MDA GRANTEE HAS HIGH-SPEED PLAN FOR FINDING ALS THERAPIES

Ralph Kuncl

"There's been a lot of poison in the air about neurotrophic factors," says neurologist and neuroscientist Ralph Kuncl, an MDA grantee at Johns Hopkins University Medical Center in Baltimore. "And that's too bad, because I think that, hidden in this group, are some of the most potent agents we have."

The question for Kuncl and other researchers is how to find them and use them as therapeutic agents in ALS.

Kuncl believes in the future of neurotrophic factors, proteins produced by the body in or near nerve cells (neurons) that help keep these cells alive under a variety of adverse conditions, including disease, injury and a natural "pruning" process that occurs during embryonic development.

He leads a team that's testing new neurotrophic factors and has had success with two new ones -- PEDF (pigment epithelium-derived factor) and neurturin. Kuncl has also developed some new ways of testing the effectiveness of existing neurotrophic factors.

Neurotrophic factors have been important in research on ALS and other neurodegenerative diseases for several years. But results in clinical trials haven't lived up to expectations derived from laboratory models.

Part of the reason, in Kuncl's view, is the inadequacy of these laboratory models in predicting what will actually happen when neurotrophic factors are tried in people.

A Realistic Environment

One way to study a substance for its effects on cells is to apply it to the cells (for example, to motor neurons, which are the muscle-controlling nerve cells lost in ALS) in a laboratory dish -- a "cell culture model" or "cell culture system." Neurons in a laboratory culture can be injured by a variety of toxins and then given various substances to see how well they "rescue" the neurons from the damaging agent.

This method, Kuncl says, has its limitations. Cells in culture are like fish out of water; they don't live very long and outside their natural environment their behavior isn't necessarily usual for them. Because of their short life span, cells in a culture dish can't be used to study chronic conditions like ALS, where damage occurs slowly over time.

Other scientists study cells in animal models of a disease. Mouse models of ALS include the SOD1 transgenic mouse, which has a genetic mutation known to cause ALS in humans, and the wobbler mouse, which has a genetic mutation that produces a disease resembling ALS.

But intact animals also have their limitations, Kuncl points out. Even with state-of-the-art imaging techniques, it's impossible to see everything that's going on at the cellular level inside a live animal. And, as with humans, there are so many biochemical processes going on at once inside the animal that it's difficult to sort out what's causing what. It's also hard to say whether the animal has the same disease that human patients do.

About seven years ago, Kuncl's group at Johns Hopkins developed an "organotypic" model for studying neurodegenerative diseases. The system consists of thick slices of the spinal cords of rats, including all the connections between the neurons and their supporting cells, the glia. Investigators can manipulate the cells with different damaging agents (for example, exposing them to too much glutamate, which is almost certainly a factor in many cases of human ALS).

This approach "provides you with an environment in which motor neurons normally live and that's much more like real life," Kuncl says.

Proof is in the Pudding

Kuncl admits that his claims are theoretical. Proof will depend on finding a correlation between his organotypic model and results of clinical trials on humans.

Kuncl believes that, if you subtract for the "delivery factor" (the difficulty of delivering neurotrophic factors to the motor neurons in animals or humans), the results seen in his organotypic model pretty well match what you see in clinical trials of neurotrophic factors.

That correlation indicates that the substances tested in his model have promising neuron preservation capabilities, he says. If scientists are sure a drug can rescue cells if it can reach them, it's worthwhile developing a good delivery system and testing it in humans, an effort that can cost millions of dollars and years of time.

"By any systemic administration, you're counting on the nerve terminals down in the muscle to gobble up this stuff and transport a small fraction of it up [to the neuron]," Kuncl says. "In order to do that, you have to give massive amounts, which is both costly and risky, leading to systemic side effects, such as occurred in the CNTF [ciliary neurotrophic factor] trial, and production of antibodies, which could diminish the [therapeutic] effect."

One way to get around the delivery stumbling block would be to implant genes for a neurotrophic factor at spots where they're likely to be able to get the factor to the motor neurons, Kuncl says. Another method would be "to implant the factors or their genetic machinery in a wafer or resin that would continually leak it out into the nervous system."

Kuncl says implanting such substances near the spinal cord would probably be effective because "most of the disability in ALS is lower motor neuron, which is spinal cord, and most of the chance for reversibility by protecting motor neurons and enhancing sprouting [growth of extensions from the neurons] is at the lower motor neuron."

