MIAMI MDA ALS CENTER TO OPEN

The 16th MDA center specifically targeted on improving the quality of life for ALS patients and their families will open March 4 at the University of Miami. The Kessenich Family MDA/ALS Center, under the direction of Dr. Walter G. Bradley, will operate within the Department of Neurology at the university's School of Medicine. This is the first MDA/ALS center to be established in Florida.

The center is named for the family of Mark F. Kessenich Jr., a Palm Beach resident who summers in Westhampton, N.Y. Although Kessenich received a diagnosis of ALS about four years ago, he continues to work actively trading government securities -- as he has for the past 34 years. His family's dedicated efforts, including fund-raising initiatives and the establishment of The Kessenich Family MDA/ALS Center Term Endowment Fund, have made the new center possible. In acknowledgment of these outstanding efforts in behalf of the ALS community, Kessenich was elected by MDA's Board of Directors to serve as an MDA national vice president.

Having received treatment at the Eleanor and Lou Gehrig MDA/ALS Center at Columbia Presbyterian Medical Center in New York, Kessenich recognized the need for Floridians with ALS to have the same kind of comprehensive care available at MDA ALS centers in other areas.

Kessenich, an avid golfer, believes in making the best of a given situation, a lesson he learned from the game in which the rule is to "play the ball where it lies." Given the reality of ALS, he decided to make the best of his situation by doing all he could to improve the quality of his life. He'd like to now do that for other patients and their families struggling against the disease.

MDA Senior Vice President and Executive Director Robert Ross said: "The center will be dedicated to providing a multidisciplinary approach to combating ALS through research and support for patients and their families, from the time of diagnosis through the course of the illness. It will advise patients and families about the disease and management of its symptoms, and provide counseling about healthcare decisions; help patients receive expert care in such areas as physical therapy, occupational therapy, speech pathology, communications, respiratory therapy and nutrition; and organize and supervise support groups.

"To have single-handedly provided all this and more for others facing the daunting challenge of ALS identifies Mark Kessenich as a man whose courage is matched only by his generosity," Ross added.

In addition, the center will conduct research and therapeutic trials seeking better treatments or a cure for ALS; serve as liaison for ALS patients with primary physicians, visiting nurse services, hospice care providers, physician specialists, medical consultants and insurance company case managers; and publish a quarterly newsletter and other educational materials.

"In my experience with ALS, I've encountered a number of specialists who have contributed greatly to the quality of my life," Kessenich said. "A major objective of the center is to provide a kind of "one-stop shopping,' where patients can consult a variety of specialists in one setting."

Bradley commented: "We also hope to develop a database, which will provide information and contacts that will be of use to people with ALS and their families, and which would be available through the Internet."

A former MDA research grantee who has overseen the MDA clinic at the university since 1992, Bradley serves as chairman of the Department of Neurology and director of its Neuromuscular Research Division. He's participated in clinical trials for a number of potential therapeutic agents in the treatment of ALS, including CNTF, BDNF and GDNF.

He's also a participant in an international effort to test the substance known as SR57746A, produced by the French company Sanofi Pharmaceuticals. The Sanofi drug may have the potential to stimulate the body's production of various neurotrophic factors.

Bradley will serve as chairperson of the center's advisory board, which will also include Beverly Barry Kessenich, wife of Mark F. Kessenich Jr., and Dr. R. Rodney Howell, chairman of the Department of Pediatrics at the university's School of Medicine and chairman of MDA's Scientific Advisory Committee.

For more information about the center, call Nadine Greenberg, MDA's local health care service coordinator, at (561) 627-5454.

