RESEARCHERS UNRAVELING GENETICS OF MS
Medical researchers have made significant progress in understanding the genetics involved in MS. In two new studies, published in the July 29th online edition of the New England Journal of Medicine and Nature Genetics, three teams of researchers say they have identified, by separate methods, new genetic variants that contribute to the disease.

MS is a disease in which the body's immune system mistakenly attacks myelin. For years, the cause of MS has been considered part genetic and part environmental. Trying to identify the genes involved, however, has proven frustrating. Consequently, researchers have been speculating about what genes might be involved and then seeing if individuals with MS have abnormal variants of that gene. In recent years, researchers have suspected more than 100 candidate genes, none of which could be confirmed, except for variations in the immune system that have been known about for some time.

One team used a new, advanced method called Whole Genome Association. The other teams used the candidate gene approach. Because all three teams identified the same gene, the researchers are confident they have opened a new avenue into the cause and possible treatment of MS.

The identified gene produces a substance called the interleukin-7 receptor, a protein that allows immune system cells to respond to a control agent. Researchers believe the receptor is part of a biochemical pathway involving many genes. Defects in any of these genes may lead to MS. Researchers now believe it is possible to explore the pathway and perhaps develop treatments to remedy the disease-causing process.

The new research is the result of several large teams at universities in the U.S. and abroad who have coordinated their publications and pooled their data for analysis.

Because the course of MS is unpredictable, clinical trials are challenging. Researchers are hopeful that the interleukin-7 receptor will provide sufficient motivation to endure the expense of long clinical trials.

With these findings, researchers may be able to perform blood tests to identify people with the flawed genes and begin to develop drugs to counteract its effects.

One drug on the market, daclizumab (Zenapax), already works on interleukin-2 and is currently in a Phase II clinical trial exploring its potential use alone and in combination with other immune-modulating drugs in MS.

Unraveling the genetic mystery of MS is proving harder than other autoimmune diseases caused by one or two malfunctioning genes. MS appears to involve defects in many genes, each with only a modest effect. The newly identified defects, by themselves, raise the risk of MS by about 20 percent. The studies also found evidence that a dozen other genes may be linked to MS, providing future potential targets for MS researchers.

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ETHNICITY IN MS
According to a recent study in Neurology, differences in immune systems have been found in African Americans with MS compared to Caucasians.  These differences could begin to explain why African Americans experience more disability with MS than Caucasians.

The study compared levels of antibodies in the cerebrospinal fluid of 66 African Americans to 132 Caucasians with MS. Antibody levels in the cerebrospinal fluid of African Americans with MS were 29 percent higher than levels found in Caucasians.

According to John R. Rinker, MD, with the Washington University School of Medicine in St. Louis, "The findings show that ethnic differences in MS extend to the immune response system, which plays a central role."  He also noted that recent genetic studies in MS have begun to identify certain genes which may explain why African Americans experience more disability, but the products of these genes and the mechanism of their effects remain unknown.

Researchers also noted that African Americans who had MS may need a cane, walker or wheelchair at an average of nine years compared to an average of 17 years for Caucasians.

"It has always been noted that, on average, African Americans seem to follow a more aggressive course with MS. For example, the Optic Neuritis Treatment Trial showed poorer recovery of visual function in African Americans than Caucasians," explains Ben Thrower, M.D. "The possible silver lining is that African Americans are generally diagnosed more quickly, perhaps due to presenting with more 'typical' symptoms. This could lead to earlier intervention."

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RESPONSE TO INTERFERON BETA PREDICTED BY MRI

According to a study presented at the 17th meeting of the European Neurological Society, magnetic resonance imaging (MRI) of brain lesions at the beginning of treatment and after one year of treatment with Interferon beta (IFN-b) can help identify individuals with MS who do not respond to IFN-b treatment.

"Early identification of nonresponders may help neurologists in their decision about MS treatment," said Carlo Pozzilli, MD, Multiple Sclerosis Centre, S. Andrea Hospital, Rome, Italy. Dr. Pozzilli is head of the research team that performed the retrospective study involving 345 patients (101 men and 244 women) who had been treated with IFN-b for an average of 4.5 years. At the beginning of the study, subjects had a mean disease duration of 5.5±4.9 years and a median Expanded Disability Status Scale (EDSS) score of 1.5 (range 0-4.5).

The researchers analyzed EDSS scores and MRI scans at baseline and after one year of IFN-b treatment of all individuals who completed the study. For subjects who discontinued IFN-b therapy, the final EDSS score was calculated at the last neurological assessment during IFN-b treatment.

Those with an increase of at least 1 point on the EDSS score (confirmed in two consecutive visits separated by a 6-month interval) were considered to have a "poor clinical response." Disease activity was determined based on the presence of gandolinium-enhancing (Gd-enhancing) lesions in post-contrast T1-weighted scans and on the accumulation of hyperintense lesions on T2-weighted images.

Individuals who had longer disease duration at the beginning of treatment and a higher baseline EDSS were more likely to have a poor response to IFN-b therapy. A relapse within the first year of IFN-b therapy also was associated with an increased likelihood of poor response over the study period.

However, investigators found that MRI data were even stronger predictors of long-term outcome, whereby both the presence of at least one Gd-enhancing lesion at 1-year and an increase in T2 lesion burden were related to a poor outcome.

"This emphasizes the importance of MRI monitoring, which not all doctors believe in," comments MSF Medical Advisor, Ben Thrower, M.D. "Beta interferon should prevent new T2 and enhancing lesions. When it does not, it probably means that the drug is not right for that person, the dose is not high enough, or there is a lack of compliance to therapy."

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MSF NEWS

IT'S BRIGHTER TOMORROW GRANT TIME AGAIN
Each year, the MSF makes dreams come true for individuals with MS through the Brighter Tomorrow Grant Program. The goal of this national program is to provide goods or services to those with MS to improve quality of life by enhancing safety, self-sufficiency, comfort, or well-being. Applications are confidential and will be reviewed by the grant committee. The Brighter Tomorrow Grant is a wish-based program and is not based solely on financial need.

Applicants are asked to provide basic personal and financial information, along with a brief essay of 100 words or less, to describe their need and how the grant might help them to have a brighter tomorrow. Applications are accepted from July 1st until October 1st. In order to be considered by the grant committee, applications must be received during these dates only.

Applications are now available on our website. Visit http://www.msfocus.org/programs_grants_bwmg_app.php. Applications will also arrive in the summer issue of MSFocus. Additional applications can be obtained by calling 1-888-MSFOCUS (673-6287). Previous grant recipients are ineligible

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SIXTH ANNUAL CAREGIVERS' NIGHT OUT CONTEST
Has someone in your life gone above and beyond the call of duty to help you?  Then, honor them this November during National Family Caregivers Month! Whether this special someone is a friend, relative, child, or significant other, we want to hear how they have made a difference in your life. Handwriting and writing style are unimportant. We're seeking stories with heart! Winners will receive dinner for two at a restaurant of their choice and their story and photo will be published in the winter issue of MSFocus.

In 100 words or less, tell us what makes your caregiver special and how he or she has made a difference in your life. Be sure to include your name, address, phone number and email address.

Submissions will be accepted from July 15th through September 1st.

Application can be emailed to homecare@msfocus.org or mailed to Caregivers' Night Out Contest, Multiple Sclerosis Foundation, 6350 N. Andrews Ave., Ft. Lauderdale, FL 33309.

Don't ignore your body's warning signs
Since heart attack symptoms can include mild pressure in the chest, lightheadedness and sweating, it's often hard for the average person to identify one. That's what researchers at the Yale School of Medicine found in a study of 24 women 55 and under who'd had heart attacks and were admitted to a hospital. It showed that 42 percent didn't recognize the warning signs.