New Factors in the Pipeline

Kuncl's team published its PEDF results in the July issue of the Journal of Neuropathology and Experimental Neurology and its neurturin results in the May issue of Molecular and Cellular Neuroscience.

Either of these substances used alone in the organotypic culture model led to "virtually 100 percent survival over a course of two months," Kuncl says, under neuron-damaging conditions "when otherwise half the motor neurons or more would have been gone."

When two such factors are combined, the results can be "even more spectacular," he says.

Kuncl is particularly enthusiastic about PEDF because it may have certain advantages over other existing factors.

For one thing, its effects aren't limited to its success as a neurotrophic factor. Recent research has uncovered a potential role for PEDF in preventing blindness in common conditions in which too many blood vessels grow in the retina or other parts of the eye. This fortuitous finding may make PEDF a hot commodity for drug companies because of its potentially broad commercial uses.

Another advantage of PEDF is the small size of some of its active parts.

Their size, Kuncl says, will make administration easier, whether a gene therapy or a drug therapy approach is used. Small molecules are much more likely to cross natural barriers and enter the nervous system, even if they're administered systemically, he says.

Kuncl is careful to say that the discovery of PEDF and neurturin as potential drugs for ALS is still a long way from the clinic. "This discovery with PEDF allows it to enter the pipeline," he says, "but the pipeline is long." 

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WHAT EVER HAPPENED TO MYOTROPHIN?

Myotrophin, a drug based on the neurotrophic factor IGF-1 (insulin-like growth factor 1), has been a source of controversy for more than three years, ever since it first went before a Food and Drug Administration advisory panel in June 1996 and then again in May 1997. Two companies, Cephalon of West Chester, Pa., and Chiron of Emeryville, Calif., developed Myotrophin and sought approval to market it for the treatment of ALS.

The controversy stems from a discrepancy in the results of two large clinical trials conducted to test the safety and effectiveness of Myotrophin, one in the United States and the other in Europe. The U.S. trial passed tests on both counts, but the European trial failed to demonstrate effectiveness, according to an FDA advisory panel.

Protests from the ALS community followed the denial of approval for Myotrophin, with lively discussions on the Internet and a spot on NBC's "Dateline," which aired in July 1997.

"POTENTIALLY APPROVABLE"

In May 1998, Cephalon received a letter from the FDA stating that Myotrophin was "potentially approvable," contingent upon the submission of additional information from ongoing studies that would demonstrate to the FDA's satisfaction that Myotrophin is safe and effective as an ALS treatment. At the time, no such information appeared.

But, says Sandra Menta, manager of corporate communications at Cephalon, that information could be available soon. "An additional source of clinical data may be available through Cephalon's partner in Japan, Kyowa Hakko Kogyo Co., which is conducting a clinical study of Myotrophin in ALS patients in that country. The results of that trial may be available later this year."

Meanwhile, investors in Cephalon stock who filed a class-action suit saying they were deceived by early, rosy reports about Myotrophin's performance in the European trial, have reached a $17 million settlement with the company.

"This settlement and the underlying case does not affect the FDA review of Myotrophin," Menta says. "In light of the settlement, on July 30, 1999, the court granted a final order dismissing the case." Menta refers those with questions about the settlement to the claims administrator at (800) 475-4699.

STAY TUNED

For those interested in other information about Myotrophin, Menta advises calling the company's Medical Information Department at (800) 896-5855.

An older information number, (800) 896-5855, is also still in operation and can offer help to people taking Myotrophin under Cephalon's expanded access program, a plan under which people with ALS can obtain the still-unapproved Myotrophin free of charge. The program is not accepting new participants but will continue to serve those already enrolled, Menta says. She estimates that some 200 people with ALS are now receiving Myotrophin through this program. 

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MARYLAND MAN WITH ALS TO APPEAR ON TELETHON

Glenn Harwood, 59, of Crofton, Md., will be the subject of a special profile scheduled to run on the Jerry Lewis MDA Telethon, which airs for 21½ hours Sept. 5-6.

Harwood, who has ALS, will also appear in person on the program with his wife, Fran, to talk about the effect ALS has had on their lives.

Harwood received his ALS diagnosis in 1994, although symptoms started as early as 1990. Despite the need to use a power wheelchair and loss of his vocal powers, Harwood maintains an active lifestyle and an upbeat attitude about life.

Harwood uses a variety of devices -- some low-tech (a pad and pen), and some high-tech (EZ Keys by Word Plus and the DEC Express synthesizer) -- so that he can continue to communicate. E-mail is another tool he uses to express his thoughts. (His e-mail address is harwood@ccconline.net.)

