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The Potential role of peripherin in motor neuron degeneration
NEW DEPARTMENT OF VETERANS AFFAIRS REGISTRY FOR VETERANS WITH ALS (USA)
ON THE TRAIL OF PROTEINS GONE AWRY , Two new ALS studies help shore up a favored idea on how the disease harms motor neurons.
ENROLLMENT TO BEGIN FOR ALSA CO-SPONSORED CLINICAL TRIAL OF MYOTROPHIN IN ALS
Advocate urges caution on accessibility
Mandated changes in U.S. created 'a lot of ill will'
Star survey finds 62 food outlets without automatic doors
Article on 13th International Symposium on ALS/MND, 17-19
: November 2003
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MDA scientists find possible key to ALS
News rom the Muscular Dystrophy Association
TUCSON, Ariz., March 10, 2003 — Research funded by the Muscular Dystrophy Association has homed in on a potential trigger for amyotrophic lateral sclerosis (ALS), a fatal disease that typically has no clear cause.
ALS, also known as Lou Gehrig’s disease, attacks the muscle-controlling nerve cells called motor neurons, causing the muscles connected to them to waste away. There is no cure, and many people with the disease succumb to respiratory failure within three to five years of diagnosis.
A new study published on-line by Nature Genetics shows that genetic defects affecting a supply line within motor neurons can lead to an ALS-like disease.
Researchers based at the National Institute of Neurological Disorders and Stroke (NINDS) in Bethesda, Md., probed the DNA of a large family from Alabama that has a hereditary motor neuron disease similar to ALS. Their analysis revealed mutations in the dynactin gene, which encodes a protein that helps move nutrients, growth factors and other cargo along axons — the long thread-like appendages of nerve cells.
“This is an important finding because it supports data from animal studies suggesting that defects in axonal transport might play a key role in ALS,” said Sharon Hesterlee, MDA director of Research Development.
Ninety percent of ALS cases are sporadic (having no known cause), and the remaining 10 percent are hereditary. About one-quarter of hereditary ALS can be traced to mutations in the SOD1 gene, but even in these cases, the details of the disease process are unclear.
In a 1999 study, MDA-funded researchers found that mice with SOD1-related ALS show impaired axonal transport before they show signs of weakness. And last year, Erika Holzbaur of the University of Pennsylvania in Philadelphia found that when normal mice are genetically engineered to produce an inhibitor of dynactin, they develop ALS.
Holzbaur, Kenneth Fischbeck and Imke Puls of NINDS, and Robert Brown Jr., director of the MDA/ALS center at Massachusetts General Hospital in Boston, were key authors on the current study.
Studies of dynactin and axonal transport might hold insights into treatments for ALS, Fischbeck said. “If we can further understand this mechanism, hopefully it will lead to a better understanding of how to keep motor neurons alive,” he said.
Mutations in dynactin or related proteins might underlie some forms of hereditary ALS, while other disruptions of axonal transport — perhaps by toxins or infectious agents — might be capable of triggering sporadic ALS, he added.
USE OF "AIDS COCKTAIL" IN PEOPLE WITH ALS
Clinical Bulletin from The ALS Association National Office Last week, Canadian media released a story about a woman with ALS who has been treated for the last 18 months with an AIDS cocktail. She and her ALS physician, Dr. John Turnbull of McMaster University in Ontario, Canada, report that her disease has slowed down and some symptoms have improved or gone away. This is an encouraging report and ALSA is pleased to learn that Dr. Turnbull has begun a small clinical trial with this cocktail of AIDS drugs. Results of this trial will be available later this year.
ALSA's perspective and comments:
·
There is no peer-reviewed evidence at this time that indicates that the "AIDS cocktail" also known as HAART (highly active antiretroviral therapy) is beneficial to people with ALS. There can be significant side effects with this therapy. Until more is learned, ALSA is cautious about taking the report of a single case study as an indicator of what the treatment might mean to a population of people with ALS.·
Two reports appeared in the medical literature in 2001 describing studies in which HIV positive patients with accompanying ALS-like syndromes showed stabilization or partial recovery of the ALS syndrome after starting antiretroviral therapy. see http://www.alsa.org/news/news092801.cfm·
Encouraged by these initial published reports, ALSA is sponsoring a small pilot study to test whether patients with ALS who are negative for HIV would show similar reversal of symptoms when treated with Idinavir, a protease inhibitor (different from that in the HIV cocktail, but in the same class). Idinavir was selected because it can cross the blood brain barrier. This study will be completed in May 2003 at which time results will be made available. (see http://alsa.org/research/scicur111.cfm)·
Studies to investigate whether retroviruses are involved in ALS are in progress. The protease inhibitor Indinavir and the related compound in the AIDS cocktail may be effective in preventing caspase-dependent apoptosis (a cell death pathway involved in motor neuron degeneration). More evidence from animal studies are necessary to support this hypothesis.·
ALSA is currently unaware of any other trials using the AIDS cocktail. ALSA will keep the ALS community informed should we be alerted to any other ongoing efforts. ALSA is always watching for anything that will make a difference in this horrendous illness. ALS medical literature includes reports of some cases in which the individual's disease fluctuates. The ALS community needs to have data from carefully controlled and well-designed laboratory and human studies to be confident that this or any treatment is truly safe and effective for ALS. The published results of this one case study, the pending results of the Indinavir study, and the data from the small clinical trial Dr. Turnbull has begun will provide important information to substantiate whether this therapeutic approach holds the promise for others with ALS.PEOPLE WITH ALS SHOULD CONSULT WITH THEIR NEUROLOGIST CONCERNING THIS INFORMATION.
Seizing life amid horror of ALS
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COMMUNICATIONS ADVISORY
January 30, 2003
RE: Media coverage of Elizabeth Grandbois' ALS drug treatment administered by Dr John Turnbull, McMaster Health Sciences
Recently Elizabeth Grandbois has been interviewed by various media outlets (CH TV, Hamilton, Hamilton Spectator, CTV National News, Michael Coren Live etc) about her treatment with the 'AIDS cocktail' drugs prescribed by Dr John Turnbull of McMaster Health Sciences, Hamilton. Dr Turnbull indicated that he is doing a small study with 15 people. Results will be available in 6 months.
The following is the official position of the ALS Society of Canada and should be communicated if questions are directed to the partner ALS Societies.
There is no peer-reviewed evidence at this time that indicates that the so-called "AIDS cocktail" is beneficial to people with ALS.
According to Dr John Turnbull of McMaster Health Sciences, there is a small drug trial. Results will be available within the year.
The ALS Society of Canada is NOT aware of any other drug trials using the "AIDS cocktail" to treat ALS currently underway in Canada.
When the ALS Society becomes aware of any such drug trials the ALS Society of Canada will announce it through the usual channels and on its web site - www.als.ca.
PEOPLE WITH ALS SHOULD CONSULT WITH THEIR NEUROLOGIST CONCERNING THIS INFORMATION.
