lack of energy, increased irritability and a feeling of demoralization – grew out of the field of cardiology. Studies have identified vital exhaustion as a risk factor for heart attacks and death from a heart attack. Depressive mood has also been widely blamed, at least in lay literature, as a risk factor for cancer. However, the scientific data is much more inconsistent than that for heart attacks. Two recent prospective studies failed to identify a link between depression and cancer. Corinna Bergelt, Ph.D. of the Danish Cancer Society's Institute of Cancer Epidemiology in Copenhagen and colleagues followed 8527 people aged 21–94 years to investigate whether depressive feelings and exhaustion were risk factors for cancer, looking at all cancers combined, smoking-related cancers, alcohol-related cancers, virus and immune-related cancers, and hormone-related cancers.

Boston, MA – Researchers from the Harvard School of Public Health, Kaiser Permanente, and a team of collaborators have found further evidence implicating the Epstein-Barr virus (EBV) as a possible contributory cause to multiple sclerosis (MS). The study appears in the advance online edition of the June 2006 issue of Archives of Neurology. MS is a chronic degenerative disease of the central nervous system. Women are more likely than men to get the disease and it is the most common neurologically disabling disease in young adults. Although genetic predisposition plays an important role in determining susceptibility, past studies have shown that environmental factors are equally important. EBV is a herpes virus and one of the most common human viruses worldwide. Infection in early childhood is common and usually asymptomatic. Late age at infection, however, often causes infectious mononucleosis. In the U.S., upwards of 95% of adults are infected with the virus, but free of symptoms. EBV has been associated with some types of cancer and can cause serious complications when the immune system is suppressed, for example, in transplant recipients. There is no effective treatment for EBV. The study population was made up of more than 100,000 members of the Kaiser Permanente Northern California (KPNC) health plan, who provided blood specimens as part of medical examinations between 1965 and 1974.

Links for keyword: Neuroimmunology