"Attitude is very important," Harwood says. "A 'can do' attitude followed by a 'will do' attitude -- this is a one-two punch that is unbeatable."

In the video profile, Harwood uses the voice synthesis technology to talk about his passion for golf, bicycling and work. He says his abilities, not his enthusiasm, have been affected by the disease.

Video footage shows Harwood in his wheelchair commuting by bus and train to his job at the U.S. Small Business Administration, a federal bureau that provides financial, technical and management assistance to help Americans start, run and expand their businesses.

Harwood, once a commander in the Coast Guard, is determined to remain active and believes that MDA-funded research will lead to new and better treatments for ALS. He's participated in several clinical trials for potential ALS treatments.

"There is always hope, and no room for despair," Harwood says in the video segment via his speech synthesizer.

Four years ago, for his 55th birthday, Harwood asked that, in lieu of gifts, his friends make donations to MDA designated to support ALS research. He has repeated the request every year since. The Fifth Annual Glenn Harwood/MDA Celebration, commemorating Harwood's 59th birthday on Aug. 11, took place recently. Once the funds are counted, Harwood hopes to top the $30,000 mark for total funds raised for MDA over the years.

In March, Harwood's voice synthesis device allowed him to testify before the Maryland Legislature in favor of an assistive technology loan program. Funding for the program was approved in large part due to the eloquence of Harwood's testimony.

"Glenn Harwood is an amazing man who refuses to let his positive outlook be dampened by the destructive and progressive effects of ALS," MDA National Chairman and Telethon star Jerry Lewis says. "I'm pleased that the Harwoods have agreed to help convey to our viewers in a very personal way the importance of our efforts to defeat this disease."

Harwood cites religious faith and the support of family and friends as being responsible for his positive mental stance. He gives special credit to his wife for helping him to remain upbeat.

"Last, but not least, you must have and maintain a sense of humor," Harwood says. "I carry a couple of jokes with me at all times and share them with all who stop to talk to me. My motto is 'Can't Walk Or Talk, But Can Always Laugh.'"

The Telethon, which originates from CBS Television City in Hollywood, supports MDA's programs of research and services for people with any of 40 neuromuscular diseases, including ALS. The Telethon often features reports about living with ALS and provides updates on ALS research.

The Telethon can also be seen live through streaming video at MDA's Web site, www.mda.org. 

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GENE THERAPY FOR ALS?

One of the strategies that's been tried to prevent the loss of motor neurons (nerve cells that activate muscles) that occurs in ALS is to make the cells "hardier" by giving them human neurotrophic, or "growth," factors like BDNF (brain-derived neurotrophic factor). Although neurotrophic factors don't attack the underlying problem that causes motor neurons to die, they may help the cells stay alive for longer, and some researchers think that their effects are strong enough to make a real difference in the course of the disease.

A better way to deliver therapeutic growth factors to motor neurons? Immature muscle cells (myoblasts) are infected with a modified virus carrying the gene for GDNF. The infected myoblasts are injected into the muscles of mice with a hereditary form of ALS. The injected cells fuse with existing muscle cells and begin producing and secreting GDNF, which is taken up by the endings of nerve fibers. GDNF is then transported through the nerve cell to the nerve cell body, where it helps to keep the cell alive.

So far, however, the results of clinical trials in humans using various neurotrophic factors, including BDNF, CNTF (ciliary neurotrophic factor) and GDNF (glial-derived neurotrophic factor), haven't lived up to their promise. Researchers suspect that results thus far have been disappointing, at least in part, because motor neurons live in a very protected environment in the body and it's hard to deliver neurotrophic factors to those areas. It's for this reason that BDNF is being administered in one ongoing clinical trial "intrathecally," or directly into the spinal fluid.

Another potential way of delivering neurotrophic factors is to take advantage of the fact that the barrier that protects the nervous system is absent where nerve cell endings contact muscle cells. The idea is that the nerve fibers may able to act like straws, slurping up neurotrophic factors from around the muscles they innervate, and transporting these factors back to the cell bodies in the spinal cord.

Now, a group of researchers led by Martha Bohn of Northwestern University Medical School in Chicago has taken this idea even further by using gene therapy to boost the production of GDNF in the muscles of mice with ALS. They were able to do this by harvesting a special kind of primitive muscle cell, called a "myoblast," from newborn mice. They infected these myoblasts with a genetically altered virus that carries the gene for GDNF, then injected the modified myoblasts back into the muscles of mice with a familial form of ALS. The modified myoblasts then began producing GDNF in the muscle, where it could be soaked up by the endings of motor neurons.