Please refer any other questions about this matter directly to
Susan Graham Walker, Director of Communications and Program,
ALS Society of Canada.
800-267-4257, sgw@als.ca
Montreal, April 1 2003 - A new three-drug cocktail used to treat mice with ALS, or Lou Gehrig's disease, may increase life span and decrease disease progression according to a study conducted at the Research Institute of the McGill University Health Centre (MUHC). The study, published in today's issue of Annals of Neurology, is the first to look at this drug combination in a mouse model of ALS. This research was made possible by a partnership led by the Canadian Institutes of Health Research (CIHR), in conjunction with the ALS Society of Canada and the Muscular Dystrophy Association of Canada (MDAC).
"Last year, we demonstrated that minocycline, a commonly prescribed antibiotic, on its own reduced disease progression, and delayed death in the ALS mice," says MUHC neuroscientist and senior author, Dr. Jean-Pierre Julien. "Findings from our current study show that a therapeutic approach based on a combination of minocycline with two other drugs is much more effective in delaying the onset of the disease and in increasing the longevity of the ALS mice."
"The results are very impressive," says Dr. Angela Genge, director of the ALS clinic at the Montreal Neurological Institute and Hospital. "The approach that Dr. Kriz and Dr Julien use is uniquely helpful in screening for potentially effective therapies in this cruel, currently incurable disease. Every gain gives us hope for the future."
"These research results give people who suffer from ALS hope, and show how well CIHR is working," said Dr. Rémi Quirion, Scientific Director of the Institute of Neurosciences, Mental Health and Addiction of the CIHR. "I have followed and admired Dr. Julien's work for many years and it is important that the Government of Canada invest in this kind of research."
"These results provide hope to ALS patients and their families," says Centre Hospitalier de l'Universite de Montreal (CHUM) ALS clinician Dr. Monique D'Amour. "Because there is little effective treatment for ALS, new drug strategies are necessary. We will have to see if this will work in patients."
A steadily progressive and fatal neuromuscular disease, ALS erodes a person's nervous system, eventually leading to paralysis and the inability to speak or swallow. People with ALS usually die within three to five years of diagnosis. Little is known about the cause of ALS and there is no cure. It is a disease of national importance, affecting between 1,500 and 2,000 people in Canada. Two to three Canadians a day die of ALS.
The discovery reported in this paper by Dr. Jasna Kriz, Ms. Geneviève Gowing and Dr. Julien is funded by a unique partnership between the ALS Society of Canada and the Muscular Dystrophy Association of Canada (MDAC). This partnership, in collaboration with the Canadian Institutes of Health Research (CIHR), has funded over $9 million of neuromuscular research since 2000.
"This is very exciting news for the ALS community," says Helene Vassos, interim National Executive Director for the ALS Society of Canada. "We are pleased that research, funded by our collaborative initiative with the MDAC and CIHR continues to result in important discoveries."
Dr. Julien, who is also a professor of Neurosciences at McGill University says that Dr. Kriz looked at the effect of combining three different drugs on the disease progression of ALS mice. The three drugs administered include minocyline- an antibiotic with anti-inflammatory properties, riluzole - the traditional ALS drug, and nimodipine - a drug that blocks calcium channels and normally used to treat brain hemorrhage and for prevention of migraine headache. Dr. Kriz compared the life span, muscle strength, nerve cell loss, and inflammatory response in ALS-mice who were fed a regular diet with those given food containing the three-drug cocktail. The mice fed the drug cocktail lived substantially longer, had a delayed onset of neuronal and muscle deterioration. "Our findings demonstrate the merit of a drug combination approach for treatment of a disease with complex degeneration pathways. The three drugs are currently available and we hope that our study will justify a trial on ALS patients," says Dr. Julien.
About the CIHR
CIHR is Canada's premier agency for health research. Its objective is to excel, according to internationally accepted standards of scientific excellence, in the creation of new knowledge and its translation into improved health for Canadians, more effective health services and products and a strengthened health care system. CIHR's Institute of Neurosciences, Mental Health and Addiction supports research to enhance mental health, neurological health, vision, hearing, and cognitive functioning and to reduce the burden of related disorders through prevention strategies, screening, diagnosis, treatment, support systems, and palliation.
For more information, please contact:
Christine Zeindler, MSc Communications Coordinator (Research)
McGill University Health Centre Communications Services
(514) 934-1934 ext. 36419
pager: (514) 406-1577
christine.zeindler@muhc.mcgill.ca
Susan Graham Walker
Director of Communications & Programs
ALS Society of Canada
(416) 497-2267, ext. 208
Center scientist spots another major path in ALS model
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Date : 14 Mar 2003
>From: ALS Center ALScenter@jhmi.edu
Robert Packard Center News Network
CENTER SCIENTIST SPOTS ANOTHER MAJOR PATH IN ALS MODEL
At least five major chemical pathways in nervous system cells go awry in ALS, researchers have noted in the last decade. Now a new study led by a Packard Center researcher points to yet another one. But this pathway may be relatively easy to put right, parts of the study suggest, and, as a new area directly on the route leading to motor cell death, it offers an attractive target for therapies.
The study, which uses mouse models of ALS, appears in the March 15 Journal of Neuroscience. It was funded by The Robert Packard Center for ALS Research at Johns Hopkins and by the Canadian Institutes of Health Research.
The work centers on a family of molecules called Cdks (for cyclin-dependent kinases), which normally either help signal cells to divide or help regulate nervous system development. Cdks are active in
growing animals. They get shut off in cells that no longer undergo mitosis, like motor neuron cells. "Problems may arise if Cdks become active in cells where they're meant to be quiescent," says McGill
University biochemist Jean-Pierre Julien, Ph.D., who oversaw the research team.
"We know that if you abnormally activate them in cultures of nerve cells, those cells die pretty handily," he says. "Now we've gone on to show that in animal models of ALS, whose nerve cells also die, those same Cdk molecules are also abnormally active."
Julien's team studied SOD1 mice, a standard animal model of the disease. These animals carry copies of a human gene that sparks a rare genetic form of ALS. Like humans, SOD1 mice undergo progressing muscle weakness and death.
By using sensitive tracers, the researchers showed levels of most Cdks were significantly higher in SOD1 mice than in healthy ones.
Two of the Cdks are especially crucial, Julien says, because, activated abnormally, they apparently trip cell suicide programs that quickly bring about cell death.
What starts it all? Scientists know cell stress; inflammation and abnormal cell chemistry in general can raise Cdks in cells. Julien speculates something similar, like inflammation, may spark the Cdk
upswing in the mice.
Interestingly, he says mice given the drug minocycline, an antibiotic that reduces inflammation, experience less Cdk uproar in their cells. "Inhibitors of Cdks, which we already know are protective in other neurodegenerative conditions," Julien adds, "might give us a reasonable avenue to explore for ALS treatment." In fact, other Packard-funded scientists are now exploring CDK inhibition as future therapy for ALS.