MDA's other ALS centers are:

• The Jerry Lewis MDA/ALS Clinical and Research Center at the University of Southern California School of Medicine in Los Angeles; Dr. W. King Engel, director; (213) 743-1611
  
  
• The MDA/ALS Center at the University of California at Los Angeles; Dr. Michael C. Graves, director; (310) 825-7266; e-mail: mcgraves@ucla.edu
  
  
• The Forbes Norris MDA/ALS Research Center at California Pacific Medical Center in San Francisco; Dr. Robert G. Miller, director; (415) 923-3604; e-mail: rmiller@itsa.ucsf.edu
  
  
• The MDA/ALS Center at the University of Colorado in Denver; Drs. Steven P. Ringel and Hans E. Neville, directors; (303) 315-7221
  
  
• The MDA/ALS Center at Yale University in New Haven, Conn.; Dr. Jonathan M. Goldstein, director; (203) 785-4867; e-mail: jonathan.goldstein@yale.edu
  
  
• The MDA/ALS Center at Emory University School of Medicine in Atlanta; Dr. Jeffrey Rosenfeld, director; (404) 727-3818; e-mail: jr@neuro.emory.edu
  
  
• The MDA/ALS Center at the University of Chicago; Dr. Raymond Roos, director; (312) 702-6390
  
  
• The MDA/ALS Center at Johns Hopkins University in Baltimore; Drs. Daniel B. Drachman and Jeffrey D. Rothstein, directors; (410) 955-6435; e-mail: ddrachm@welchlink.welch.jhu.edu
  
  
• The MDA/ALS Center at Massachusetts General Hospital in Boston; Dr. Robert H. Brown, director; (617) 726-5750; e-mail: brown@helix.mgh.harvard.edu
  
  
• The MDA/ALS Center at Washington University School of Medicine in St. Louis; Dr. Alan Pestronk, director; (314) 362-6981; e-mail: pestronk@kids.wustl.edu
  
  
• The Eleanor and Lou Gehrig MDA/ALS Center at Columbia University in New York; Dr. Lewis P. Rowland, director; (212) 305-8551; e-mail: djl1@columbia.edu
  
  
• The MDA/ALS Center at Duke University Medical Center in Durham, N.C.; Dr. Janice Massey, director; (919) 684-5422
  
  
• The MDA/ALS Center at the University of Texas in Dallas; Drs. Richard J. Barohn and Wilson W. Bryan, directors; (214) 648-6419; e-mail: cbeise@mednet.swmed.edu
  
  
• The MDA/ALS Research and Clinical Center at Baylor College of Medicine in Houston; Dr. Stanley H. Appel, director; (713) 798-4072; e-mail: lappel@bcm.tmc.edu
  
  
• The MDA/ALS Midwest Regional Research Program at the University of Wisconsin in Madison; Dr. Benjamin R. Brooks, director; (608) 263-9057; e-mail: brooks@neurology.wisc.edu

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PROFILE OF A MOTOR NEURON

An Interview with MDA Grantee Heather Durham

Among the most important lines of research in ALS is the question of how and why motor neurons die in this disorder. Motor neurons are nerve cells located in the upper part of the brain (upper motor neurons) and in the brain stem and spinal cord (lower motor neurons).

MDA science writer Margaret Wahl recently talked with neurobiologist Heather Durham of Montreal Neurological Institute, part of McGill University. Durham is working with fellow MDA grantee Denise Figlewicz, a neurobiologist at the University of Rochester (N.Y.), to figure out why motor neurons die and what might save them.

The researchers are using a cell culture model, meaning cells in a laboratory dish. They're adding to their cultures genes for mutant SOD-1, which is known to cause ALS. (People with mutated SOD-1 genes develop ALS.) So far, this is the best laboratory model of ALS, in animals and in culture systems, that researchers have found. They're studying what happens to lower motor neurons with the mutant SOD-1 protein under a variety of conditions and in response to a variety of therapies.

Upper motor neurons transmit messages to lower motor neurons via a chemical neurotransmitter called glutamate. Some drugs, such as riluzole (Rilutek) and gabapentin (Neurontin), partially block glutamate and are thought to have a disease-slowing effect in ALS because of this action. Understanding the effects of glutamate and of glutamate blocking is a line of research being pursued in Durham's lab.

Glutamate affects lower motor neurons only after it "docks" at a glutamate receptor on the surface of the cell. Once this docking has occurred, a channel opens. In some cases, calcium can flow through this channel.