Editorial: This health program is too important to let die

Congress must stand up to the president if he vetoes health benefits for children

If Congress and President Bush fail to come to agreement soon, 6.6 million children -- 800,000 in California -- could lose their health insurance coverage when the State Children's Health Insurance Program (SCHIP) expires Sept. 30....(more)

New MS Genetic Risk Factors Found

By Michael Smith, Senior Staff Writer, MedPage Today
Reviewed by Zalman S. Agus, MD; Emeritus Professor at the University of Pennsylvania School of Medicine.
July 30, 2007
BOSTON, July 30 -- New genetic contributors to multiple sclerosis have been uncovered for the first time in 35 years, according to researchers here.

Action Points

• Explain to interested that it has long been known that multiple sclerosis has a genetic element, but only the human leucocyte antigen (HLA) gene complex has been conclusively linked to the disease.
• Note that these research reports suggest that variations in two genes outside the HLA complex may also play a role in the pathogenesis of the disease.

In related papers in the New England Journal of Medicine and Nature Genetics, scientists confirmed the importance of the human leucocyte antigen (HLA) gene complex in the pathogenesis of MS and reported two new risk factors:

• Variations in the gene for the alpha chain of interleukin receptor seven (IL7R-alpha), on chromosome five. The protein produced by the gene is also known as CD127.
• Variations in the gene for the alpha subunit of interleukin receptor two (IL2R-alpha), on chromosome 10. The alpha subunit of the receptor is also known as CD25.

Both genes play a role in T-cell-mediated immunity, which makes them plausible candidates for a role in MS.

But the increased risk associated with carrying the risk variants is small, reported David Hafler, M.D., of Harvard, and colleagues in the International Multiple Sclerosis Genetics Consortium.

Writing in the NEJM, Dr. Hafler and colleagues said each of the variants they uncovered in the two genes explained less than 0.2% of the variation in the risk of developing MS.

By contrast, variations in the HLA complex - first linked to MS in 1972 - remain the largest genetic risk factor for the disorder, explaining nearly 50% of the risk, according to Jonathan Haines, Ph.D., of Vanderbilt University Medical Center in Nashville and colleagues in the Multiple Sclerosis Genetics Group.

Dr. Haines and colleagues, reporting in Nature Genetics, said a variation in the IL7R-alpha gene influences the amount of the protein available in the body, hinting that the ups and downs of the alpha chain may be part of the mechanism that leads to MS.

The three papers -- including a second in Nature Genetics by Jan Hillert, M.D., of Karolinska University Hospital in Stockholm, and colleagues -- all report that a single-letter genetic variation in IL7R-alpha is significantly associated with the risk of MS.

The variation - or single nucleotide polymorphism (SNP) -- is dubbed rs6897932.

Dr. Hafler and colleagues and Dr. Haines and colleagues put the significance of the association at about P=2.9×10⁻⁷. The other research group used different statistical methods, but concluded that "all analyses point toward (rs6897932) as being most strongly associated with risk of multiple sclerosis" among a number of SNPs they investigated.

But Dr. Halfer and colleagues also reported that a cluster of SNPs in the HLA gene complex was highly associated with MS (at P=8.94×10⁻⁸¹), confirming the importance of the HLA system.

Also, they said, two SNPs that are usually inherited together in the IL2R-alpha gene were associated with the disease, at (P=2.96×10⁻⁸).

Many of the findings were made using the increasingly popular method of genome-wide association scanning, in which researchers compare the genes of cases and controls, using a panel of many thousand of SNPs to tease out variants linked to the disease in question.

The method has been called "hypothesis-free" because investigators don't have a pre-conceived notion of where in the genome to look for suspected links. Instead, they scan large numbers of cases and controls to see which SNPs are more common among cases.

Recent studies have found previously unsuspected links to heart disease and diabetes, among other disorders. (See Common Genetic Variation Increases Heart Disease Risk)

These new findings "strongly support the dominance of the HLA locus in the genetic background of patients with multiple sclerosis," said Leena Peltonen, M.D., Ph.D., of the University of Helsinki.

But they also support the notion that there are many risk variations for MS outside the HLA complex, she said in an accompanying editorial in the NEJM.

Dr. Peltonen noted that genome-wide scanning -- unlike other studies in other disorders -- did not find any new major risk factors for MS.

And she cautioned that -- by definition -- such a method relies on variations that are common in the population and would miss genetic risk factors that are not widely distributed.

"We need to define the full allelic diversity of the 'suspicious genes' that are initially identified by genome-wide studies," Dr. Peltonen said. Doing so might uncover "rare, high-impact" variants that play an even larger role in the risk of disease, she said.
The International Multiple Sclerosis Genetics Consortium study was supported by the National Multiple Sclerosis Society, the National Institute of Neurological Disorders and Stroke, the National Institute of Allergy and Infectious Diseases, the Wellcome Trust, the National Center for Research Resources, the Penates Foundation, the Nancy Davis Center Without Walls, and a Jacob Javits Merit Award. The researchers said they had no potential conflicts.

The study by the Multiple Sclerosis Genetics Group was supported by the NIH and the National Multiple Sclerosis Society. The researchers said some members had potential conflicts.

The study by Dr. Hillert and colleagues was supported by the Swedish Research Council, the Norwegian Research Council, the Eastern Norwegian Regional Health Authority, the Danish Multiple Sclerosis Society, the Warwara Larsen Foundation, NeuroproMiSe, the Swedish Society of the Neurologically Disabled, the Bibbi and Nils Jensens Foundation and the Swedish Foundation for Strategic Research, and the Karolinska Institutet. The researchers said they had no potential conflicts.
Additional Multiple Sclerosis Coverage
Primary source: New England Journal of Medicine
Source reference:
Hafler DA et al. "Risk Alleles for Multiple Sclerosis Identified by a Genomewide Study." N Engl J Med 2007;357.
Additional source: New England Journal of Medicine
Source reference:
Leena Peltonen. "Old Suspects Found Guilty - The First Genome Profile of Multiple Sclerosis." N Engl J Med 2007;357.
Additional source: Nature Genetics
Source reference:
Gregory SG et al. "Interleukin 7 receptor a chain (IL7R) shows allelic and functional association with multiple sclerosis." Nature Genetics 2007; doi:10.1038/ng2103.


http://www.medpagetoday.com/Neurology/MultipleSclerosis/dh/6287

New MS Genetic Risk Factors Found (CME/CE)
BOSTON -- New genetic contributors to multiple sclerosis have been uncovered for the first time in 35 years, according to researchers here. [more]
http://www.medpagetoday.com/Neurology/MultipleSclerosis/dh/6287