Other scientists in the study were Minh Dang Nguyen, Mathiew Boudreau, Jasna Kriz, Sibastien Couillard-Despris, Holger Patzke, Michael Ahlijanian and David Kaplan.
About The Robert Packard Center for ALS Research
Located in Baltimore, the Robert Packard Center for ALS Research at Johns Hopkins University is a collaboration of scientists worldwide working aggressively and rapidly to develop new treatments and find a cure for amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease. It is the only institution of its kind dedicated solely to the disease. Research conducted by the Center is meant to translate from the laboratory bench to the clinic in record time. Scientists and clinician members of the Center are unsurpassed at moving drugs reliably and rapidly from pre-clinical experiments to human trials.
The nature of ALS shapes the Center's aggressive, results-oriented scientific approach. ALS is a devastating, progressive neuromuscular disease that causes complete paralysis and loss of function -- including the ability to eat, speak and breathe -- and eventually, death. ALS progresses quickly and is not curable. Most patients die within five years of diagnosis.
To learn more about The Robert Packard Center for ALS Research at Johns Hopkins, including the latest information on ALS research and treatment, log on to www.alscenter.org.
The Potential role of peripherin in motor neuron degeneration
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Date : 14 Mar 2003
>From: webmaster@alsa.org
Research News from The ALS Association National Office
THE POTENTIAL ROLE OF PERIPHERIN IN MOTOR NEURON DEGENERATION
The current issue of The Journal of Cell Biology* contains Dr. Janice Robertsons published study describing the different forms of the protein peripherin and their potential role in motor neuron
degeneration in ALS. Dr. Robertsons study was funded through The ALS Associations Investigator-Initiated grant program.
Peripherin is a protein found in neurons, normally at low levels in motor neurons. After injury, levels of the protein are increased and are found in association with abnormal accumulations of other proteins in motor neurons of patients with ALS and the mutant SOD1 mouse models of ALS.
Over-expression of peripherin in mice leads to selective motor neuron degeneration mimicking several aspects of ALS.
Peripherin is present in different forms termed Per 58, Per 56 and Per 61. This study is the first to describe the differential expression of these forms both in a normal and a pathogenic setting. Why the different peripherin forms exist is unknown, however, it is possible that they have different functional properties. This study demonstrates that Per 61 is toxic to motor neurons in culture and is found in association with the abnormal protein accumulations both in the SOD1 mouse model of ALS and in two cases of familial ALS. These findings suggest that the presence of this toxic form of
peripherin may contribute to the neurodegenerative mechanism in ALS.
Janice Robertson said, The different peripherin isoforms are generated by a process called alternative splicing. Our findings show that abnormalities in alternative splicing lead to expression of a neurotoxic variant of peripherin, called Per 61, in motor neurons of mutant SOD1 mice. Most importantly we provide evidence for the expression of the human equivalent of Per 61 in motor neurons of ALS patients, suggesting that abnormalities in alternative splicing of peripherin may represent a new mechanism for understanding the neurodegenerative process.
Janice Robertson, PhD, is located at McGill University, Montreal, Canada. The ALS Associations funding of this study was in part made possible through the generosity of its National Capital Area
Chapter.
*Robertson, J., Doroudchi, M.M., Nguyen, M.D., Durham, H.D., Strong, M.J., Shaw, G., Julien, J.P., Mushynski, W.E., 2003, A Neurotoxic Peripherin Splice Variant in a Mouse Model of ALS.
The Journal of Cell Biology online, March 17, 2003
Creatine provides no help for ALS
Creatine, an over-the-counter supplement popular with weight lifters, has been used by thousands of people suffering from amyotrophic lateral sclerosis, or A.L.S., since they learned of a 1999 study involving mice. In it, creatine extended the lives of mice with the disease.
Now, a new study, conducted in the Netherlands and published online yesterday by The Archives of Neurology, has found that creatine provides no significant benefit in humans with the disorder, which is also known as Lou Gehrig's disease.
Dr. Geert Jan Groeneveld of Utrecht University, the lead researcher, wrote that the study also illustrated the difficulties of studying commonly available dietary supplements, particularly in connection with dire conditions like A.L.S., which causes nerves to waste away steadily.
He said it would have been impossible to find enough patients to meet standard statistical criteria when those who suspected they were being given a placebo could buy creatine almost anywhere.
Instead, Dr. Groeneveld and his colleagues enrolled a smaller number of A.L.S. patients, 175, in an experiment of the most rigorous design. In it, neither the patients nor the researchers knew who was getting the drug and who was not.
The researchers found no significant difference in survival rates, the rates at which muscle mass wasted or in quality of life ratings, according to the study.
Dr. Jeffrey D. Rothstein, an A.L.S. expert at the Johns Hopkins Medical Center, who was not connected with the study, said that it was possible that creatine had some small benefits, but that he doubted it.
"I believe the trial effectively rules out the value in ongoing use of creatine, at least at that dose," Dr. Rothstein said in a statement. "And my suspicion is that higher doses, if effective at all, would be of marginal benefit."
NEW RESEARCH SUGGESTS REVERSAL OF ALS MAY NOW BE POSSIBLE
MIAMI, April 2 /PRNewswire/ -- Reversal of Lou Gehrig's disease may now be possible using thrombopoietin and thyroid hormone to cause regeneration of endogenous stem cells of the central nervous system. Evidence suggests spinal cord injury can be reversed through regeneration by stem cells. This research will be presented by George R. Schwartz, M.D., a senior researcher at Neuroregeneron Co., this week at the annual meeting of the American Spinal Injury Association held in Miami, Florida.
The Food and Drug Administration (FDA) biologics division approved a unique clinical trial in May 2002, authorizing the use of thrombopoietin for Lou Gehrig's disease (amyotrophic lateral sclerosis) in a 40-year-old mother of three small children whose clinical condition was deteriorating rapidly. She was more than 90% paralyzed, with minimal speech capability, tremendous difficulty swallowing, and rapidly failing respiratory function.
The new treatment was approved for a clinical trial after it was demonstrated that platelet growth factors could be tremendously increased through use of thrombopoietin. Platelet growth factors act as stimulants for the growth and development of glial cells which act as repair cells for dying nerve cells. In addition, platelet growth factors can stimulate immature cells to differentiate into cells which act as neurons. Thyroid hormone was added to the trial after experimental evidence demonstrated that thyroid hormone acted as a signaling substance helpful for repair cells to function.
Platelets were raised in cycles to more than 10 times the normal level resulting is blood serum rich in platelet growth factors.
At day 42 of this clinical trial, this patient showed remarkably improved head and neck control and strength. At day 45, she exhibited improvement in tongue strength and motion with improved swallowing functions. As a result, a feeding tube was not necessary.
At day 60, increased leg muscle strength was clearly evident. Along with this motion, the patient was able to turn her arms and hands which had been paralyzed for more than a year. At day 110, she began to move her hands. Muscle strength throughout her body increased and her pelv could support more weight.
