Date: Thu, 3 Nov 94 10:34:32 EST From: Bob Broedel To: Stuart.Neilson@brunel.ac.uk Subject: Re: ALS Interest Group List =============================================================== == == == ----------- ALS Interest Group ----------- == == ALS Digest (#121, 26 August 1994) == == == == ------ Amyotrophic Lateral Sclerosis (ALS) == == ------ Motor Neurone Disease (MND) == == ------ Lou Gehrig's disease == == ----- == == This e-mail list has been set up to serve the world-wide == == ALS community. That is, ALS patients, ALS researchers, == == ALS support/discussion groups, ALS clinics, etc. Others == == are welcome (and invited) to join. Currently there are == == 310+ subscribers. == == == == To subscribe, to unsubscribe, to contribute notes, == == etc. to ALS Digest, please send e-mail to: == == bro@huey.met.fsu.edu (Bob Broedel) == == Sorry, but this is *not* a LISTSERV setup. == == == == Bob Broedel; P.O. Box 20049; Tallahassee, FL 32316 USA == =============================================================== CONTENTS OF THIS ISSUE: 1 .. Editorial - Thanks 2 .. Questions about Riluzole trial 3 .. Neurontin 4 .. IGF-1 5 .. re: Riluzole 6 .. re: Riluzole - 2 7 .. re: Intravenis Vitamin C and ALS 8 .. Remacemide 9 .. ALS/SOD mice 10 . conference announcement (1) ===== Editorial - Thanks ========== Thanks to Kathy Goeddel (Kathy=Goeddel%CGG%InfoSys@banyan.BV.TEK.COM) for posting a message to the Prodigy system's ALS BBS that informed them of the ALS Interest Group. To join the Prodigy system, interested folk should call Prodigy Customer Service at 1-800-PRODIGY. Thanks to John Bartels (71170.464@compuserve.com) for discovering the CUTTING EDGE article that was sent out as ALS Digest 117. (2) ===== Questions about Riluzole trial ========== >From : BWRAYNSTRM@aol.com X-Mailer: America Online Mailer Date : Mon, 22 Aug 94 16:24:28 EDT Subject : Questions about Riluzole trial To All, I am participating in the Riluzole trial. After 11 months, I feel my progression rate has not changed. Can anyone report on his/her experience with the trial? I've heard conflicting reports about the release of Riluzole for "compassionate use". Does anyone know if "compassionate use" is a real possibility for the near future? (3) ===== Neurontin ========== >From : SadieJanie@aol.com X-Mailer: America Online Mailer Date : Wed, 24 Aug 94 21:21:18 EDT Subject : Neurontin My mother in law was diagnosed one year ago with bulbar ALS. Two days ago she was put on Neurontin. Has anyone had any experience with this drug? If so, how long has the patient been taking it? Any positive results? Negatives? Any differences in speech and/or swallowing? We heard that someone in Florida showed a remarkable recovery in regaining speech and eating abilities. This news came via Prodigy. Anyone with any info at all, please e-mail me. Thanks in advance! (4) ===== IGF-1 ========== >From : Teach21@aol.com X-Mailer: America Online Mailer Date : Mon, 22 Aug 94 10:38:51 EDT Subject : IGF-1 I am interested in learning more about IGF-1, the experimental treatment for ALS. Any information about success, side effects, and dosages would be very much appreciated. My father has ALS and we are investigating all possible treatments. Thank you in advance, Teach21@aol.com (5) ===== re: Riluzole ========== Date : Mon, 22 Aug 94 10:13:35 EST >From : "Mike Doliton" To : "Dr. Kenneth Fischbeck" , : als@huey.met.fsu.edu Subject: Re: Riluzole Dr. Fischbeck, I read about the study in March 1994. My problem is my voice and swallowing are deteriorating and by the time Riluzole gets on the market it would be too late to do any good. I'm trying to avoid the feeding tube. I missed the trials by 1 week. They closed the trials just when I found out about them. I have so much anger for Rhone-Poulenc Rorer. I asked them if they could add just one more person to their trial and they refused. I'm trying Neurontin like many others are. I heard it was a glutamate blocker like Riluzole thru Dr. Munsat in Boston. Do you have any comments about glutamate blockers and Neurontin. Neurontin was originally a anti-convulsive drug. Thanks for your taking the time to write to us. Regards, Michael Doliton Sony Medical Systems (6) ===== re: Riluzole - 2 ========== Date : Mon, 22 Aug 94 15:33:01 -0400 >From : "Dr. Kenneth Fischbeck" To : "Mike Doliton" Cc : "Dr. Kenneth Fischbeck" , : als@huey.met.fsu.edu Subject: Re: Riluzole Mr. Doliton: Sorry to hear about your situation. I agree that it is not too cool of Rhone-Poulenc Rorer to come out with an encouraging preliminary trial and then not be able to accomodate patients like yourself in further studies. A good contact for information about glutamate blockers in ALS is