July 30, 2007
Advances Cited in Research on Multiple Sclerosis
By NICHOLAS WADE
Medical researchers have made a significant advance in understanding
multiple sclerosis, a common neurological disease that causes symptoms
ranging from muscle weakness to paralysis.
The disease is one in which the body's immune system mistakenly attacks
the electrical insulation of nerve fibers. The cause is part genetic and
part environmental, but researchers trying to identify the relevant
genes have endured repeated frustration. Their approach has been to
guess what genes might be involved and see if patients have abnormal
versions.
This guesswork has produced more than 100 candidate genes in recent
years, none of which could be confirmed except for long-known variants
in the mechanism used by the immune system to recognize proteins that
are foreign to the body.
In three articles published online yesterday in The New England Journal
of Medicine, three teams of researchers say they have identified, by
separate routes, new genetic variants that contribute to the disease.
One team used a new, advanced gene-hunting method called Whole Genome
Association, which has racked up a string of successes with major
diseases in the last few months. The other teams used the candidate gene
approach, but because all three teams identified the same gene, the
researchers say they are confident they have opened a new window into
the cause and possible treatment of multiple sclerosis.
The gene makes a substance called the interleukin-7 receptor, a protein
that enables cells of the immune system to respond to a control agent.
Researchers believe the receptor is part of a biochemical pathway
involving many genes; defects in any of these genes may lead to the
disease. It is now possible to explore the pathway, they say, in the
hope of devising treatments to correct the disease-causing process.
The new research is the product of several large teams at universities
in the United States and abroad who have coordinated their publications
and pooled their data for analysis.
The leaders of the Whole Genome Association Study include David A.
Hafler of Brigham and Women's Hospital in Boston; Stephen L. Hauser of
the University of California, San Francisco; and Jonathan L. Haines of
Vanderbilt University Medical Center in Nashville. The two candidate
gene studies were headed by Dr. Haines and Jan Hillert of the Karolinska
Institute in Stockholm.
Because the course of the disease is unpredictable, clinical trials are
hard to conduct, said Dr. Kári Stefánsson, chief executive of Decode
Genetics in Reykjavik, Iceland. "But once you have an ironclad
discovery, as I believe the interleukin-7 receptor is," Dr. Stefánsson
said, "then you have the motivation to endure the expense of a long
clinical trial."

New Multiple Sclerosis Gene Found WebMD Mon, 30 Jul 2007 8:41 AM PDT Three new studies show that variations in the IL7R gene, which affects the immune system, are more common in people with multiple sclerosis.

Genetic breakthrough in multiple sclerosis -- biggest for decades AFP via Yahoo! News Sun, 29 Jul 2007 2:55 PM PDT Investigators on Sunday reported the biggest breakthrough in decades into the genetic drivers for multiple sclerosis (MS), identifying two genes that each boost the risk of developing this tragic disease by up to 30 percent.

3 genes linked to multiple sclerosis / Mutations may increase risk of developing disease San Francisco Chronicle Mon, 30 Jul 2007 3:47 AM PDT New DNA scanning technologies, which have uncovered genetic traits tied to a growing list of human ailments, have spotted three gene mutations that may raise the risk of a person developing multiple sclerosis, the most common neurological disease among young...

Scientists identify 2 genes linked to multiple sclerosis Boston Globe Mon, 30 Jul 2007 1:37 AM PDT CHICAGO -- After decades of dead ends, scientists have identified two genes that might raise the risk of multiple sclerosis, providing insight into the causes of the debilitating disease.

Gene found that may provide breakthrough for multiple sclerosis patients ABC 7 Chicago Mon, 30 Jul 2007 9:26 AM PDT The most significant genetic breakthrough in multiple sclerosis research in three decades.

Researchers identify gene causing multiple sclerosis International Herald Tribune Sun, 29 Jul 2007 11:14 AM PDT Three teams of researchers, working separately by different methods, have succeeded in identifying the gene linked to the causes of multiple sclerosis.

Scientists identify genes that can cause multiple sclerosis The Kansas City Star Sun, 29 Jul 2007 8:23 PM PDT FORT LAUDERDALE, Fla. | After three decades of work, scientists said Sunday they have identified two human genes that can cause multiple sclerosis, illuminating a new road toward a treatment for the disease.

Studies link genes to multiple sclerosis Arizona Daily Star Mon, 30 Jul 2007 0:18 AM PDT RALEIGH, N.C. — An international team of scientists has pinpointed genes that increase the risk of developing multiple sclerosis.

Genome detectives discover culprits in multiple sclerosis News-Medical-Net Mon, 30 Jul 2007 3:39 AM PDT Genome detectives have done it again by revealing at least three genes which are implicated in the incurable nerve disorder Multiple Sclerosis (MS).

Breakthrough could help treat multiple sclerosis
Dallas Morning News Sun, 29 Jul 2007 10:51 PM PDT
After three decades of searching, scientists said Sunday they have identified two human genes that can cause multiple sclerosis, which could lead to breakthroughs in understanding and treating the often-devastating disease.

MS: Is it all in the genes

A MAJOR advance in the search for new treatments for multiple sclerosis was heralded yesterday, with news of the first genetic breakthrough in the understanding of the disease for 30 years.

The Many Myths Of European Health Care

July 29, 2007 -The New Republic - By Jonathan Cohn.

CBS News

You hear it over and over again, in casual conversation and in serious debates among experts: If we create universal health insurance here in the U.S., then we'll end up with less responsive, less advanced medical care. Few arguments have done as much political damage to the cause of universal health care. And, as wonks like me have been arguing in recent months, few arguments fall apart more quickly under scrutiny.

After all, if universal health insurance means long queues for treatments, then why aren't patients in Paris or Hamburg waiting months for routine services — while patients in Boston and Los Angeles are?

If it means getting rushed, impersonal treatment, then why do France and Germany give new mothers more than four days to recover in the hospital, while insurance companies in the U.S. push new mothers out before two?

If it means making do with less advanced technology, then why does Japan have more CT and MRI scanners per person than we do?

And if it means worse health care overall, then why do so many studies show the U.S. scoring so poorly on international comparisons, including those examining "mortality amenable to health care" — a statistic devised specifically to test the quality of different health care systems across the globe?

CONTINUED -

http://www.cbsnews.com/stories/2007/07/27/opinion/main3105523.shtml

Fish Oil May Help Keep Inflammation at Bay

Scientists pinpoint 2 DNA variants linked to MS

BY DELTHIA RICKS

delthia.ricks@newsday.com

July 29, 2007, 6:12 PM EDT

In what is being hailed as a genetic bonanza, scientists have pinpointed two key DNA variants that elevate the risk of multiple sclerosis.

Since 1868 when the degenerative neurological disorder was first described, medical investigators have tried to shed light on its underlying cause. And even now with the announcement of two genetic discoveries -- the first in more than three decades -- scientists say they still have years to go before they fully understand MS.
advertisement

"We have been working on this for 25 years so this is a landmark achievement for MS, but we have a long way to go," said Dr. David Hafler, the Breakstone professor of neurology at Harvard Medical School and Brigham and Women's Hospital in Boston.

An estimated 400,000 people in the United States have MS, the most common neurological disorder in people 40 and younger.

Five years ago, Hafler organized the International Multiple Sclerosis Genetics Consortium, pooling the talents of the world's top experts to accelerate the gene hunt. The consortium scanned the entire human genome, using DNA samples from more than 12,000 people.

What they found, Hafler said, was a stunning genetic relationship between multiple sclerosis, type 1 diabetes and the thyroid condition known as Graves' disease. Type 1 diabetes and Graves are two major autoimmune diseases characterized by the body's capacity to attack itself, a key characteristic of MS.

One of the newly identified MS genes is known as the IL-2 receptor, which previously had been linked to type 1 diabetes and Graves. The other is called IL-7. When healthy, both are intimately involved in the body's immune response.

Prior to today's announcements, the only other DNA links to MS were discovered in the 1970s when British scientists spotted a large DNA cluster known as MHC -- the major histocompatibility complex -- which is flawed in patients with the condition. This segment of DNA also is responsible for many immune functions, Hafler said.

Given the complexity of MS, Hafler added, scientists were certain that a constellation of genes that included MHC must be related to the disorder. That notion, he said, inspired the hunt for additional suspects.

"We did a scan of the whole genome," Hafler said, describing a sweeping search of the entire complement of human genes to find those related to MS. "We didn't focus on one spot, looking for a single lamp post. We searched everywhere."