The patient showed clear reversal of a previously deteriorating condition, and return of functions. Her downhill course stopped.
TO READ THE FULL TEXT OF THIS STORY CLICK THE LINK BELOW:
http://www.rideforlife.com/MT/archives/als_research/000483.html#483
SOURCE : Daily Miner & News (Kenora, Ontario)
DATE : April 30, 2003
HEADLINE: RESEARCH ADVANCE: LOU GEHRIG'S DISEASE
BYLINE : BY CHEN CHEKKI, MINER AND NEWS STAFF
A drug cocktail discovered by a Quebec researcher may substantially extend the life of the estimated 50 people in Northern Ontario suffering from Lou Gehrig's disease.
Dr. Jean-Pierre Julien of the McGill University Health Centre has for several years been researching the disease, scientifically known as amyotrophic lateral sclerosis, or ALS. It erodes the nervous system and has no known cause, cure or treatment. The disease usually kills people between two and five years after they have been diagnosed with the
disease.
Julien found last summer that the mixture of drugs extend the lifespan of mice with the deadly disease by six weeks. "Getting six weeks is quite spectacular," Julien, senior author of the study, said in an interview.
He said six weeks may not sound like much more time, but the normal lifespan of healthy mice is two to three years. Julien said the extended lifespan found in mice with the disease may translate into a proportional extension of life expectancy for humans.The experimental treatment uses three particular drugs. It uses minocycline, or a well-known antibiotic that helps reduce inflammation. It also uses riluzole, which has previously been found to reduce the amount of glutamate -- or neurotransmitter commonly found in Lou Gehrig's sufferers.
The third drug is nimodipine, a drug often used to prevent migraine headaches and help those recovering from brain damage. Julien said the the study is valuable because the disease exists in mice very similar to the way it does in humans. Julien also said the Lou Gehrig's-infected mice were studied at 7 to 9 months of age when they began to show symptoms of the disease -- making for a life-like situation commonly found in people.
"This way, it makes for a realistic situation," said Julien. "Humans don't always develop symptoms at birth, but later in life. "Some mice were fed food without the drug cocktail and some were given only food with the drugs. They were compared for their lifespan, muscle strength, nerve cell loss and inflammatory response. The mice taking the drugs lived longer and had delayed deterioration of their motor neurons and muscles.
"The results are very impressive," said Dr. Angela Genge, director of the Amyotrophic Lateral Sclerosis clinic at the Montreal Neurological Institute and Hospital.
Julien said the findings merit a drug combination approach for treatment of the disease.
His study follows his previous research that found that minocycline alone extended the life-expectancy of Lou Gehrig's mice by three weeks. The three drugs are available for use and Julien is already planning human trials.
"We will set up a human trial as soon as possible, maybe in the next three mont said. Julien believes such tests would include people living in Nova Scotia,Ontario, Alberta and British Columbia.
The study was made possible by a partnership led by the Canadian Institutes of Health Research, The ALS Society of Canada and the Muscular Dystrophy Association of Canada.
About 400 people are registered with the Amyotrophic Lateral Sclerosis Society of Ontario and 1,000 people are believed to suffer from provin
With about five per cent of those cases known to be in Northern Ontario,an official with the society believes there are many more who have notbeen diagnosed for the disease or have reported it to them. "There definitely is more," said Ravi Jain, director of services for the
society. "But a lot of people may not choose to report with us."He believes the new study gives great hope for those with the disease that he said may be 5 to 10 per cent genetically caused.
A steadily progressive and fatal neuromuscular disease, Lou Gehrig's damages motor neurons that control muscle movement. Situated in a person's spinal cord and brain, the damaged neurons lack the ability to send instructions to muscles in the body, rendering a person unable to control them.
Other cells surrounding the neurons also become inflamed and damaged."They create a bad environment for the motor neurons," said Julien.The first symptoms of the disease usually occur in the legs, arms, throat, or upper chest area. Along with muscular weakness, one may also have muscular fatigue and may begin to trip and fall. Others lose the use of their hands, arms and find it hard to swallow and speak without slurring their words.Muscle twitching may also be an indication of the fatal disease. There is no precise order in which the symptoms appear and any one of them may indicate the presence of Lou Gehrig's. Because the disease often takes its toll before being diagnosed, many become debilitated before they find out they have the disease. Progression of the disease further paralyzes limbs and respiratory system.However, senses such as taste, touch, sight, smell and hearing remain unimpaired and the intellect is usually remains normal. About 1,500 to 2,000 people have the disease across Canada and up to three of them die everyday. Julien said the chance of men getting the disease is 1 in 800 and the chance of women getting the disease is 1 in 1,200.Facts about Lou Gehrig's Disease:- In at least 90 per cent of cases, the disease strikes people with no family history of Lou Gehrig's disease.- It can strike anyone, regardless of age, sex, or ethnic origin.- The usual age of onset is 55 to 65, but some have been younger than- Lou Gehrig was a famous baseball player for the New York Yankees who died of the disease in 1941.- The disease was first identified by the famous French neurologist, Dr.Jean-Martin Charcot in 1874.- The disease killed 1,423 Canadians in 2001
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NEW DEPARTMENT OF VETERANS AFFAIRS REGISTRY FOR VETERANS WITH ALS
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Genetic Basis for Motor Neuron
SOURCE : PR Newswire
DATE : May 2, 2003
HEADLINE: International Coalition Publish in Journal 'Science'
: Groundbreaking Research On Genetic Basis for Motor Neuron
: Degeneration; Results from Model-based Functional Genomics: Research Provides New Insight on the Pathogenetic Mechanism: Which Causes Diseases such as MND/ALSDATELINE: MUNICH and LONDON, May 2Ingenium Pharmaceuticals AG and a coalition of international research organizations announced today the publication in Science of research describing a fundamental discovery about the genetic and molecular basis for Motor Neuron Disease (MND), which includes Amyotrophic Lateral Sclerosis (ALS). The research explains a key pathogenetic mechanism of motor neuron degeneration, potentially opening new therapeutic avenues for treating motor neuron diseases including ALS, also known as Lou Gehrig's Disease, the third most common neurodegenerative disease after Alzheimer's and Parkinson's. The research was conducted by Ingenium; University College London; the Queen Mary, University of London; UK Cancer Research; Munich Technical University; and Institute of Experimental Genetics at the GSF-National Research Center for Environment and Health, Germany. The UK work to find the gene mutation in the mouse was funded by the Motor Neurone Disease Association. The National Genome Network funded the GSF research.Today's Science publication explains the mechanism for how widely-expressed genes can cause selective death of motor neurons, resulting in MND. By identifying two specific mutations in the same gene, the combined research group has produced a precise mammalian model of MND and described the pathogenetic link between specific gene mutations and selective, progressive degeneration of motor neurons. The research groups initially began their research with two distinct mouse