The researchers were able to show that the mice treated with GDNF gene therapy retained specific motor neurons and physical skills longer than their untreated littermates. These results are difficult to compare with the results obtained from studies with other compounds, such as creatine and riluzole, because the researchers didn't measure the effect of the therapy on survival and used a different technique for counting motor neurons than was used in those other studies. The findings were published in the July issue of Human Gene Therapy.

The researchers suggest that this approach would ultimately be easier and safer to perform in humans than delivering neurotrophic factors directly to the spinal fluid, as in the intrathecal BDNF trial. Transplanting genetically modified muscle cells, however, brings its own set of safety issues.

First, the immune system has a tendency to reject foreign cells -- this is the reason that organ donors must be so carefully matched with recipients. Thus, this type of treatment may ultimately require carefully matched donors to avoid rejection of the transplanted cells. To date, myoblast transfer hasn't been successful in humans because the transplanted cells tend disappear after a few weeks, even with carefully matched donors.

Second, the presence of viral proteins or even the therapeutic GDNF protein in the transplanted cells may trigger unwanted attention from the immune system. Even though GDNF is a normal body protein, when it's found in abnormal body locations or in abnormal amounts, the immune system may treat it as if it were a "foreign" protein. At best, the transplanted cells may merely be eliminated. At worst, the immune system may develop antibodies to GDNF or the delivery virus and prevent future gene therapy treatments.

Despite these potential problems with using gene therapy and transplanted cells to deliver neurotrophic factors to treat ALS in humans, the Bohn study represents a good preliminary start at identifying and working out these problems.

Other researchers funded by MDA are studying ways to put genes for neurotrophic factors directly into neurons, and still others are studying ways to avoid triggering immune reactions against the delivery viruses and their therapeutic genes.

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MAKING THE MOST OF YOUR MDA CLINIC EXPERIENCE -- HAVE YOU TRIED OCCUPATIONAL THERAPY?

What comes to mind when you think of "occupational therapy"? Making stuffed animals? Weaving baskets? If you think of occupational therapy as "just diversion" or "busywork," you're not alone -- but you're wrong.

Today's occupational therapists are highly skilled professionals whose job it is to help people who have impairments in their ability to perform an occupation -- whether that means a profession or other work-related role, hobby, special skill or simply taking care of activities of daily living -- to regain that ability using whatever adaptations are necessary.

Unfortunately, in ALS, referrals to occupational therapy aren't always made, or may be made too late, says Glen Gillen, senior occupational therapist at Columbia-Presbyterian Medical Center in New York.

"A lot of times, we're missing the window of opportunity where people could have maintained function," Gillen says. "By the time we get them, there's little they can do and they've missed out on a lot of activity that could have been important to them."

When people ask Gillen, "When is a good time to order occupational therapy?" he tells them, "If the patient has complaints that they can't do a certain thing, an activity that they could do before, and they have an interest in regaining that, that's a good time to call in an occupational therapist. Usually, our interventions are a couple of sessions at different times throughout the disease progression."

Gillen cites two recent examples in which occupational therapy has been helpful in clients with ALS.

"I had a patient recently who had ALS and was ventilator-dependent, and she wanted to be able to suction herself," Gillen recalls. "She didn't have the upper extremity control to do that, and it was annoying and painful to her to have her home health aide do her suctioning. She thought she was rough."

Gillen was able to modify the patient's suctioning technique and apparatus so that she was able to suction herself.

"I saw someone else recently who wanted to have more control over his environment -- the television, radio and some lighting -- and he couldn't get around," Gillen says.

"I purchased for him a simple environmental control unit that cost $30 at Radio Shack, and he was able to turn things on and off in the whole room. He did a fan, he did lighting, he did TV and radio. So with a simple intervention and the right setup, he had full mastery of his environment."

Most MDA clinics and ALS centers can refer you to occupational therapists, so don't hesitate to ask your doctor or nurse practitioner to make the referral. 

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JAMES KELLER DIES

James Keller, the award-winning college baseball coach from Austin, Texas, died in July after a six-year battle against ALS.

Keller was a celebrated and beloved figure not only to the young athletes he coached before ALS caused his early retirement from Concordia Lutheran College in Austin, but also to the many people who heard him speak about ALS through his appearances on the national broadcast of the Jerry Lewis MDA Telethon.