Calcium is vital to many cellular functions, but its concentration has to be tightly controlled. Too much can kill a cell. (Reducing dietary calcium won't control excess calcium's entry into cells. Blood calcium levels stay the same, controlled by hormones that take calcium from the bones if dietary calcium is low.)

Do motor neurons have too much calcium to handle, and does that bring them closer to their "safety threshold" than they would be otherwise? If so, can we do anything about that?

Do motor neurons lack stress-relief proteins that most other cells have in abundance? Can we give them some?

These are among the intriguing questions being asked by Durham and Figlewicz.

HD : What we're trying to do in my lab now is to look at the properties of the motor neuron that might make it more stressed than other cells, make it more vulnerable. We've suspected for a long time that there may be many initiators of a disease like ALS. You may not have to know exactly what all the initiators are. You have to look at what's happening, though, in the context of the cell and its environment. That can be just as important in terms of how that disease progresses and whether the cell lives or not as understanding exactly what started the process.

So, for example, when we put mutated SOD-1 genes into many different types of cells in culture, we see that all these cells are expressing the mutant protein, yet the motor neurons are particularly vulnerable to its presence, just as they are in the organism. Why?

We're trying to understand whether it's the other stresses that the motor neuron has to cope with all the time, or the methods it has at its disposal to protect itself compared with other cells -- in other words, what combination of such factors determines whether it's going to succumb or survive.

MW : Tell us some things that are different about motor neurons compared with other cells.

HD : One of the things we've shown in our culture model, where we have motor neurons that express mutant SOD-1 proteins, is that, if we block the effects of glutamate, the cells don't die. So there's some kind of interaction that's happening there. Many types of neurons have glutamate receptors and receive glutamate signals, so why don't they die as readily as motor neurons? Why don't they die, too? It's clearly not just the glutamate; it's something about motor neurons and glutamate.

We're looking at a number of possible differences in the motor neuron. One is the type of glutamate receptor that motor neurons have versus the kinds other cells have.

In the nervous system, there are basically two kinds of glutamate receptors -- NMDA and non-NMDA receptors. When glutamate "docks" at these receptors, calcium comes through them. We used to think it was only the NMDA receptors that allowed calcium to enter the cell, but now it seems that, in some neurons, including motor neurons, the non-NMDA receptors also open themselves up to calcium ions when they're stimulated by glutamate.

These glutamate receptors are composed of various combinations of proteins, called subunits. Recently, another group published a paper showing that these non-NMDA receptors are composed of various combinations of subunits, and that one subunit in particular determines whether or not the receptor is permeable to calcium. It seems that if this one subunit, called GluR2, is there, and if it has undergone certain processing in the cell, calcium doesn't come through and doesn't get into the cell.

Some studies indicate that motor neurons may be deficient in GluR2 subunits, although that remains controversial. In any case, studies in cultured motor neurons have shown that calcium does enter these cells in some way when non-NMDA glutamate receptors are activated.

MW : So, motor neurons let in more calcium than other cells do?

HD : Yes. And there's another problem with calcium that we're looking at too. Motor neurons may also be deficient in proteins called calcium binding proteins, like calbindin and parvalbumin. These are molecules whose job is to mop up excess calcium. There have been a few papers that show that motor neurons are deficient in these proteins compared with other kinds of neurons.

MW : Anything else, besides calcium, that makes motor neurons particularly vulnerable?

HD : Yes. There are the so-called "stress proteins" that help protect cells against adverse conditions of various kinds. These proteins -- some of which are called "chaperone" proteins and "heat shock" proteins -- help maintain other proteins in their proper shape, or transport them to places in the cell. They aid in the metabolism of abnormal proteins. Cells that are subjected to stress normally increase their synthesis of these stress proteins and for a time become more resistant to further stress, even if it's more severe. Motor neurons may be less efficient than other cells in increasing their expression of these stress proteins.

MW : What kinds of agents do you consider promising to help these relatively vulnerable motor neurons? For example, what about agents that block glutamate, and what about neurotrophic factors?