models of late-onset MND and traced the genetic cause of the symptoms to specific point mutations in one gene, Dnchc1. Based on that discovery, the combined research team defined that the mutations in the Dnchc1 gene impaired axonal transport in the nerve cell, which specifically caused cell-death in motor neurons without affecting other cell types. This type of selective motor neuron degeneration is clinically similaron a cellular and organismal level to the human disease state seen in ALS and other motor neuron diseases."This publication is exciting as it provides a fundamental step toward explaining the pathobiology that results in MND, but it also, although at an early stage, could significantly impact our understanding of neurodegeneration in general," commented Dr. Gabriele Stumm, study co-author and Director of the Neurobiology Program at Ingenium. "The key discovery is that an inherited moderate impairment of nerve cell transport functions indeed can result in age dependent distinct motor neurodegeneration. This finding was enabled by Ingenium's research approach and our valuable collaboration with the UCL and detected in the neuropathology laboratories of Prof. Joanne E. Martin, Queen Mary, University of London, and Prof. Juergen Schlegel, TU Munich.""The pathogenetic link between specific gene mutations and selective, progressive degeneration of motor neurons has been the fundamental question in MND research," stated Professor Elizabeth Fisher of the Department of Neurodegenerative Disease at the National Hospital forNeurology & Neurosurgery at UCL. "Using similar technology, both research groups identified a mutated gene which provides an answer to this question."<"I am delighted that this paper has helped open up new approaches in the study of motor neuron disease; it is the culmination of many years of work with national and international colleagues," added Joanne E. Martin, Professor of Neuropathology at Queen Mary, University of London.The research teams used ethylnitrosourea (ENU) as a chemical mutagen to produce random point mutations in the mouse genome. The researchers identified a mouse phenotype that displayed progressive loss of muscle tone and locomotor ability, in a similar fashion to the ALS disease progression in humans, and the research groups performed positional cloning to locate the mutated gene responsible.The collaborative research began with the further biological analysis of the two models and the respective similarities produced by two different missense mutations. The findings reported are also important in demonstrating the value of random point mutation research in a model system since prior studies of the particular gene in knock-out animal models produced embryonic lethalities, with no discernable link to MND research."The ability to correlate a biological phenotype similar to a human disease state with a specific gene mutation is a powerful approach to discovering biological mechanisms that will have real importance in developing new therapeutics," said Dr. Michael C. Nehls, Chief Executive and Chief Scientific Officer of Ingenium. "The next step for Ingenium's research is to demonstrate the application of this knowledge to the human disease and we are moving forward with this in collaboration with the University of Ulm and Professor Ludolph, a noted specialist in treating ALS patients."Dr. Hrabe de Angelis, Director of the Institute of Experimental Genetics in Munich said: "We would have not been able to conduct this study without the industrial-academic consortium. The interdisciplinary and interstructural approach was essential for the successful discovery of this new disease mechanism. In addition, mouse models have proven again to be key for the molecular understanding of disease."Dr. Brian Dickie, Director of Research Development at the Motor Neurone Disease Association in the UK, said: "In the vast majority of cases of MND the causes remain unknown. This discovery opens up a promising new avenue of research into definitive causes of MND and will doubtless accelerate our search for a cure."The paper published in the May 2, 2003 issue, Vol. 300, Nr. 5620, pages 808-812 is entitled "Mutations in dynein link motor neuron degeneration to defects in retrograde transport". Contributing authors include M. Hafezparast, R. Klocke, C. Ruhrberg, A. Marquardt, A. Ahmad-Annuar, S. Bowen, G. Lalli, A. S. Witherden, H. Hummerich, S. Nicholson, P.J. Morgan, R. Oozageer, J. V. Priestley, S. Averill, V. R. King, S. Ball, J. Peters, T. Toda, A. Yamamoto, M. Augustin, D. Korthaus, S. Wattler, P. Wabnitz, C. Dickneite, S. Lampel, F.Boehme, G. Peraus, A. Popp, M. Rudelius, J. Schlegel, H. Fuchs, M. Hrabe de Angelis, G. Schiavo, D. T. Shima, A. P. Russ, G. Stumm, J. E. Martin and E. M.C. Fisher.University College London (UCL) has been consistently rated amongst the top three multi-faculty universities in the UK. With an international reputation for excellence and innovation in teaching and learning, UCL has occupied a pioneering role in higher education since its inception. As well as being the first English university established after Oxford and Cambridge, UCL was the first university to offer undergraduate teaching in physics, chemistry and engineering.The Provost and President of UCL is Sir Derek Roberts FRS. Queen Mary is the fourth largest of the Colleges of the University of London. Its roots lie in four historic colleges: Queen Mary College, Westfield College, St Bartholomew's Hospital Medical College and the London Hospital Medical College. Pooling strengths, expertise and resources, Queen Mary is now fully integrated. It is a research university, which ranks in the top 20 of English universities. It also has a strong international reputation, with over 20 per cent of students coming from over 100 countries.The basis of Ingenium's business is its knowledge and expertise in generating the biological information critical to the discovery, validation and development of therapeutics. Ingenium's biology-based target discovery technology, Deductive GenomicsTM, involves a functional genomics analysis of an entire mammalian genome to locate novel therapeutic entry points to treat disease. From the breadth of knowledge generated by Deductive GenomicsTM, Ingenium is currently advancing a pipeline of novel models and biologically validated drug targets in the areas of obesity, lipid metabolism, neurodegeneration and autoimmune disease. Ingenium has research partnership agreements with Elan Corporation, F. Hoffmann-La Roche Ltd., Sequenom Inc. and Lynkeus BioTech GmbH, in addition to numerous international academic collaborations. The company benefits from funding from premier investors, an experienced management team, top industry advisors and a growing patent portfolio.The Motor Neurone Disease Association (MNDA) is the only organization of its kind in England, Wales and Northern Ireland dedicated to working on behalf of people living with MND. It funds the largest number of MND research projects in the UK. It is currently funding 29 projects ranging from mechanisms of disease pathogenesis through to health and social care research. The Association also provides information, advice and support to people affected by MND.For more information contact: For Ingenium : Gretchen Schweitzer, Ph: +49 (0)89-8565-2398, gretchen.schweitzer@ingenium-ag.comFor UCL : Heidi Foden, Ph: +44 (0)20-7679-1621Peripheral, motor nerve cells created from ES cells.
SOURCE : Jiji Press Ticker Service
DATE : May 6, 2003, Tuesday
HEADLINE: Jiji Press Roundup of Recent Bio News
DATELINE: Tokyo, May 6
PERIPHERAL, MOTOR NERVE CELLS CREATED FROM ES CELLS--Japanese scientists
have succeeded in creating peripheral nerve cells from the embryonic stem cells of a mouse and a monkey, an achievement that could open the way for treatments of certain difficult neural diseases.
The scientists, led by Prof. Yoshiki Sasai of Kyoto University, alsosucceeded in cultivating motor neurons from the ES cells of a monkey.