Dr. Jeff Rothstein at Johns Hopkins. Also, Dr. Munsat is highly experienced with ALS therapeutic trials; I would certainly value his opinion on the matter. K. Fischbeck, M.D. (7) ===== re: Intravenis vitamin C and ALS ========== The newsletter (Spring/Summer 1994) of the Linus Pauling Institute of Science and Medicine is a special issue, "Spotlighting the Biological Antioxidants". Included is an article by C.A. Douglas Ringrose, MD, FRCS, entitled THERAPEUTIC USE OF IV VITAMIN C IN DEGENERATIVE DISEASES. Dr. Ringrose practices medicine in Edmonton, Alberta, CANADA. He is affiliated with the Norman Bethune University. An excerpt from his article: "Subjects undergoing this therapy to counteract free radicals have included those with no illness, Parkinsonism, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), atherosclerosis, osteoarthritis, rheumatoid arthritis, angina pain, and metastatic cancer with side effects from chemotherapy. It was the latter problem that initially interested the writer in intravenous megadoses after being a long-time advocate of lesser oral doses (1-2 g per day) to enhance healing and as a prophylaxis against disease. (See sidebar for summary of anecdotal responses)" > From the sidebar: "An ALS patient on a similar regimen -- plus alfalfa-sprout tablets -- noted improved strength in afflicted areas." Here is a subnote from the article: "A note to practitioners: Commercially prepared vitamin C for intravenous infusion can be obtained from Merit Pharmaceuticals in Los Angeles." == = Linus Pauling Institute; 440 Page Mill Rd.; Palo Alto, CA 94306 = TEL 415-327-4064 == (8) ===== Remacemide ========== FISONS (COMPANY REPORT) TS=FISNY // UK Pharmaceuticals // MORGAN STANLEY & CO. INC.: Moore, D., et al 06-15-94 15 Pages Includes Abstract Research & Development Meeting New Chemical Entities Fisons have set themselves the goal of bringing to clinical trials a new chemical entity (NCE) every three years. This compares with Zeneca (708p) who intend to bring one NCE to the market every year. This seems to be a realistic goal especially in the light of what we learned at the R&D meeting. Remacemide The key NCE product in the pipeline currently is Remacemide, which continues to look promising and has potential in four separate indications: namely, epilepsy, acute stroke treatment, the prevention of clotting in coronary bypass surgery and Huntingdon's disease. Theoretically, the drug may also have applications in Parkinsons disease, motor neurone disease, dementia, head injury and stroke prevention. ===================== The drug is still on hold in the US, pending the outcome of an investigation into a histopathological finding. The fact that European regulatory authorities have not expressed concern, which would have limited further clinical development, is at least encouraging. In addition Remacemide is in a Phase II trial for Huntingdon's disease and has been through a Phase II study for epilepsy in the US. We expect the Phase II studies in epilepsy to be complete by the end of the year and the Phase III study to be under way soon after. The first filings to regulatory authorities should be in 1996-97 and the first sales booked in 1998. The secondary indications from epilepsy will follow after the initial epilepsy approvals. One of the key advantages of the drug at this stage is its lack of negative interaction with other drugs. Studies show that it might be superior to Wellcome's (594p) Lamotrigine and Warner Lambert's ($70.88) Neurontin in suppressing convulsions, but ========= the samples are small and it would be unwise to make any extravagant claims at this stage. Remacemide lags the competition in stroke management, both for the initial treatment and in the prevention of a second stroke. Ciba's (SFr 855) glutamate antagonist has already been through a randomised Phase ==================== II trial and Roche's (SFr 6,790) dextorphan, which is an NMDA blocker similar to Remacemide, has shown some efficacy in a Phase II study. Remacemide may arguably have a lower degree of side effects but this is less of a problem in acute indications. (9) ===== ALS/SOD mice ========== Citation: Science, June 17, 1994 v264 n5166 p1663(2) ---------------------------------------------------------------------------- Title: Mouse model found for ALS; mice carrying mutant gene associated with a hereditary form of ALS develop motor neuron degeneration much like that of the human disease. (amyotrophic lateral sclerosis) Authors: Marx, Jean ---------------------------------------------------------------------------- Abstract: Mark Gurney and his team have developed transgenic mice that that could serve as an animal model for