Even though multiple sclerosis is a neurological condition, scientists also believe that it is an autoimmune disease, driven by turncoat components of the immune system, explained Simon Gregory, a molecular geneticist at Duke University. Gregory pinpointed IL-7's exact location on chromosome 5. People have 46 chromosomes, 23 inherited from each parent.

In MS, turncoat immune-system cells attack the insulating fatty coatings of nerves -- the myelin sheath. With the sheathing destroyed, nerve function is damaged, causing a range of symptoms from muscular weakness and loss of coordination to speech and visual disturbances. The disorder primarily occurs during young adulthood.

Gregory added that MS also must have an environmental trigger, perhaps a viral infection that sets off the cascade of ill-fated genetic events.

In Manhattan, Dr. John Richert, executive vice president of research for the National Multiple Sclerosis Society, said there is practical meaning in the discoveries. Scientists now have new targets for diagnostics and therapeutics.

"These advances open a door for a landslide of new gene discoveries for MS," Richert said.

The complete report of the consortium's research is posted in the online edition of the New England Journal of Medicine. Gregory's analysis is published in Nature Genetics.

http://www.amny.com/news/health/ny-hsms0730,0,6544271.story?coll=am-topheadlines

Think About This One!!! It is short but very interesting!
A car company can move it's factories to Mexico and claim it's a free
market.
A toy company can out source to a Chinese subcontractor and claim it's a
free market.
A shoe company can produce its shoes in south East Asia and claim it's a
free market.
A major bank can incorporate in Bermuda to avoid taxes and claim it's a
free market.
We can buy HP Printers made in Mexico. We can buy shirts made in
Bangladesh. We can
purchase almost anything we want from 20 different countries.
BUT, heaven help the senior citizens who dare to buy their prescription
drugs from a
Canadian or Mexican pharmacy. That's called un -American! And you think
the pharmaceutical
companies don't have a powerful lobby? Think again!
It is an interesting
thought. Maybe this
is an issue that should come up in the next election!
Forget the 50, send it to everyone. We're all in this boat together!
Even if you aren't in this
boat now, you're standing on the pier.

Gene findings: Disease-by-disease

Scientists analysed DNA from 17,000 people

A team of UK researchers have identified several genes and regions of the genome involved in seven common diseases - but what are the implications for people suffering from the conditions?

Bipolar disorder

The first genome-wide study of bipolar disorder has shown that there are many genes that influence an individual's susceptibility to the condition and that each gene on its own makes a relatively small contribution to risk.

Several of the genes identified are involved in how nerve cells in the brain talk to each other.

Bipolar mood disorders affect around 100 million people worldwide.

Professor Nick Craddock, professor of psychiatry, at the University of Cardiff said: "By helping to unravel the mechanisms of illness, the findings will help pave the way to better diagnosis and treatment.

"Some new therapies based on a better understanding of the illness will involve novel drugs but others are likely to include forms of education, lifestyle advice and talking treatments."

Coronary heart disease

Various genetic regions that increase the risk of coronary artery disease have been found.

There is a lot of follow-up work required to fully understand the impact of the genetic associations that we have identified. However they have already provided some major leads regarding possible new treatment option Dr Miles Parkes

One region on chromosome 9, increases the risk by almost 50% in people with one copy of the variant, and almost doubles the risk in people who carry both copies.

Two other studies recently reported the same finding.

Heart disease is the UK's biggest killer.

Professor Nilesh Samani, head of cardiovascular sciences at the University of Leicester, said: "Identifying these new genetic variants is a first step that can help us to better predict who are at higher risk, to identify more specific ways of prevention by understanding how these genes operate and potentially, and most excitingly, in developing new treatments."

Crohn's disease

Three new genes increasing a person's susceptibility to Crohn's disease and a region containing several genes were identified in the study.

One gene, involved in regulation of the immune system, is shared with type 1 diabetes - the first genetic link between the two diseases.

A process known as autophagy - a process of clearing bacteria from within cells - was found to be associated with the development of the disease, which affects up to 60,000 people in the UK.

Dr Miles Parkes, consultant gastroenterologist at Addenbrooke's Hospital and the University of Cambridge said: "The study has substantially advanced our understanding of what causes Crohn's disease.

"There is a lot of follow-up work required to fully understand the impact of the genetic associations that we have identified. However they have already provided some major leads regarding possible new treatment options."

Hypertension

Hypertension was found to be due to numerous interacting factors rather than any major genetic influence but several genetic markers are being studied further.

Greater understanding of the genetic basis of susceptibility is important to the development of novel therapies particularly those aimed at arresting the disease process before significant disability has occurred Professor Jane Worthington

High blood pressure affects over 16 million people in the UK

Professor Mark Caulfield, Barts and The London School of Medicine, Queen Mary's University, London said: "Our study has highlighted the complex nature of the disease, with few clear cut genes emerging at this stage.

"This is probably in part because of the high number of genes involved, which helps to explain why patients with hypertension need to be treated with a combination of multiple drugs."

Rheumatoid arthritis

Several genes have been implicated in rheumatoid arthritis for the first time.

Further work will be needed to understand how the variation within these key genes influences the development of the condition, the course of the disease and response to treatment.

Around 387,000 people in the UK have rheumatoid arthritis.

Professor Jane Worthington, professor of chronic disease genetics at the University of Manchester said: "Greater understanding of the genetic basis of susceptibility is important to the development of novel therapies particularly those aimed at arresting the disease process before significant disability has occurred."

Type 1 diabetes

Four new chromosome regions and two further possible regions that increase the risk of developing type 1 diabetes - one of which is shared with Crohn's disease.

Around five million people worldwide have type 1 diabetes, including over 250,000 in the UK.

This research helps us to understand that, for most people at least, an individual's risk of developing diabetes as they get older is influenced by a number of genes, as well as by their environment Professor Mark McCarthy

Professor John Todd, professor of Medical Genetics at the University of Cambridge: "We now have confirmation that there are at least ten genes or chromosome regions that increase the chances of developing type 1 diabetes.

"The pathways that lead to Crohn's disease are increasingly well understood. We hope that progress in treating Crohn's disease will give us clues on how to treat type 1 diabetes."

Type 2 diabetes

Data from the project led to the discovery of several novel genes involved in the development of type 2 diabetes and obesity.

One of these genes influences risk of diabetes through an effect on weight and risk of obesity and others have a direct effect on diabetes risk.

Around 1.8 million people in the UK have type 2 diabetes

Professor Mark McCarthy, professor of diabetic medicine at the University of Oxford, said: "This research helps us to understand that, for most people at least, an individual's risk of developing diabetes as they get older is influenced by a number of genes, as well as by their environment.

"Clearly, the more 'high risk' alleles a person inherits, the higher the likelihood that they will go on to develop diabetes."
http://news.bbc.co.uk/2/hi/health/6727043.stm

BBC NEWS | Health | New MS genes after 30 year hunt
New MS genes after 30 year hunt

Many genes are thought to play a role in MS

The first new genes for three decades linked to multiple sclerosis have been identified by UK and US researchers.

Approximately 60,000 people in the UK suffer from the incurable disease of the nervous system.

The finding, published in two journals, will not lead directly to new tests or treatments, as experts say as many as 100 more genes may play a role in MS.

However, a Cambridge University researcher said he now expected swifter progress to reveal them all.

The joint project used the latest genome-scanning technology to look at the genetic make-up of thousands of MS patients, looking for signs of tiny genetic differences which might mean a greater risk of developing the illness.

It concluded that people carrying either of two genetic variants, called IL7R-alpha and IL2R-alpha, had an increased risk of between 20% and 30%.