The report was published Tuesday in the electronic edition of theProceedings of the National Academy of Sciences of the United States.
It was previously known that early exposure of ES cells to BMP4, a protein found in an embryo that later develops into a brain and a spinal cord, promotes change in skin cells.
The scientists discovered that late BMP4 exposure, conducted after a fourth day of coculture, caused change in peripheral neural cells.
They also reported that upon ES cells' exposure to another type of protein called Sonic hedgehog (Shh), ES cells were transformed into motor neurons.
The findings are expected to lead to treatments for such diseases as congenital megacolon and amyotrophic lateral sclerosis
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Gene for incurable neuron disease found
SOURCE : Jiji Press Ticker Service
DATE : May 6, 2003
HEADLINE: Jiji Press Roundup of Recent Bio News
DATELINE: Tokyo, May 6
GENE FOR INCURABLE NEURON DISEASES FOUND--
Japanese and European researchers have jointly identified a gene that could cause such motor neuron diseases as amyotrophic lateral sclerosis, or Lou Gehrig's disease, according to the U.S. journal Science.
Studying one of genes coding for a motor protein called dynein, a team of Japanese, British and German researchers found that mice with a mutation in one copy of the dynein gene, Dnchc1, showed degeneration of their motor neurons.
The gene gave rise to motor problems similar to Lou Gehrig's disease and spinal muscular atrophy in humans, and determining the molecular processes underlying these diseases is the first step toward potential treatment, the journal said.
Motor proteins carry waste products in nerve cells, which die if the proteins stop working.
Cherishing every moment - an ALS story
Diagnosed with a terminal illness, Patsy Seguin-Tremblay discovers more laughter with her family, learns to appreciate often-overlooked moments and sets herself solid goals for the future.
Despite the fact that she was diagnosed with amyotrophic lateral sclerosis (ALS) on September 1, 1998, One has become Patsy Seguin-Tremblay's favourite number. It represents how she's learned to live her life; it stands for every single thing she takes comfort in and every little event she cherishes being a part of.
A recent article in the ALS newsletter entitled "ALS - A Disability or a Fatal Disease?" by Cheryl Carter-Newhas solidified Patsy's unwavering spirit, having reminded her that others share her thoughts and her determination to battle the degenerative disease that many experts claim will take a life in three-to-five years.
"I've encountered some health care professionals and people who view ALS as a death sentence. If you don't see it their way they treat you as non-compliant, in denial or a difficult patient," she said. "I have accepted my fate. I have accepted that I have ALS but I don't feel I'm terminal."
The article, she said, singled out some important challenges facing ALS sufferers. It dealt with the dismissive attitudes some doctors have towards the disease, and the general belief that ALS is too expensive to consider prolonging your life after the disease reaches its later stages.
We also have encountered health care professionals who have said that. "It's too much of a burden on caregivers; you don't want to live that way do you?", Seguin-Tremblay revealed. "What value does my life have? Just ask my children, my husband, my friends."
She added that every day becomes important, that every accomplishment becomes a celebration of life.
"I take pleasure in more things. When I write an e-mail, a page takes a day for me. I enjoy seeing my children coming home from school. We have had many dark days but there have been many more filled with love and faith. Those are far more frequent."
Having worked as a registered nurse for 15 years, Patsy said she knows the odds she's facing. In the past five years her symptoms have progressed to the point where she needs assistance to move around. her arms and legs have weakened and she's lost her ability to talk. Today, Patsy communicates mostly through communications devices and her computer.
"Carter-Newhas article talks about our battles with real-life demons, with the lack of faith in us, our family and our situation - sometimes on a daily basis from people who are supposed to provide support," Seguin-Tremblay explained. "Luckily , we've also been blessed with those professionals and people who treat us with dignity, who respect our decisions and treat us intelligent people."
One.
It's an important number in Patsy's life, just as each day, each hour, each breath has taken on a whole new meaning since her diagnosis five years ago. It stands for her family - sons Alexandre and Patrick, and husband Stephane. It stands for each day. It stands for a single, positive attitude that refuses to accept three to five years.
Pride of a Century
SOURCE : The New York Post
DATE : June 19, 2003
HEADLINE: PRIDE OF A CENTURY - YANKS COMMEMORATE LEGENDARY LOU GEHRIG
BYLINE : KEVIN KERNAN
AS the gold bracelet slipped onto Teresa Wright's wrist she immediately felt a closeness to Lou Gehrig. This was 61 years ago during the filming of "Pride of the Yankees."
"To me," says Wright, who played Lou's wife Eleanor, "Pride of the Yankees" was a love story. That bracelet was an example of their love. Just wearing it was special. I'll never forget it."
Gehrig's wife had brought the bracelet onto the set so it could be used in the film. The bracelet, which Eleanor later presented to the Hall of Fame, is made up of 17 metal elements celebrating Gehrig's mythical career, including seven World Championships and six All-Star Games.
The bracelet remains one of the Hall's most valued treasures and is on tour in Chicago as part of the record-shattering "Baseball As America" exhibit. The Yankee first baseman gave the bracelet to his wife on their fourth anniversary.
"Mrs. Gehrig was so sweet and warm," recalls Wright, 85. "I got to know her better through the years through her work with ALS. Her love for Lou endured. I think the film has endured because people love Lou Gehrig and they love a love story."
Today, on the 100th anniversary of Gehrig's birth, Wright will be at Yankee Stadium as part of a celebration presented by the ALS Association-Greater New York Chapter. There will be a pre-game wreath ceremony at Gehrig's monument.
Catfish Hunter's wife Helen will be present as well as Ray Robinson, author of "Iron Horse," and Dorine Gordon, president of the New York chapter of the ALS Association.
Amyotrophic Lateral Sclerosis is the insidious disease that took the lives of Gehrig and Hunter and is better known as Lou Gehrig's Disease.
Gehrig died on June 2, 1941, 17 days before his 38th birthday. The day he died, Joe DiMaggio was 19 games into his 56-game hitting streak, picking up two hits off of Bob Feller.
"Having Gehrig's name associated with ALS does help our cause," explains Gordon, citing the Lou Gehrig Challenge: the Campaign to Cure ALS
. "Putting a face to the disease helps raise awareness. It also serves as inspiration for people with ALS and their families because Lou Gehrig's legacy is that of strength, courage and a positive attitude in the face of adversity."Tom Shieber, curator of new media at the Hall of Fame, has studied the bracelet and Gehrig and offers this insight.
The popular notion is the bracelet is made up of Gehrig's World Series and All-Star rings, but Shieber believes it's possible that jewelers Dieges & Clust, who created the jewelry for the World Series rings at the time, made the bracelet for Gehrig using molds of World Series and All-Star designs that were used in rings and pins.
As for the man himself, Shieber has no questions about why Gehrig, who was the first New York-born baseball hero, remains such a mythical figure.