He received his ALS diagnosis late in 1992. Keller and his wife, Caroline, immediately began to read up on ALS research. Keller, a charismatic speaker, began to make public appearances on behalf of MDA, and then was featured in a special video profile on the national broadcast of the 1993 Telethon.

Via the profile, Telethon audiences were introduced to a handsome, athletic man with a sharp intelligence and innate decency, who was equally comfortable hitting balls to his young players out on the field or romping with his young sons in his backyard.

At the time, the effects of ALS were hardly noticeable. Keller proved himself an accomplished spokesperson for MDA. He appeared on the cover of the 1994 Labor Day weekend issue of Parade magazine, which included a story about his battle against ALS and his role on the Telethon.

In subsequent appearances on the Telethon, it was clear that ALS had begun to take its toll on Keller. Yet he remained unfailingly positive and spoke often of the faith he had in work being done by MDA-funded researchers to defeat ALS.

"We're making progress. It's like a puzzle," Keller said on one Telethon. "You put a couple of pieces together, the next piece is easier to put in there. We're making a lot of progress."

Keller began using a wheelchair and a feeding tube. His sister, Brenda Keller Spiker, said, "James displayed his courage as he continued to coach, no longer from the coach's box but from a wheelchair in the dugout, using a voice synthesized computer operated by his toes.

"The lessons he taught his athletes will affect their entire lives," said Spiker, who herself became a member of the MDA family and works as an MDA district director in Austin.

By 1997, Keller's ALS progression forced him to retire as baseball coach at Concordia. At his retirement ceremony on May 3, Keller received an unusual honor. His Number 19 coaching jersey was permanently retired from play. It was the kind of tribute usually reserved for baseball legends such as Lou Gehrig. For Keller, it seemed entirely fitting. Keller proudly attended the ceremony in his wheelchair, with sons Wesley and Louis at his side.

Keller received further tribute when the Greater Austin Sports Foundation created the James Keller Award to honor other distinguished athletes.

Keller's death in July was a cause for sadness for the many who had been inspired by his singular example of bravery and service to others.

"During his battle with ALS, Coach Keller was the embodiment of personal dignity and courage," MDA National Chairman Jerry Lewis said. "He loved baseball, and he loved instilling the qualities of sportsmanship and decency into the young men he coached. He was also truly gifted at speaking about ALS and impressing upon people the urgent necessity of defeating this terrible disease."

"He was a true gentleman," said MDA Senior Vice President and Executive Director Robert Ross of Keller. "It was a distinct honor to have had this remarkable man as part of our MDA family." 

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HELP FIGHT ALS TODAY AND TOMORROW

Many people who know the devastating effects of ALS are providing lasting support for MDA's battle against the disease. Through your will, you can designate a gift to MDA earmarked to support ALS research or services.

Bequests to MDA can be made with cash, securities, real estate, or other property. You can bequeath a percentage of the entire estate to MDA or make a bequest of the residue, donating property remaining after all bequests to family and others have been satisfied. You may also name a memorial gift in honor of a family or individual.

To give what remains of your estate after other bequests have been satisfied, just include the following language in your will:

"I give, devise and bequeath all (or a specified fraction of) the rest, residue and remainder of my estate, whether real or personal, of every kind and description, and wherever situated, to Muscular Dystrophy Association Inc., a New York not-for-profit corporation having its principal office at 3300 East Sunrise Drive, Tucson, Arizona, 85718-3208, for its program of research and services related to amyotrophic lateral sclerosis."

To give a dollar amount or percentage of your estate:

"I give, devise and bequeath the sum of $________ (or ________ percent of my estate) to Muscular Dystrophy Association Inc., a New York not-for-profit corporation having its principal office at 3300 East Sunrise Drive, Tucson, Arizona, 85718-3208, for its program of research and services related to amyotrophic lateral sclerosis."

Your attorney or financial adviser can help you work out the details of a bequest to MDA's ALS program. For more information, call MDA's Planned Giving Department at (800) 572-1717. 

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GENETIC PREDISPOSITION TO GULF WAR SYNDROME FOUND
Experts Want to Look at ALS in Vets

Robert Haley of the University of Texas Southwestern Medical Center in Dallas, along with Scott Billecke and Bert la Du of the University of Michigan in Ann Arbor, recently reported that the activity of an enzyme involved in detoxifying chemicals such as sarin nerve gas is lower in veterans affected by Gulf War syndrome.