No test

Dr Stephen Sawcer, from Cambridge University, said that even though this only represented a tiny increase in risk, it was a "landmark" discovery.

"This ends 30 years of complete frustration," he said. "But now we finally have the technology we need to help us find these genes."

These finds are the first of many, and after three decades finding nothing, we would expect to find many more of these genes over the next few years Dr Stephen Sawcer, Cambridge University

A test for this gene alone would reveal nothing about a person's chances of developing MS later in life, he said, as only one in 10 people in the UK did not carry it.

"We estimate that there are between 50 and 100 other genes which carry an additional risk.

"These finds are the first of many, and after three decades finding nothing, we would expect to find many more of these genes over the next few years."

It was only once many more "MS genes" were revealed, he said, that scientists would then be able to identify people carrying large numbers of them and examine what other factors might be triggering their illness.

Both of the genes identified by the research are known to have a role in the body's immune responses.

MS is caused when the immune system wrongly attacks the sheaths surrounding the nerves, destroying them and the body's ability to send signals along them.

This leads to muscle weakness, difficulties with balance and speech and vision problems.

Joint effort

The Harvard Center for Neurodegeneration and Repair was one of several US universities and research institutes which worked together on the project.

Adrian Ivinson, its director, said: "This study illustrates the power of collaboration - individually, none of us could have completed a study of this scale and complexity."

Dr Lee Dunster, head of research and information at the MS Society, welcomed the publication of the studies in the journals Nature Genetics and the New England Journal of Medicine

He said: "One of the great unknowns about MS is what causes it and this looks like a welcome breakthrough in getting to grips with the genetics behind the disease.

"People with MS often worry about what caused it, and particularly whether it will affect their children, so a better understanding of the role of certain genes is good news.

"These latest findings will be of great interest to researchers trying to develop future treatments."

The research is published in the New England Journal of Medicine and Nature Genetics.
http://news.bbc.co.uk/2/hi/health/6919613.stm

"Under The Influence"

VIDEO LINK

http://www.cbsnews.com/sections/i_video/main500251.shtml?id=3108688n

Zenapax (Daclizumab) drug description - prescription drugs and medications at RxList
ZENAPAX^®
(Daclizumab)
STERILE CONCENTRATE FOR INJECTION

WARNING Only physicians experienced in immunosuppressive therapy and management of organ transplant patients should prescribe ZENAPAX® (Daclizumab). The physician responsible for ZENAPAX administration should have complete information requisite for the follow-up of the patient. ZENAPAX should only be administered by healthcare personnel trained in the administration of the drug who have available adequate laboratory and supportive medical resources.

ZENAPAX^® (Daclizumab) is an immunosuppressive, humanized IgG1 monoclonal antibody produced by recombinant DNA technology that binds specifically to the alpha subunit (p55 alpha, CD25, or Tac subunit) of the human high-affinity interleukin-2 (IL-2) receptor that is expressed on the surface of activated lymphocytes.

Daclizumab is a composite of human (90%) and murine (10%) antibody sequences. The human sequences were derived from the constant domains of human IgG1 and the variable framework regions of the Eu myeloma antibody. The murine sequences were derived from the complementarity-determining regions of a murine anti-Tac antibody. The molecular weight predicted from DNA sequencing is 144 kilodaltons.

ZENAPAX 25 mg/5mL is supplied as a clear, sterile, colorless concentrate for further dilution and intravenous administration. Each milliliter of ZENAPAX contains 5 mg of Daclizumab and 3.6 mg sodium phosphate monobasic monohydrate, 11 mg sodium phosphate dibasic heptahydrate, 4.6 mg sodium chloride, 0.2 mg polysorbate 80 and may contain hydrochloric acid or sodium hydroxide to adjust the pH to 6.9. No preservatives are added.

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Multiple Sclerosis Linked to 3 Genes in Studies; More Likely
Bloomberg - USA
The research also could prompt new interest in developing Roche Holding AG's Zenapax, a drug that blocks the action of one of the genes, said researchers ...
See all stories on this topic

Elan says its loss widened in the second quarter
Boston Globe - United States
Cooke also said the company's multiple sclerosis drug Tysabri had a "solid quarter" with about 14000 patients on therapy as of mid-July -- an increase of ...
See all stories on this topic

New Genes Discovered For MS- TIME

Sunday, Jul. 29, 2007 By ALICE PARK

The best way to understand a disease is to get at its root cause, and most of the time, that means hunting down the genes that trigger it. In three papers published this week, researchers report that they have identified two new genes that may contribute to the immune disorder multiple sclerosis (MS). The hope is that the discovery will someday lead to the development of more efficient and much-needed MS drugs, as today's therapies carry serious side effects and address the disease's symptoms, but not its cause.

The new genes are the first to be linked directly to MS since the 1970s, when researchers initially identified a cluster of DNA on chromosome 6 associated with immune system function. Doctors believe MS is an autoimmune disease, in which the body mistakenly attacks its own healthy cells. But they have never been able to figure out why the body turns on itself, and they hope these new genes may offer a clue. "This is by no means the final, whole answer, but we've gotten an incredible glimpse into the cause of the disease," says Dr. David Hafler, professor of neurology at Harvard Medical School and Brigham and Women's Hospital and an author of one of the papers, which appears in the New England Journal of Medicine. In the other reports, published in Nature Genetics, two independent research teams confirmed the role of one of the genes described by Hafler's group.

For decades, MS researchers have been forced to make their best guess as to what causes the disease, which affects 300,000 Americans, mostly women, between their 20s and 40s. Since 1990, thanks to work done in Hafler's lab, however, they've known that MS sufferers have hyperactive T cells — cells that cruise the body looking for bacteria, viruses and other pathogens — a condition that triggers an inflammatory response and destroys the protective myelin sheath around nerve cells in the central nervous system, which connects the brain and body. This can lead to gradual nerve damage and weakening of the muscles in the arms as legs, as well as problems with vision.

What doctors didn't know was why these immune cells went into a hyperalert state to begin with. Was it caused by a virus? Was it nutritional, as suggested by a study last week in the journal Neurology, which found that having too little vitamin D, normally produced in the body during exposure to sunlight, increases the risk of MS? Or, were genes to blame for inciting the immune system to rebel? Or, was it, as most experts believe, some combination of all of the above?

To get a better answer, leading MS scientists in the U.S., including Hafler, teamed up with researchers in England and formed the International Multiple Sclerosis Genetics Consortium in 2002. The plan was to take their genetic study to the next level. So, they pooled their resources and examined the entire genomes of more than 2,000 MS sufferers, their families and control subjects. "People had been studying the genetics of MS for 20 years, and nothing had come out of it," says Hafler. "I felt we needed a genetic roadmap to show us what pathways to study that would help to explain the disease."

What they found were two new genes, IL2 and IL7, which code for receptors for interleukin — the proteins that regulate how T cells work in the body. People with certain forms of these genes have a 20% increased risk of developing MS. It is not, however, a defective or mutated form of the genes that causes MS; rather, it's certain forms of the genes, known as variants, that increase risk. The etiology of MS is complicated and appears to involve many genes, so the next challenge will be to figure out precisely what role these two new genetic variants play.

As exciting as the discovery is, it's a small part of the story: the new genes account for less than 1% of the risk of developing MS. In addition, about 70% of the normal, non-MS affected population has the same variants. "Every single time we have looked for genes for MS, the genes turn out to have a very small effect," says Dr. Moses Rodriguez, professor of immunology at the Mayo Clinic and a leading MS researcher." That suggests that either the disease is not genetically controlled in a significant way, or that if it is, that there are at least a 100 or so more genes that account for the entire disease process."