"Not only was he a great ballplayer," Shieber says, "but he was one of the first ballplayers that was super muscular. That was a new thing.
Ruth was barrel-chested and had those great wrists, but Gehrig was so strong . . . he hit prodigious home runs.
"Part of his mystique also is that he played in the shadow of Ruth, the quiet hero," Shieber adds. "He let his bat do his talking. He was this Iron Man, this Iron Horse, who was unstoppable, yet he succumbed to this terrible disease."
Shieber also notes, "Gehrig didn't have any children. In that way he was less tangible."
With no descendants to color public opinion, the legend grew around this historic number: 2,130 consecutive games. Gehrig's lifetime statistics also represent the sadness of unfulfilled milestones. The first baseman finished seven home runs below 500, 279 hits short of 3,000 and five RBIs shy of 2,000. On his headstone, his year of birth is wrong, listed as 1905.
A year after the luckiest man on the face of the earth died, "Pride of the Yankees" was made with Gary Cooper in the lead.
The movie was more than a baseball story. It was about love, pride, courage, family, and all things good. Explains Teresa Wright in her still youthful voice: "Mr. [Samuel] Goldwyn loved the movie so much I remember him saying: 'I don't care if the picture makes a dime. I want every man, woman and child in America to see this movie.' Obviously it made a lot of money."
Lou Gehrig was America's hero. So much so that during World War II, a Merchant Marine troop transport ship was named in his honor. The Liberty ship Lou Gehrig was commissioned in 1943. It carried 480 men and 120 vehicles and was involved in Operation Neptune one year later.
The ship landed in Normandy, 13 days after D-Day.
On Lou Gehrig's birthday.
Watson and Caddie Add a Memory
SOURCE : The New York Times
DATE : June 13, 2003, Friday, Late Edition - Final
HEADLINE: Sports of The Times: Watson and Caddie Add a Memory
BYLINE : By DAVE ANDERSON
DATELINE: Olympia Fields, Ill.
INSIDE the scorer's room, 53-year-old Tom Watson was checking his 65 that shared the first-round lead in the 103rd United States Open, but soon his 48-year-old caddie, Bruce Edwards, walked quickly over to where more than a dozen reporters were waiting.
Waiting for him even more than they were waiting for Watson. "The way I talk," Edwards said with his boyish smile, "you want to talk to me?"
His words were slightly slurred. Late last year, Edwards was found to have A.L.S., amyotrophic lateral sclerosis, the neurological illness known as Lou Gehrig's disease. But he has continued to carry Watson's 50-pound golf bag on the Champions Tour, and he trudged with it yesterday in one of the most emotional golfer-and-caddie rounds in Open history.
"The fact that they gave him a spot," Edwards said of Watson's exemption in the Open, "was very special."
And when Edwards was asked what Watson's friendship and financial help -- the annual medical cost of treating his disease is reportedly about $200,000 -- has meant to him, he said, "He's a " and he burst into tears.
"It was very emotional," Watson said later of the round. "We were taking care of business, but he had tears in his eyes and he made me cry."
Edwards, who lives in Ponte Vedra Beach, Fla., with his wife of five months, Marsha, has been Watson's caddie for 30 years, except for the three years when he worked for Greg Norman. "I have so many memories," Edwards said. "This is another major one in my career with him."
This memory may be the best of all, the one that will stay with him when, inevitably, he won't be well enough to carry the golf bag, stir Watson when he's down, calm him when he's angry; to do all the little things that a good caddie does besides suggesting a club or reading a green.
"We turned back the clock," Edwards said of Watson's 65. "We had a blast."
Turned back the clock to all those glorious years when Watson was the world's best golfer, winning the 1982 Open along with five British Opens and two Masters, back to when Edwards, tanned and slim and with that boyish smile, was at his side not only as the best-known caddie, but the best caddie.
"If anything," Edwards was saying now, "the disease I have, what I'm trying to do is show other people to keep going. I don't know when I won't be able to do it any more, but I feel pretty good. I sound like the town drunk but to hell with that. I love what I do. I love working for him."
What had Watson whispered to him as they walked off the final green? "Not bad for old folks, huh?"' Edwards said. "He's 53 going on 24."
Asked if yesterday's 65 rated with Watson's chip-in at Pebble Beach to win the 1982 Open, Edwards said: "It was just a game back then. It's a lot more than a game now."
Not far away, Watson was talking about how, with some 30,000 people affected by A.L.S., medical research has been concentrated on trying to find cures for the millions with cancer and heart disease, to name two illnesses. "In five or ten years," Watson said, "we'll find a cure forA.L.S., but we need the money for research."
Watson acknowledged that Edwards was his inspiration in trying to win this Open at what would be a record age. "Bruce doesn't have a mean bone in his body, " Watson said. "He always has a positive attitude. He stands above most of the caddies out here in how to do his job."
Despite his debilitating illness, which requires him to take some 150 pills a day, Edwards declined to accept the option of using a golf cart in the Open. "I'm doing really well," he said. "My legs are good."
So are his instincts as a caddie. Edwards was at Watson's home outside Kansas City on Monday when they were looking over some of the golf clubs that Watson had used in other years. "He told me to put my old Ping putter in the bag," Watson said.
With that old putter, Watson needed only 23 putts yesterday in his five-under-par 65. That tied his lowest Open round, a 65 in the second round at Olympic outside San Francisco in 1987. But on No. 12, a 458-yard par 4, Watson didn't need to putt.
"When he holed that 6-iron there," Edwards said of Watson's eagle 2, "I said, 'Looky here, we might have something going today.' He never made a bogey after that."
And can Watson keep it up today? "Why not?" Edwards said. "I'm not going to stand here and tell you he can win or he's going to win, but if he keeps his emotions better thanI have and that putting stroke works like it did today, we'll give 'em a go."
It's always been "we" with Tom Watson and Bruce Edwards, but never as much as it was yesterday.
| PUBLICATION: | The Telegram (St. John's) |
| DATE: | 2003.06.14 |
| SECTION: | News |
| PAGE: | A4 |
| SOURCE: | The Western Star |
| BYLINE: | Gary Kean |
| DATELINE: | PASADENA |
Christopher Dennis had his retirement plans all set. He had his house renovated -- and the contractors did a good job putting in new stairs. He had nearly $5,000 tucked away in the kitty for his "retirement quad" all-terrain vehicle.
Everything seemed to be falling into place, but there was one other thing he had that forced the 52-year-old Pasadena resident and his family to reset their priorities.
Last May, the highly active vice-principal of Deer Lake elementary, who loved running, tending to over 60 varieties of roses in his garden and cooking gourmet meals for his family, was diagnosed with amyotrophic lateral sclerosis ( ALS ).
Also known as motor neuron disease, ALS is a rapidly progressive fatal neuromuscular disease. It's characterized by the degeneration of a select group of nerve cells that gradually paralyze the voluntary muscles and eventually affects breathing and swallowing.
