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After a decades-long search, scientists identify new genetic risk factors for multiple sclerosis

07-29-2007 · EurekAlert!

A pair of large-scale genetic studies supported by the National Institutes of Health has revealed two genes that influence the risk of getting multiple sclerosis -- data sought since the discovery of the only other known MS susceptibility gene decades ago. The findings could shed new light on what causes MS -- a puzzling mix of genes, environment and immunity -- and on potential treatments for at least 350,000 Americans who have the disease.

Keywords: decades-long, search, scientists, identify, genetic, risk, factors, multiple, sclerosis, decades, long, scientist, factor, sclerosi

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Advance in understanding of blood pressure gene could lead to new treatments
02-04-2007 · EurekAlert!
Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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Scientists find major susceptibility gene for Crohn's disease
04-15-2007 · EurekAlert!
Using a novel approach, researchers identified that the PHOX2B, NCF4 and ATG16L1 genes constitute genetic risk factors for Crohn's disease. In addition, their study identified two regions of the genome where genetic risk factors are located but no known genes were implicated -- further work will be necessary to identify the causal genes in these regions.
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Scientists find major susceptibility genes for Crohn's disease
04-16-2007 · EurekAlert!
A consortium of Canadian and American researchers led by Dr. John D. Rioux, PhD, Associate Professor of Medicine at the Montreal Heart Institute and the Université de Montréal, report in the April 15 online edition of Nature Genetics the results from a search of the entire human genome for genetic risk factors leading to the development of Crohn's disease.
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Risk genes for multiple sclerosis uncovered
07-29-2007 · EurekAlert!
Using a whole-genome association scan, an international consortium of scientists has found genetic variations in multiple sclerosis patients, findings that suggest a possible link between MS and other autoimmune diseases.
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Lupus in women: New genetic risk factors identified
01-20-2008 · EurekAlert!
An international consortium of clinical scientists and genomics experts, including researchers from the Montreal Heart Institute and Université de Montréal, have uncovered multiple new genetic risk factors for systemic lupus erythematosus, commonly known as lupus. The large-scale genomic study is the first of its kind to investigate the genetic basis of lupus.
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Studies identify DNA regions linked to nicotine dependence
02-14-2007 · EurekAlert!
Genetic factors play an important role in cigarette addiction, suggest scientists at Washington University School of Medicine in St. Louis. They show that certain genetic variations can influence smoking behaviors and contribute to a person's risk for nicotine dependence.
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Genome-wide search unearths surprising clues for diabetes and triglycerides
04-26-2007 · EurekAlert!
Scientists from the Broad Institute of Harvard and MIT, Lund University and Novartis today announced the discovery of three unsuspected regions of human DNA that contain clear genetic risk factors for type 2 diabetes, and another that is associated with elevated blood triglycerides. The study is among the first to apply a suite of genomic resources to clinical research, including the Human Genome Project, the SNP and HapMap Projects, and genome-scale laboratory and analytical tools.
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Feinstein researchers develop new genetic method and identify novel genes for schizophrenia
12-03-2007 · EurekAlert!
Scientists at the Zucker Hillside Hospital campus of the Feinstein Institute for Medical Research have identified nine genetic markers that can increase a person's risk for schizophrenia. In a study published this week in the Proceedings of the National Academy of Sciences, the research team uncovered original evidence that this disabling brain disease can be inherited in a recessive manner. A recessive trait is one that is inherited from both parents.
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Israeli scientists identify: Genes that affect responses of multiple sclerosis patients to copaxone
10-10-2007 · EurekAlert!
Getting the drug dosage correct can be a tricky exercise in trial and error in a disease like multiple sclerosis. Scientists from the Weizmann Institute and the Technion have identified two genes that affect a patient's response to the drug Copaxone, a finding which may help take the some of the guesswork out of treatment.
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Landmark study highlights complex genetic risk factors behind type 2 diabetes
04-26-2007 · EurekAlert!
A UK collaboration of scientists has identified three new genes that predispose individuals to develop type 2 diabetes, bringing scientists a step closer towards understanding what causes this complex disease. The findings bring the total number of genes known to be involved in type 2 diabetes to nine.
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