Hafler acknowledges that these findings are only the first step. Uncovering additional genes will require analyzing an even larger pool of MS patients and their families — Hafler is hoping to find at least 9,000 more patients. He calculates that with that much DNA, he'll be able to tease out 90% of the genetic culprits involved in MS. "These first genes give us a working hypothesis for what may be causing MS," says Hafler, "and a lot more work needs to be done. But we have finally begun."

http://www.time.com/time/health/article/0,8599,1647940,00.html?xid=rss-topstories

Two genes may raise risk of MS

JULIE STEENHUYSEN

Reuters
July 29, 2007 at 12:55 PM EDT
CHICAGO — After decades of dead ends, scientists have identified two genes that may raise the risk of multiple sclerosis, lending insight into the causes of the debilitating disease.
The findings, released in two medical journals on Sunday, represent the first genes conclusively linked to multiple sclerosis in more than 20 years, experts said.
MS is a disease of the central nervous system that affects about 350,000 people in the United States and more than 2.5 million people globally.
In a large-scale study appearing in an online version of the New England Journal of Medicine, teams of international researchers scanned the entire human genome of more than 12,000 people for MS risk factors.
That study uncovered two new gene suspects, both of which are thought to play a role in autoimmune disease.
Until now, the only genetic link identified with MS was the major histocompatibility complex, or MHC, a large cluster of genes essential to the immune system.
Neither of the newly discovered genes appears to be as instrumental to developing the disease as MHC, but the research is important because it lends insight into other genetic factors that raise a person's risk of multiple sclerosis.
"Having this genetic road map will be of incredible importance in developing new therapies," said Dr. David Hafler of Harvard Medical School, who worked on the genome study.
The role of one of the gene suspects in MS — a variant of the interleukin-7 or IL-7 receptor — was confirmed in two papers published online on Sunday in Nature Genetics.
The gene helps control the activity of regulatory T cells, which suppress the activation of the body's immune system.
"This discovery brings us into a whole new pathway that could have a very important role in understanding the fundamental mechanisms that trigger MS," said Dr. Stephen Hauser, professor of neurology at University of California San Francisco, who worked on studies released online in the New England Journal of Medicine and Nature Genetics.
While the studies used different methods, they both pointed the finger at IL-7.
The Nature Genetics study, led by Jonathan Haines of Vanderbilt University Medical Center in Nashville, Tennessee, and Margaret Pericak-Vance of the University of Miami, examined variants in three genes suspected to have a role in the disease. It found variants in IL-7 receptors were consistently more common in MS patients than in healthy people.
Researchers observed a similar association in a separate study in Nature Genetics by Jan Hillert of the Karolinska Institutet in Stockholm and colleagues, who looked at a large collection of people from Denmark, Finland, Norway and Sweden.
The other gene identified by the whole genome scan — the IL-2 receptor — has been linked to two other autoimmune diseases: type 1 diabetes and autoimmune thyroid disease.
"The story here is the commonality of autoimmune disease," Dr. Hafler said.
Researchers believe both environmental and genetic factors play a role in the development of MS, which attacks and destroys the insulation along nerve fibers.
MS symptoms range from mild muscle weakness to partial or complete paralysis.
http://www.theglobeandmail.com/servlet/story/RTGAM.20070729.wmsgene0729/BNStory/specialScienceandHealth/?page=rss&id=RTGAM.20070729.wmsgene0729

Multiple Sclerosis Linked to 3 Genes in Studies; More Likely
Bloomberg.com Sun, 29 Jul 2007 10:33 AM PDT
July 29 (Bloomberg) -- Scientists who screened the entire human genome have implicated at least three genes in the incurable nerve disorder Multiple Sclerosis, and hinted a dozen more might be involved.

After a decades-long search, scientists identify new genetic risk factors for multiple sclerosis
EurekAlert! Sun, 29 Jul 2007 10:08 AM PDT
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 (MS) – data sought since the discovery of the only other known MS susceptibility gene decades ago.

Risk genes for multiple sclerosis uncovered
EurekAlert! Sun, 29 Jul 2007 10:10 AM PDT
BOSTON, Mass. (July 29, 2007)—A large-scale genomic study has uncovered new genetic variations associated with multiple sclerosis (MS), findings that suggest a possible link between MS and other autoimmune diseases.

Risk genes for multiple sclerosis uncovered
CTV.ca Sun, 29 Jul 2007 10:07 AM PDT
Researchers have uncovered new genetic variations that appear to put one at increased risk for multiple sclerosis, in a discovery that's being called the first real progress on the genetics of MS in 30 years.

New Genes Found for Multiple Sclerosis
Time Magazine Sun, 29 Jul 2007 10:34 AM PDT
Researchers uncover two new genes that may cause MS, raising hopes for better treatments

Research identifies new genes linked with MS
Reuters via Yahoo! News Sun, 29 Jul 2007 10:04 AM PDT
After decades of dead ends, scientists have identified two genes that may raise the risk of multiple sclerosis, lending insight into the causes of the debilitating disease.

Two genes may raise risk of MS
The Globe and Mail Sun, 29 Jul 2007 10:20 AM PDT
Two more genes have been conclusively linked to multiple sclerosis, opening pathways to possible future treatments for the debilitating disease

Man with multiple sclerosis goes halfway down state in triathlon
Ventura County Star (subscription) - Ventura county,CA,USA
Rosales said his faith prevents him from condoning the use of embryonic stem cells in the search for a cure for multiple sclerosis and other diseases. ...
See all stories on this topic

Significant MS Clues Already Discovered

The Multiple Sclerosis Genetic Group (MSGG) is a collaborative effort between the Center for Human Genetics at Duke University Medical Center, Vanderbilt University Medical Center, the University of California at San Francisco and UC Berkeley. In 1996, the MSGG completed one of the first genomic screens aimed at identifying the location of MS susceptibility regions.

The genomic screen used 471 individuals from 80 families and the strongest evidence for an MS susceptibility gene was found in a region on chromosome 6 known as the Major Histocompatibility Complex (MHC). The MHC group of genes acts as the "master switch" for our body's immune system. This finding supports the hypothesis that MS is an autoimmune disease. Since the publication of this genomic screen, many other research groups have conducted similar studies, which confirmed the important role of the MHC in contributing to MS and also suggested other chromosomal regions likely to harbor MS susceptibility genes.

The MSGG second-generation screen of a much larger number of MS families was completed and published in 2004, and the research group is currently following up the most strongly implicated genomic regions to zoom in on the actual genes that increase MS risk. Breathtaking advances in molecular and statistical genetics, including the completion of the human genome sequence, give us the necessary tools to identify these MS genes. Understanding the genetics of MS will provide us with significant insights into the causes of disease and hopefully guide us to new treatment opportunities.

The Promising Future for MS Genetic Studies
Several steps in the genetic dissection of MS must follow the current work. The first is to try to weed out the false-positive results from the genomic screens, by testing more markers within each of these regions and testing more families. Based on the initial genomic screening results, the most interesting regions for further consideration are on chromosomes 3, 5, and 19. Potential linkage to chromosome 19 was first reported by our group in 1993.

The next step is to take these confirmed regions and narrow the likely candidate gene region as much as possible. While this has been viewed as a very difficult task, several new developments will simplify the problem.