In the past year, Dennis has lost 20 pounds of muscle. He had to retire from his job last September.
"The progress for me has been very rapid and there's nothing I can do about it," said Dennis, showing how the muscles in his leg and in between his thumb and index finger have wasted away.
"I can't regain muscle. Exercise does no good. If I lie on my back, I can't breathe. If I sit on the floor, I wouldn't be able to get up unless I could get hold of something to pull myself up.
"I used to cook. Now, I have trouble putting something in the microwave."
The Dennis house has since undergone new renovations. There's a chairlift to help Dennis get up over his new stairs. He has a walker, a wheelchair and rails in the bathroom and bedroom to help him get around. His retirement quad fund has been spent on a scooter to help him get around his garden.
When most people hear ALS , the first thing that comes to mind is Lou Gehrig ' s disease . Beyond the fact this condition ended the great New York Yankees baseball player's career and eventually his life in 1941, most people don't know a whole lot about ALS .
ALS kills two to three Canadians every day. The average lifespan of someone diagnosed with ALS is between two and five years. There is no family history of the disease in 90 per cent of the cases and the number of deaths caused by ALS is more than twice the number caused by cystic fibrosis and multiple sclerosis combined.
While research is being conducted along several fronts, there is no cure for ALS . Dennis did try an experimental treatment, but had to stop after experiencing an allergic reaction to the drug.
His family is coming to grips with the inevitable and there is an undeniably positive aura in the Dennis household.
"We're still very happy people and we find many reasons to laugh," said wife Wanda. "Christopher is a very strong person. I think one of the keys is not to overeducate yourself about ALS .
"We could be off at some clinic, but things work right for us in this house and we have chosen to be happy staying here."
That atmosphere is something that Cheryl Power of Corner Brook, who became president of the provincial chapter of the ALS Society of Canada after the disease claimed her father, picks up on whenever she visits the home.
"I don't know what it is, but I always feel better when I leave here," said Power. "It's like that in most of the homes of ALS patients I visit."
That positive attitude is the epitome of why the ALS Society of Canada chose the cornflower as its emblem. Despite its fragile appearance, the hearty wildflower represents how
people living with ALS tend to show remarkable strength in coping with a devastating disease.
June is ALS Awareness Month in Canada. Today is ALS Flower Day and cornflowers are being sold at various locations to raise money for research.
There are currently 30 people with ALS in Newfoundland and Labrador, but Power said that figure doesn't reflect how common ALS is.
"If everybody who had ALS lived a long time, there'd be an awful lot of ALS patients around, but their lifespan is so short," said Power. "We've had six patients pass away and we have had four new diagnoses this year."
While this is ALS Awareness Month and he encourages everyone to purchase a blue cornflower today, Dennis said the annual ALS walk in September, which raises money to assist people living with ALS , is also very important.
"There's not a darn thing we can do other than make people more aware," he said. "Sixty per cent of the money raised in Newfoundland at the walk in the fall stays here to buy equipment and the walk helps the association continue to buy these things and lend them out.
"We have bought some things ourselves, but there are some people who are not as well off or don't have an insurance plan that would give them things that are very necessary when you're sick."
Dennis would also like to see Ottawa change employment insurance rules so spouses of ALS patients can stay home and avoid the expense of a home-care worker.
"That could take a huge strain off families," he said.
United States: the impact of ADA on employment opportunities for people with disabilities
By Andy Imparato, President and CEO of the American Association of People with Disabilities (Andy Imparato is president and CEO of the American Association of People with Disabilities, a cross-disability membership organization committed to total integration of people with disabilities into all aspects of society. This article was originally published in SCI Life)
On July 26 of this year, we in America celebrated the 10th anniversary of implementation of the employment provisions of the Americans with Disabilities Act. After ten years of civil rights protections in the workplace, what impact has the ADA had?
Some scholars suggest the ADA's impact on the workplace should be measured by the extent of the increase in employment rates among working-age people with disabilities. By this standard, existing data would show that the ADA has had little impact on increased employment rates, at least among those with severe disabilities. Accordingly, they would argue that the employment provisions of the ADA have been a failure.
Another measure of the ADA's impact is the expectations for jobs and careers of young people with disabilities leaving school. Although I am unaware of any quantitative research in this area, I am convinced that the ADA's vision of full participation has had a profound impact on young people with disabilities. They have high expectations, and they are breaking down barriers. For example, I recently had the pleasure of meeting the first Yale Medical School student to complete medical school as a wheelchair user.
Much attention has been given to the line of U.S. Supreme Court decisions that have narrowed the scope of the protected class under ADA and generally made it more difficult for victims of disability discrimination in the workplace to prevail. Some in the disability rights movement have argued that the Supreme Court has "gutted" the employment provisions in the ADA and that what is left provides little protection. Although the Supreme Court has definitely undermined Congressional efforts to ban employment discrimination on the basis of disability, it is important to recognize that disabled workers and job applicants continue to enjoy important rights and continue to use the ADA successfully to challenge discrimination.
Some sub-populations within the disability community have been particularly hard hit by the Supreme Court rulings, including state workers, individuals who are able to function well with medications or other "mitigating measures," people with well-controlled epilepsy, diabetes, depression, and other physical and mental health conditions.
At some point, perhaps very soon, the diverse coalition that passed the ADA will need to reassemble and recruit new allies to fix some of the damage done by the Supreme Court and the lower federal courts. More important, from my perspective, disability advocates and leaders will need to reform the disability benefit and health care systems so that they consistently promote work and economic empowerment.
However, even if these reforms don't occur for years, the ADA has redefined the disability experience in the U.S., and most employers have come to accept the rightful place of disabled individuals within our society. In recent years, I have seen a growing recognition by business of the large disability market, and I believe this recognition is due in large part to the increased political visibility of disabled people and their families that accrued from the effort to pass and implement the ADA.
As Dr. Martin Luther King observed with regard to the civil rights movement, "the greatest victory of this period was... something internal.... The greatness of this period was that we armed ourselves with dignity and self-respect."
[Disability World] A bimonthly web-zine of international disability news and views • Issue no. 14 June-August 2002
2003-2004 RESEARCH FUNDING ANNOUNCED
JULIEN AWARDED CANADA RESEARCH CHAIR
STEM CELL RESEARCH ON MUSCLE REGENERATION
2003-2004 RESEARCH FUNDING ANNOUNCED
Nearly $3.9 million of neuromuscular research funded has been approved for 2003-2004. The partnership between The ALS Society of Canada and Muscular Dystrophy Canada with the support of the Canadian Institutes of Health Research (CIHR) will fund 10 multi-year projects.
Included for funding is the work of Dr. Jean-Pierre Julien, now at the University of Laval, into the role of inflammation in pathogenesis of ALS; Dr. Elizabeth Meiering, of the University of Waterloo, into folding and aggregation of ALS-associated mutant superoxide dismutases and Dr. Janice Robertson