HD : If we block the glutamate receptors in culture, it protects the neurons. Now, in a culture model, we can block glutamate neurotransmission completely, because we don't have to keep an animal alive. When we did that, it was amazing. The motor neurons lived. I was really quite astonished. We were able to do the same thing with the drug riluzole [Rilutek].

Under these circumstances, however, the transmission of messages from the upper motor neurons in the brain to the lower motor neurons in the spinal cord would be completely blocked. So, as far as the muscle is concerned, it still wouldn't receive any signals. The muscle doesn't care if the motor neurons up above are dead or if they're just not transmitting; either way, the muscle can't contract. Maybe that's why riluzole isn't a wonder drug. By the time you block enough glutamate so that you're saving motor neurons, you're also inhibiting the flow of messages through the motor system. Either way, there's impairment of movement.

As for neurotrophic factors, I don't want to put a wet blanket on this idea, but things haven't turned out as well as people had hoped. They're no magic bullet. The question is why. It could be that there's already enough around and adding more doesn't help. Maybe if we could find a few different ways to support the motor neuron, though, it would make a difference.

MW : What about stopping the cell death program with substances that block apoptosis, the programmed cell death pathways?

HD : The problem is that those pathways get activated because the cell is very stressed. When you block them, you really haven't alleviated these stresses that are getting the cell into trouble. What these experiments accomplish is to inform us of what's happening in the cell, what pathways might be involved. Then we can work backwards to identify the key stresses.

We've looked at Bcl-2, which is one of the substances in this category, and obtained only minimal benefit. Other investigators have found a marginal effect with these in mice, a couple of additional weeks of life, but I don't know if that translates into a couple of years in humans. We just don't know. The cells are still dying.

MW : What substances do you think will be useful leads to therapies? And, how do you foresee delivering them? Is gene therapy in the cards?

HD : We can probably overcome the immunologic problems associated with gene therapy. We're not just stuck with adenoviruses as vectors [delivery vehicles] for gene therapy now.

As to what to put into the vectors -- that's what we're looking at in my lab. We're trying to say, for example, what happens if you give the motor neurons a GluR2 subunit by a gene therapy approach? How would that work?

What happens if we give the motor neuron the calcium-binding protein calbindin?

We also want to look at free radical scavengers, like glutathione, vitamins C and E, and the carboxyfullerenes. The less specific the scavenger, the better. You need scavengers that can work on a lot of different free radicals. [Free radicals are byproducts of many biochemical reactions. They're atoms or molecules that steal electrons from other substances and damage them in the process, and they've been implicated in ALS. Free radical scavengers detoxify free radicals and protect cells.]

And, we have evidence that increased expression of the stress proteins can protect cells from mutant SOD-1. We're investigating ways to increase their expression in motor neurons.

Also, it turns out that the drug FK506 [tacrolimus, Prograf] has another property besides being an immunosuppressant. It has some kind of neuroprotective effect inside the cell that isn't completely understood. So we're asking about these types of molecules, too.

As to the gene therapy approach, the key issues regarding gene therapy in ALS are identifying the appropriate genes to transfer, meaning gene products that are safe and effective; and developing vectors that can deliver the therapeutic gene to motor neurons scattered throughout the spinal cord, brain stem and brain. Viral vectors are very effective in transferring the therapeutic gene into the motor neurons, but getting these vectors to where the motor neurons are located is still a major problem.

MW : Are you optimistic about ALS research?

HD : Yes. What's really important is that now we can generate models in the lab, using mutant SOD-1, that we know for certain have a relationship to ALS in humans. Before the gene defects in ALS were identified, we were kind of spinning our wheels. We didn't know the sequence in which things happened. We didn't know how cells died in ALS. Of course, few people with ALS have the SOD-1 gene defects, but we suspect everybody's motor neurons may die in similar ways, and we're beginning to see how.

If we can create a profile of the motor neuron, identify what the stresses are on the motor neuron and what it needs to protect itself, we can help not only people with genetic forms of ALS; we can help everybody.