New Molecular Resources
The goal of the Human Genome Project is to provide the complete human DNA sequence. As a by-product of this effort, complete (if still somewhat inaccurate) genetic and physical maps have been generated for all the chromosomes. Expressed sequence tags for the majority of human genes are now available, although the known or predicted function of these genes is still largely unknown. Thus for any candidate region, many genes are now readily available for study. Within the near future, complete gene sequences and intron-exon structures will become widely available, greatly simplifying the candidate gene search. In addition, new genotyping techniques, such as single nucleotide polymorphism genotyping on silicon chips may make gene mapping and identification even faster and more accurate. The Duke CHG is a leader in the application of these new techniques to human disease.

New Statistical Methods
One problem with the case-control study design is that positive results can arise for disease irrelevant reasons. To eliminate non-genetic influences, family-based association methods have been developed. The most commonly applied is the transmission-disequilibrium test (TDT) which examines the frequencies of alleles transmitted and not transmitted to children. This allows the use of single affected individuals, but also requires sampling their parents. The power of this simple test arises from its reliance on linkage disequilibrium, which usually exists over only very small intervals (usually less than 1 cM). Thus it is very complementary to standard linkage analysis, where the effect is broad (up to 30 cM), but its discriminative power over small regions is low. The TDT is best applied to the candidate genes that will fall within the critical regions. Large data sets of such TDT trios (an affected patient and both parents) are currently being collected by several research groups around the world.

The Duke CHG has played a significant role in expanding and extending these new methods for application to diseases such as MS.

Genetic Interactions
Virtually all genetic studies to date have examined only a single gene/marker/region at one time and yet we know that MS is influenced by multiple genes. It is likely that these genes interact with each other, and perhaps with environmental influences, to generate the MS phenotype. These complex interactions can be examined by a number of approaches. Thus future studies of MS will need to incorporate both genetic and environmental information in their data collection and analysis. The Multiple Sclerosis Genetics Group is collecting this important environmental information on their patients in order to examine gene/environmental interactions.

Chromosome 19
Previous genetic studies have indicated a region on chromosome 19 near the APOE gene as containing a susceptibility gene for MS. We recently examined this region in detail in a large data set of multiplex (> 2 MS patients per family) US MS families. We were able to confirm our earlier findings of potential linkage and association in this are in a much la. In addition to our analysis of US MS families, we have recently studied a population of MS patients from San Marino, Italy. San Marino is a small somewhat isolated population with a high frequency of MS (1/1000). There is no HLA-DR2 association in these families. Thus, we performed a genomic screen on the San Marinese families and then analyzed these data using family based association methods. We identified seven regions exhibiting evidence of potential association with MS. One of the most interesting areas was the region on chromosome 19 previously identified in our studies in the US series of families. These data provide further evidence of a locus on chromosome 19 that confers susceptibility to MS. Efforts are currently underway to identify the chromosome 19 gene.

Exploring Chromosome 3
Another region under investigation is chromosome 3p21. There are two candidate genes of interest in this region, CCR5 and CCR2B. These genes are interesting because aberrant expression of the proteins coded for by these genes has been detected in instances of demyelination. We found that some MS patients carry a CCR5 allele with a 32 base pair deletion. These patients had an age of onset 3 years later than those patients without the deletion.

International MS Genetics Consortium Successfully Launched

In 2003, a large international collaboration focused on the genetic dissection of MS was formed. It includes all the members of the MSGG research group as well as groups from Harvard University, the Broad Institute of the Massachusetts Institute of Technology (MIT), and the University of Cambridge in the United Kingdom. By bringing together many experts on MS genetics and combining some of the largest family data sets available in the US and UK with the most cutting-edge molecular-genetic and statistical resources from several institutions, we hope to accelerate the process by which we will gain more insight into the causes of MS. Visit their website to find out more information about the International MS Genetics Consortium (IMSGC)'s research goals and ongoing projects.

Multiple Sclerosis Study Participation

This study is a collaborative effort between many universities. The CHG’s role in the study is to do the laboratory and data analysis.

Our colleagues at University of California at San Francisco (UCSF) enroll qualifying families.

You can reach the UCSF study coordinator at
Phone: (toll free) 866-674-3637 ss
E-mail: msdb@itsa.ucsf.edu.

// top //

CHG Multiple Sclerosis Publications

As CHG researchers continue to define the genetic causes of MS, they publish their findings in leading academic journals and share their knowledge with colleagues at meetings and conferences.

Multiple Sclerosis Research Publications


// top //

Additional Multiple Sclerosis Information

MS Support Groups and Information Sources

The Multiple Sclerosis Genetic Group

National Multiple Sclerosis Society
733 Third Avenue
New York, NY 10017
Phone: (800) FIGHT-MS
Phone: (800) 344-4867
E-mail: info@nmss.org

// top //http://wwwchg.mc.duke.edu/diseases/ms.html
http://wwwchg.mc.duke.edu/diseases/ms.html

Multiple Sclerosis Gene Cluster Pinpointed

Wednesday, September 28, 2005

By Charlene Laino

The most comprehensive genetic study to date of multiple sclerosis has pinpointed a cluster of genes on chromosome 6 as playing the major role in causing the disorder.

The findings will ultimately help doctors to develop better treatments for MS, researchers say.

Researcher Margaret Pericak-Vance, MD, director of the Center for Human Genetics at Duke University in Durham, N.C., says previous studies had already pointed to this area on chromosome 6 as playing a role in MS.

“What’s different here is that we now know that it is the major effect -- that is, no other genes have an effect as large on causing MS,” she tells WebMD.

What Causes MS? Learn More

Having the Genes Doesn’t Equal MS

A person who harbors the genetic defect will not definitely develop MS, Pericak-Vance adds. “It does, however, make them more susceptible.”

As a result, she says she does not recommend people be tested for the genes.

Related

• Links

  • What Causes MS? Learn More
  • Why More Women Get Multiple Sclerosis
  • Learn How Multiple Sclerosis Progresses
  • Visit WebMD's Multiple Sclerosis Health Center

Nearly 400,000 Americans have MS, according to the National Multiple Sclerosis Society.

Worldwide, up to 2.5 million may be affected by the chronic disease of the brain and spinal cord.

In healthy people, nerve fibers are wrapped in a protective coating called myelin. But MS inflames or destroys myelin, disrupting the flow of nerve impulses. That can prompt problems with muscle control and strength, vision, balance, sensation, and mental function.

Why More Women Get Multiple Sclerosis

Coming to Terms With MS

Genes and Environment Play Role in Causing MS

Pericak-Vance says no one knows exactly what causes MS, but it is thought to be a complex interaction of genetic and environmental factors.

The genes pinpointed on chromosome 6 are known as major histocompatibility complex genes.

“These are genes that play a critical role in helping the body to distinguish its own cells from outside invaders such as bacteria or other microbes,” Pericak-Vance says. “If the system breaks down, the immune system may attack your body’s own cells, as happens in MS.”

For the study, presented here at the annual meeting of the American Neurological Association, the researchers used the latest genetic techniques to analyze data on 730 families in which more than one family member was affected by the disorder.

The next step, Pericak-Vance says, will be to hone in on other genes that may play smaller roles in causing the disease.

Henry McFarland, MD, chief of the neuroimmunology branch at the National Institute of Neurological Disorders and Stroke in Bethesda, Md., says the findings are “significant.”

“Identifying these genes starts to give us new clues into the causes of MS as well as how to treat it,” he tells WebMD.

Birth Control Pills May Lower MS Risk

Visit WebMD's Multiple Sclerosis Center

By Charlene Laino, reviewed by Michael W. Smith, MD

SOURCES: American Neurological Association 130th Annual Meeting, San Diego, Sept. 25-28, 2005. Margaret Pericak-Vance, MD, director, Center for Human Genetics, Duke University. Durham, N.C. Henry McFarland, MD, chief, neuroimmunology branch, National Institutes of Neurological Disorders and Stroke, Bethesda, Md.

http://www.foxnews.com/story/0,2933,170721,00.html

Stem Cell Robbery in Missouri?

by diverdonreed

Fri Jul 27, 2007 at 11:49:03 PM PDT

- WHICH WAY, MISSOURI?