Gulf War syndrome is the name given to a broad group of medical problems experienced by some members of the U.S. military who served in the 1991 Persian Gulf War.

The finding indicates that some people may have a genetic predisposition to serious illnesses, including ALS, that could be triggered by exposure to those chemicals.

The enzyme in question, called PON1 type Q, normally acts in the blood to break down a category of chemicals called organophosphates that are found in some pesticides, such as DEET, and in sarin nerve gas. These chemicals were used during the Gulf War.

The researchers found that veterans with Gulf War syndrome were less likely to have the gene for one type of PON1 type Q than Gulf War vets who are well. The finding appeared in the July issue of Toxicology and Applied Pharmacology.

Now, Haley, who has been in contact with the families of Gulf War vets who have ALS, is asking whether there might be a connection between the lack of PON1 type Q and ALS. Haley has also correlated specific changes in brain structures with Gulf War syndrome and would like to see whether Gulf War vets with ALS also show these changes.

Haley said he'd like any Gulf War veterans who've been told they might have ALS to call him about possible participation in a study that involves both sick and well Gulf War vets.

Haley also wants to collect an accurate roster of Gulf War vets with ALS to determine whether the number is higher than the national rate for men in the same age groups. Haley can be reached at (214) 648-3110. 

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TWO QUEST STORIES HAVE ALS FOCUS

Two articles in the August issue of Quest, MDA's bimonthly national magazine, may be of special interest to readers affected by ALS.

The magazine, which subscribers will receive in late August, contains stories about dysphagia and communications technology, both written by MDA Senior Writer Phil Ivory.

The dysphagia article describes problems with swallowing that can occur in neuromuscular disorders, including ALS. The story describes treatment options for dysphagia, ranging from lip and tongue exercises to food modifications to surgery. It also lists resources for more information.

"Voice of Tomorrow" describes technological solutions that help people write or speak, including software and specialized equipment.

The current issue of Quest also contains a preview of the Jerry Lewis MDA Telethon, which will be broadcast worldwide Sept. 5-6. See "Maryland Man".

Anyone with ALS who is registered with MDA should be receiving a free subscription to Quest. Others can subscribe at a cost of $12 per year. A subscription form is available on this Web site, or for questions, call MDA's Publications Department at (520) 529-2000. 

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MDA OPENS ALS CENTER IN SYRACUSE

A new MDA/ALS center at the State University of New York Health Sciences Center in Syracuse brings to 19 the number of the Association's multidisciplinary centers devoted to ALS care and research.

The new center is under the direction of Jeremy M. Shefner. MDA also maintains a clinic at SUNY in Syracuse for treatment of all 40 neuromuscular diseases.

The new MDA/ALS center is located in the Department of Neurology, 750 E. Adams St.; telephone (315) 464-4627. For further information, call Kristen Clogg, MDA's Syracuse program service coordinator, at (315) 451-8417.

In New York, Hiroshi Mitsumoto has been named director of the Eleanor and Lou Gehrig MDA/ALS Center at Columbia University, following the retirement of Lewis P. Rowland in September. Mitsumoto, an international authority on ALS, will also head the ALS and Muscle Disease Division at the Neurological Institute at New York Presbyterian Hospital.

Rowland, a national MDA vice president, will continue in private practice and will remain involved in clinical trials at the Gehrig center after his retirement.

MDA/ALS centers offer highly focused programs of research and medical management directed at combating ALS (complete list of MDA/ALS centers).

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KUDOS FOR MDA'S ALS PROGRAM

The following letters were sent to Quest, MDA's national magazine. Robert Ross, MDA senior vice president & executive director, wanted to share them with readers of The ALS Newsletter as well. 

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DO YOU HAVE MDA'S CAREGIVER'S GUIDE?

To assist families affected by ALS, MDA offers "When a Loved One Has ALS: A Caregiver's Guide." This 94-page manual is filled with helpful advice for all family members.

If your family doesn't have a caregiver's guide, ask the health care service coordinator at your local MDA office for one. Anyone with a diagnosis of ALS who's registered with MDA can receive the book free.

Other MDA publications on ALS are also available through your local MDA office and on ALS Web site.

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The Association welcomes gifts for ALS research honoring significant occasions of achievement. These gifts may be made in tribute to special people or to mark such events as anniversaries, birthdays, weddings, graduations or retirements.

THE ALS NEWSLETTER
Muscular Dystrophy Association
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Tucson, Arizona 85718-3208

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