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BARRY GOLDBERG DIES

Barry H. Goldberg, a well-known leader of MDA's campaign against ALS, died at his Plano, Texas, home Jan. 5. Goldberg, 51, had received his ALS diagnosis eight years earlier.

Goldberg was known for his sense of humor and sensitivity to others. He became familiar to television audiences nationwide for his appearances on MDA's Jerry Lewis Labor Day Telethon every year beginning in 1991. On the 1997 Telethon, TV personality Leeza Gibbons said she treasured the Energizer bunny that Goldberg had given her as a reminder that he "keeps going and going."

Goldberg was a founding member of MDA's National Task Force on Public Awareness and a one-time member of its steering committee. In addition, he volunteered as a systems operator for the MDA Forum on CompuServe, and communicated with many others affected by ALS.

He also shared his experience by writing motivational articles for a variety of print and electronic media around the world, including MDA's Quest magazine and The ALS Newsletter. He was a featured speaker at MDA's National Development Conference in 1991 and was active in MDA's ALS support group in the Dallas area.

MDA National Chairman Jerry Lewis said, "Though this disease severely limited his time and energy, Barry gave much of his immense talent to help MDA and people with ALS. He was a living example of grace and positive thinking."

Goldberg traveled throughout Texas and Oklahoma speaking to MDA staff, making presentations at fund-raisers and giving media interviews about the importance of MDA's ALS research. In recognition of his voluntary contributions to the Association, he received the J.C. Penney Golden Rule Award.

At the time of his diagnosis, Goldberg was a director of corporate marketing for the SABRE Group, a sister company of American Airlines, based in Fort Worth, Texas. His company provided the equipment necessary for him to work at home, which he continued to do for several years.

Goldberg is survived by his wife, Vickie; daughter, Michelle; and son, Danny, all of Plano; his parents, Jack and Gertrude Goldberg of Los Angeles; and his sister and brother-in-law, Phyllis and Al Brotman of Cypress, Calif.

Memorial donations may be made to the Goldberg Family Fund, P.O. Box 868065, Plano, TX 75086-8065. A portion of the fund will go to MDA for ALS research in Goldberg's name.

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MDA OFFERS PRINT, WEB, VIDEO HELP

MDA's extensive program of services for people affected by ALS and for their families includes a number of publications and other informational materials. The following are available through local MDA offices, the Program Service Department at (800) 572-1717 or on the MDA Web site (www.mda.org).

Newly added in 1997 are:

When a Loved One Has ALS: A Caregiver's Guide: A comprehensive, 94-page, illustrated manual filled with practical advice for meeting the medical, emotional, financial and everyday challenges faced by primary caregivers for people with ALS. The guide contains an extensive list of resources, including books, organizations and Web sites. The primary caregiver for anyone with a diagnosis of ALS who is registered with MDA can receive a copy of the guide free. For others, there's a charge of $10.

MDA's World Wide Web site has been expanded and redesigned. Among its features are: a What's New section with late-breaking MDA news and a zip code directory for locating the nearest MDA offices and clinics. Information about support groups and assistance with a wheelchair purchase is included in the MDA publications section, including The ALS Newsletter, which can also be read on and downloaded from the Web site.

Other MDA publications include:

Facts About Amyotrophic Lateral Sclerosis: A detailed description of the disease's symptoms, causes, treatments and current research. Free.

The ALS Newsletter: A bimonthly publication designed to provide up-to-date news, with a focus on current ALS research. Mailed free to those registered with MDA who have ALS.

Quest: MDA's bimonthly national newsmagazine has in-depth stories about issues involved in living with any of the 40 neuromuscular diseases MDA covers, as well as about Association activities, helpful products and research. Mailed free to those registered with MDA; $12 yearly subscription for others.

With Strength and Courage: Understanding and Living With ALS: A 24-minute video geared for newly identified ALS patients. Hosted by actor Ed Fry, and featuring MDA/ALS Center Director Dr. Stanley H. Appel, the video was produced in 1996 with assistance of Rhone-Poulenc Rorer, maker of Rilutek. It's available for viewing from local MDA offices.