The great state of Missouri has been robbed of eight hundred and fifty million dollars.

Who are the thieves? That's up to you to decide.

By my way of thinking, the Republican Party and the Religious Right should divide the guilt. Their political games denied Missouri eight hundred and fifty million dollars, which should have gone to that state's economy and to medical research, the fight against incurable disease.

First, let us judge the magnitude of what was lost.

$850,000,000.00 Big bucks. Thar's enough to pay for a McDonald's double cheeseburger for each of America's three hundred million citizens.

How significant is that? Yesterday, another state, New Jersey began a battle to raise $450 million (over ten years) for stem cell research. Governor Jon S. Corzine signed legislation to allow New Jersey voters to make the decision whether or not to spend $450 million roughly half the amount of money that was lost to Missouri?

And golden California, our glorious Proposition 71, three hundred million a year and Missouri could have had $850 million? That's almost like three extra years of full funding from the number one source in the world.

Jim and Virginia Stowers had planned an enormous expansion of their medical research institute in Missouri, but only if full stem cell research would be allowed.

The way I see it, the Stowers are heroes. These two cancer survivors have dedicated their fortune, the hard work of their lives-- to the battle against chronic illness.

Their motivation? We founded the Institute so our grandchildren may have better options. Jim and Virginia Stowers.

But anti-science Republicans attacked the research at every step. They were trying to criminalize the science which may day allow my paralyzed son Roman to fulfill Christopher Reeve's great prediction, to stand up from (his) wheelchair, and walk away from it forever.

The state of Missouri took notice. Citizens came together in the Missouri Cures Coalition, and fought for a Constitutional Amendment.

Amendment 2 was offered, saying: to ensure that Missouri patients have access to stem cell therapies and cures, that Missouri researchers can conduct stem cell research in the state, and that all such research is conducted safely and ethically, any stem cell research permitted under federal law may be conducted in Missouri, and any stem cell therapies and cures permitted under federal law may be provided to patients in Missouri.

A huge battle was fought.

The Stowers helped provide a budget. Some trash was talked about them for this, implying they were trying to make a dollar by backing the research. That was dumb, even by the standards of the opposition the Stowers are billionaires already, they do not need more money they are actively engaged in giving it away.

Of course, the Religious Right and anti-abortion groups went to work, developing and distributing the most poisonous propaganda imaginable. (I have never understood why anti-abortion groups oppose embryonic stem cell research, since there is no pregnancy involved, and therefore no possibility of either a child or an abortion). Conservative churches ignored the Constitutional separation of church and state, and functioned as headquarters for the anti-research efforts. Week after week, lawn signs were passed out in church, and church bulletins and lectures ranted on and on and on.

President George Bush visited Missouri so often it might have been thought he was changing residence.

But Missouri won anyway, passing Amendment 2.

As The Jurist (University of Pittsburgh School of Law) put it:

What right is more fundamental than a citizen's right to equal treatment under laws that govern access to medical therapies and cures? On November 7, Missourians stated clearly that they do not want to be second-class citizens when it comes to decisions about the health of their families. By passing Amendment 2, Missouri voters ensured that these important decisions will be made by patients, their families, and their health care providers, not by politicians in the state capital.. November 13, 2006

The Stowers Institute could go forward. Happy ending, right?

Unfortunately Religious Right Republicans like Senator Matt Bartle and Representative Jim Lembke are now trying to overturn Amendment 2, trying to block the will of the Show Me state. They tried to work within the State government to get a bill to overthrow the Amendment. When that didn?t succeed, they supported an initiative to do the same.

But I am an outsider, what do I know about Missouri?

Good point. So let's listen to a couple Missourians.

Like Henry J. Waters III, publisher of the Columbia Daily Tribune.

Except for the perverse attitude of Missouri Right to Life, the Catholic Conference and their lapdogs in the Missouri General Assembly, life sciences research and development could be one of the largest and most promising industries in our state.

cultural conservatives are doing all they can in the Missouri legislature to prohibit life sciences research, particularly in the promising area using stem cells...

Amid this poisonous atmosphere, the highly prestigious Stowers Institute for Medical Research announced it will put on hold resources to fund a major expansion Henry J. Waters III, July 3, 2007

The Kansas City Star weighed in.

Missouri politicians like to talk about the state's promise as a bioscience hub. But those same politicians are undermining efforts to advance medical research by pandering to groups opposed to embryonic stem-cell research

The passage of Amendment 2, which protects all forms of medical research allowable under federal law, should have removed the barriers to scientific progress. But too many lawmakers continue to cower before groups such as Missouri Right to Life.

These lawmakers delude themselves by thinking life science can flourish here if the climate remains hostile to promising forms of stem cell research.. May 22, 2007, the Kansas City Star.

How do scientists feel about it?
I couldn't possibly come to a place where I thought the potentially lifesaving research I want to do could become illegal. said Dr. Kevin Eggan.Stem Cell Movement Faces Setbacks, Andale Gross, AP, July 24, 2007

What is the situation right now?
A press release from the Stowers Institute for Medical Research states:

the Institute has transferred approximately $850 million from Missouri non-profit corporations whoosh, there went the money, out of the state.

Is there a chance the money can come back, and Missouri take its rightful place among the great research centers of the world?

We remain steadfastly committed to the search for life-saving cure through research with human embryonic stem cells, said Bill Neaves, President and CEO of the Stowers Institute. Unfortunately. As long as the political climate in Missouri remains unfavorable, outstanding scientists who work with human embryonic stem cells will prefer to work elsewhere, and Missouri will be denied the opportunity to advance what many consider the single most field of biomedical science.

So the Stowers pulled their money out.

However? they also bought 100 acres of land in Kansas City, Missourigetting ready for the day, whenever it comes, when the politicians get out of the way.

The way I see it, the Stowers have faith in us. We should not let them down.

So what do we do?

I can tell you in two words.
We fight.

Yesterday, I gave away twenty-five dollars.

That's two ten dollar bills and a five, twelve double cheeseburgers from McDonald's, or six bridge tolls and a dollar, from an old retired schoolteacher.

I plan to do it again, next month, when I can afford it again.

That particular $25 went to www.Kay4Congress.com an up-and-coming Democratic representative, Kay Barnes, stem cell supporter, 21st district, Missouri, USA.

The way I see it, people like Ms. Barnes are going to help right a terrible wrong that was done to America. Her opponent is against the research we support. So I will do what little bit I can to help her, and every stem cell research supportive leader, from whichever party they may come.

We are all Missourians. What happens in the Show Me state affects everyone. We can and should take part in that great struggle, supporting leaders like Kay Barnes, and Senator Claire McCaskill, and Senator Chuck Graham, and Representative Teresa Schooley stem cell research supporters all, working together for the public good.

Which way, Missouri?

Forward.

P.S. A personal message from Donn Rubin, who led Missouri's Amendment 2 effort:

With Missouri's world class medical research institutions and its growing life sciences industry, last fall's vote demonstrated that our citizens want our state to be at the forefront of advancing medicine and finding new cures. It is disappointing that there remain some politicians and interest groups, in Missouri and around the country that would prefer to go backwards. These are the same people who used every deception in the book last year in their unsuccessful attempt to defeat the Missouri Stem Cell Amendment. But they will fail, and I am confident we will soon get past this unfortunate, divisive chapter that has threatened to slow medical progress.