the study of ALS. The team introduced a gene into the mice that has been associated with the hereditary form of ALS. ============================================================================ The existence of an animal model offers a ray of hope for understanding the mechanism underlying development of the always-fatal condition, which also goes by the name Lou Gehrig's disease. Gurney and his colleagues, including Northwestern's Haifeng Pu and Arlene Chiu of the Beckman Research Institute of the City of Hope Medical Center in Duarte, California, produced the model by introducing into mice a mutant gene that has been linked to a hereditary form of ALS. Neurobiologist Donald Price of Johns Hopkins University School of Medicine, who has seen a videotape of Gurney's transgenic mice, says their clinical signs are just what "you would think they should be" for an ALS model. "I'm on such a high about Mark's work," enthuses Price. That high is augmented by work by Price's colleagues, including Donald Cleveland at Johns Hopkins and Nancy Jenkins of the National Cancer Institute who introduced a different SOD gene mutant into mice; one line of their transgenic mice is beginning to show clinical features similar to those of Gurney's. And at least one additional group, led by Jon Gordon of Mount Sinai Medical Center in New York City, has found that giving mice a mutant SOD gene can cause them to develop ALS-like features. Neither the Price nor the Gordon groups have yet published their work. Robert Abendroth, who has chaired the research committee of the ALS Association for the past 15 years, describes the Gurney paper as an "important development." Another hope is that the mouse model will help in the development and testing of effective therapies for ALS of all types. "Use of a mouse would be a tremendous advancement in terms of safety, expense, and speed" over tests conducted in humans, Abendroth says. The development of this mouse model has come remarkably quickly. The SOD gene was implicated in hereditary ALS only about 18 months ago, through a genetic linkage age study conducted by a large multilab team including Robert Brown Jr. of Harvard University's Massachusetts General Hospital, Robert Horvitz of the Massachusetts Institute of Technology, and Teepu Siddique of Northwestern, a co-author of the current paper. Exactly what that critical alteration is remains to be established, but some clues may lie in evidence that SOD does more than break down superoxide radicals. Joseph Beckman's group at the University of Alabama, Birmingham, has found, for example, that the enzyme reacts with peroxynitrite, forming a product that may damage proteins by adding nitrate groups to them, and Irwin Fridovich of Duke University has shown that the enzyme is also a nonspecific peroxidase, an enzyme that might damage many cell constituents. ALS researchers are optimistic that the mouse models will not only help pin down exactly what these mutations do, but also provide a better understanding of the pathological changes underlying ALS. By following the course of the disease in the animals, researchers might be able to detect early degenerative changes in the motor neurons even before they cause paralysis. If so, the results might provide clues to therapies that can slow or prevent the debilitating symptoms of ALS. ============================================================================ (10) ===== conference announcement ========== Date : Thu, 25 Aug 94 11:39:42 EDT Sender : healthnet@calvin.dgbt.doc.ca >From : r.rosner@ucl.ac.uk (Roland Rosner) Subject : Announcement X-Comment: Networking in Canadian Healthcare ===================================================================== --- CONFERENCE ANNOUNCEMENT --- International Conference on TeleMedicine ******************************************* * TeleMed 94 - * * Medicine on the SuperHighway * ******************************************* November 3-4 1994 The Wolfson Conference Centre, Hammersmith Hospital, London, UK AIMS AND SCOPE TeleMed 94 will present an exciting picture of the emerging techniques in telemedicine and how they might benefit the delivery of health care to the end of the century and beyond. The conference will comprise papers, poster sessions and live demonstrations of telemedical applications. Live demonstrations from overseas will indicate the international scope of TeleMed 94. The two day conference will be accompanied by an exhibition from suppliers of equipment and services in the areas of telemedicine and related high performance data networking. FURTHER INFORMATION Further information can be obtained by email from: Telemed@indesols.demon.co.uk == end of als 121 ==