Four publications prepared by the MDA/ALS Center medical team at Baylor College of Medicine are also available through MDA.

Amyotrophic Lateral Sclerosis: A 28-page publication offering details about diagnosis and medical management. Free.

ALS: Maintaining Mobility: A 149-page book written specifically for people with ALS to assist in prolonging muscle function and enhancing independence. $6.

Meals for Easy Swallowing: A 125-page book containing a collection of recipes for easy-to-swallow foods and beverages, as well as suggestions on food preparation and service. $6.

ALS: Maintaining Nutrition: Designed primarily for use by health professionals who care for those with ALS, this 130-page book covers swallowing, diet, alternative feeding methods and tube feeding. $6.

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CLINIC AND ALS CENTER NAMED FOR VICKI APPEL

MDA's clinic and the MDA/ALS Center at the Baylor College of Medicine in Houston were recently renamed in honor of Vicki Appel. A registered nurse and coordinator of the ALS Center at Baylor from 1982 to 1997, Appel was honored for her devotion to helping those affected by ALS and other neuromuscular disorders.

The wife of Dr. Stanley H. Appel, director at MDA's Baylor clinic and the ALS Center, she died in October.

In a Jan. 22 ceremony, representatives from the College of Medicine and MDA officially dedicated the Vicki Appel MDA Neuromuscular Clinic and the Vicki Appel MDA/ALS Center. Speakers included MDA Vice President and actor Ed Fry, MDA

Vice President and Chancellor Emeritus of Baylor College of Medicine Dr. Michael E. DeBakey, and MDA Director of Research and Patient Services Administration Ronald J. Schenkenberger.

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RILUZOLE REPORT CARD

The Quality Standards Subcommittee of the American Academy of Neurology (AAN) has released its consensus statements on the use of riluzole (Rilutek) for ALS.

Riluzole, the only medication approved by the U.S. Food and Drug Administration for the specific treatment of ALS, partially blocks the natural neurotransmitter glutamate. Neurotransmitters are chemical carriers of signals from nerve cells to nerve cells or to other kinds of cells, such as muscle.

Riluzole has been available by prescription since January 1996. The cost of the drug is about $700 per month.

In the September 1997 issue of Neurology, the AAN subcommittee stated the following:

1. Patients taking riluzole still need all the rehabilitation and quality of life assistance that any other patient with ALS needs.

2. Riluzole is not a cure for ALS, but a modest prolongation of survival, which represents a first step in treating ALS.

3. No data exist to help predict how any individual patient will benefit from riluzole treatment. Responses can only be described for broad, general groups of patients.

4.General recommendations for the use of riluzole can be made by dividing ALS patients into three groups -- A, B and C.

For group A patients, the committee found, there is evidence that riluzole may prolong survival. These patients are defined by the following criteria:

a. definite or probable ALS by World Federation of Neurology criteria, with other causes of progressive muscle atrophy excluded

b.symptoms present for less than five years

c. forced vital capacity (amount of air that can be exhaled forcefully after a full breath) at least 60 percent of volume predicted for age, sex, size and other criteria

d. no tracheostomy needed

For group B patients, the committee said, there is no hard evidence to support the use of riluzole. However, the panel concurred that there may be potential benefit for this group. The criteria for group B are as follows:

a.suspected or possible ALS by World Federation of Neurology criteria

b. symptoms present for more than five years

c. forced vital capacity less than 60 percent of predicted volume for age, sex, size and other criteria

d.tracheostomy in place but only for prevention of aspiration; patient not dependent on ventilator

The committee suggested that riluzole is of uncertain benefit for patients in group C.

Criteria defining these patients are:

a. tracheostomy in place for ventilation

b.other incurable, life-threatening disorders present

c. other forms of anterior horn cell (motor neurons in spinal cord) disease present (in other words, diagnosis of ALS is not certain)

The statement didn't address how to proceed when patients "cross the lines" of these groups; for example, if someone has had symptoms present for more than five years but is still without a tracheostomy. While the details are left to the individual patient and physician, the overall implication of the AAN consensus is that, the more severe or advanced the disease, the less benefit riluzole is likely to have.

The statement also implies that, at this time, there is no evidence that riluzole would be effective in disorders other than ALS, even if they involve some of the same nerve cells.

The committee's report goes on to say that "no evidence exists to define the duration of the benefit of continued riluzole use." The report states that "there is no evidence of additional benefit if riluzole were continued after tracheostomy is performed for ventilation."

Several MDA/ALS center directors, including Dr. Robert Brown of Massachusetts General Hospital in Boston, Dr. Lewis P. Rowland of Columbia Presbyterian Medical Center in New York and Dr. Steven Ringel of the University of Colorado Health Sciences Center, gave their input to the committee for preparation of this consensus statement. MDA/ALS Center director Dr. Robert Miller of California Pacific Medical Center was a member of the subcommittee.

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ALS RESEARCH AND TREATMENT BILL NEEDS SUPPORT

The Amyotrophic Lateral Sclerosis Research, Treatment and Assistance Act of 1997, introduced in the House of Representatives in June, is still awaiting hearings in two House subcommittees.

Since the Oct. 28 death of Rep. Walter H. Capps, D-Calif., co-sponsor Benjamin Gilman, R-N.Y., has become the bill's primary sponsor. A total of 76 House members have signed on as sponsors. Capps died unexpectedly of a heart attack.

Among other provisions, the act, H.R. 2009, would amend the Social Security Act to waive the 24-month waiting period for Medicare eligibility on the basis of disability for those with ALS. Under current regulations, people under age 65 with disabilities are eligible for Social Security Disability Insurance after a five-month waiting period, and then for Medicare after another 24 months.

The bill would also provide Medicare coverage for outpatient drugs and therapies for ALS. In addition, it would double federal funding for ALS research to $25 million in 1998.

The bill was referred on June 26 to the Commerce Committee's Subcommittee on Health and Environ-ment and the Ways and Means Committee's Subcommittee on Health. No action had been scheduled by either committee as of press time.

Increasing the number of the bill's sponsors could speed action on it. You can write or call your congressional representative and ask him or her to sign on as a sponsor of H.R. 2009. Succinctly explain how the bill would benefit you and how ALS has affected your life. Letters from caregivers and others will also have an impact. A couple of weeks after you've sent a letter, make a follow-up phone call.

The address is: (Name of Representative), House of Representatives, Washington, DC 20515. You can also write to your representative's local office, or get the exact office address and phone number from either of two congressional Web sites: www.house.gov or thomas.loc.gov.

Supporters can also call or write members of the Commerce Committee at (202) 225-2927, or the Ways and Means Committee at (202) 225-3625, to urge them to schedule hearings. Names of committee members are available on the Web sites or by calling the Legislative Resource Center at (202) 226-5200.

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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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EVERYTHING YOU ALWAYS WANTED TO KNOW

(and maybe some things you didn't) is in a new book, Amyotrophic Lateral Sclerosis, by Drs. Hiroshi Mitsumoto, David Chad and Erik Pioro, 1998. 480 pages, $140. F.A. Davis Company, 404-420 N. Second St., Philadelphia, PA 19123; phone (215) 440-3001; fax (215) 440-3016.

It would be hard to imagine a more comprehensive book on ALS than this one. It covers everything from the basic anatomy and physiology necessary to understanding the disorder, to the latest theories about how nerve cells live and die, to the latest experimental treatments, right up to last year's news. (In fact, the publisher also sent an additional update in August to everyone who purchased the book after Aug. 15.)

The chapters about daily living, including problem solving with respect to communication, nutrition and mobility, are as excellent as the "hard science" chapters, as is the chapter on medical economics, ethics and legal issues.

The book is directed at doctors and other health professionals but is well written and, with the aid of a medical dictionary and perhaps some other basic reference books, it can be understood by the educated reader.

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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
National Headquarters
3300 East Sunrise Drive
Tucson, Arizona 85718-3208

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