: TO : MTS@gnv.ifas.ufl.edu ............ Tom Sanford : murray@sumax.seattleu.edu ....... MaryAnne Murray : stever@tessi.com ................ Steve Rintala : SMIRNES@IMIHSRA.BITNET .......... S. Palazzi, MD : PHIP@TEMPLEVM.BITNET ............ Tina Phipps : RRICCIUT@WCU.BITNET ............. Rae Ricciuti : andrew@uaneuro.uah.ualberta.ca .. Andrew Penn, MD : IEQZ96M@TJUVM.BITNET ............ Michele Lee : sissi@tinman.gene.com ........... Sissi Tchehrazi : linda@nuhub.acs.northeastern.edu Douglas Hanson : smith@alexia.lis.uiuc.edu ....... Linda Smith : Jim.Knox@um.cc.umich.edu ........ Jim Knox : Tom.Butts@um.cc.umich.edu ....... Tom Butts : Lori.Nelson@Forsythe.Stanford.edu Lorene Nelson : E1.R17@STANFORD.BITNET .......... Bob Hess : Norm_Oliver%NINDS31%NIH@fedtcp.ninds.nih.gov Norman Oliver : dlmc@med.unc.edu ................ David McIlwain : FROM: bro@huey.met.fsu.edu ............ Bob Broedel : RE : ALS DISCUSSION GROUP : Here is a contact person at the Food & Drug Administration (FDA) who is keeping informed about the CNTF clinical trials re ALS. ---- Lorie Harrison Division of Congressional & Public Affairs FDA-CBER Suite 200N 1401 Rockville Pike Rockville MD 20852 TEL 301-295-9000 FAX 301-295-8938 EMAIL ???????? ---- UPI 01/26 1044 Guam veterans studied for disease FORT LAUDERDALE, Fla. (UPI) -- Veterans in Florida are being asked to help in a study of whether servicemen stationed on the Pacific island of Guam during World War II have contracted neurological diseases. A nationwide survey of veterans of that period may help explain a high incidence of Parkinson's disease and amyotrophic lateral sclerosis, known as Lou Gehrig's disease, among Chamarro natives of the island, the Fort Lauderdale Sun-Sentinel reported Tuesday. If a high incidence of the diseases is found it could mean they are service-related and that would help American veterans obtain medical care, the newspaper said. "One of the most plausible theories links a high incidence of the diseases to the cycad palm, which grows abundantly on the island," said Dr. John Peacock, chief of neurology at the Veteran Administra- tion's Ioannis A. Lougaris Medical Center in Reno, Nev., where the study is based. The natives would grind the seed, leech out a poison called cycasin and produce flour for cooking, Peacock said. The study was begun after a former chaplain for the Navy's Seabees on Guam developed Parkinson's disease and questioned whether his case might be related to living on the island. "He had dinner once a week with a princess of Guam and knew about the large amount of neurological disease there," Peacock said. "That gave us the idea to find as many of the 57,500 people who served on the island and see if they have a greater incidence than the general population." Peacock announced the study recently in a Veterans of Foreign Wars newsletter and about 11,000 people have already responded. Doctors at the VA Medical Center in Miami and the University of Miami School of Medicine are aware of the Guam theories and are looking into other toxins that could produce brain damage. "The situation on Guam remains a mystery," said Dr. Juan Sanchez-Ramos, an associate professor of neurology at the university. "At one time, some investigators thought the water might be to blame," he said. "But the incidence of neurological disease has started to decline, and the water hasn't changed. What has decreased is the use of cycad palm seeds to make flour." Cycad palms are not actually palm trees, but are a cousin of the pine tree. ====== According to an article in the TALLAHASSEE DEMOCRAT of 18 JAN 93: "Veterans and their families who want more information regarding this research can contact: Susan F. Schweitzer, Neurological Clinical Nurse Specialist and Coordinator of the APDA Information and Referral Center, 1000 Locust Street, Reno, Nevada, 89520 or call (702) 328-1766. Thanks to Tom Baxter of Tallahassee Veterans for Peace for FAXing us the article. ---- Date : Tue, 26 Jan 1993 12:06:39 -0800 From : Daniel L. Wendling To : broedel@geomag.gly.fsu.edu Subject: USPS post rec. 1/21 I work for the National Rehabilitation Information Center, and Bill Shutz has passed your ALS information request to me. I don't currently have any information for you; perhaps by now you have come up with something that might help me in my quest to catalog online resources for people with disabilities. The only things I can suggest are these: You don't seem to have a Fidonet address on your post; you call in to ADANet One, in Alabama, to see if they have a conference. They have many, and I can't remember if the one I saw was for ALS or ASL (American Sign Language). Can't seem to get a connect with them today. They're at 205/854-0698. This is a data number. Also, Edward J. Madara, who helped compile the _Self-Help Sourcebook: Finding and Forming Mutual Aid Self-Help Groups_, seems to be knowledgeable about online resources. He/they (I haven't figured out which yet) might know of something. Reach them at 70275.1003@compuserve.com. This is a long shot, but the disabilities gopher server at SUNY-Buffalo might have something in the section on databases, from _National Information Sources on Disabilities_. They're at val-dor.cc.buffalo.edu 70. A few misc. resources can be got from bulletin 25 (I think) on our computer bulletin board, at 301/589-3563. Let me know what you find out, and I'll post it in our resource files. Dan Wendling = National Rehab. Info Ctr. = danlw@well.sf.ca.us ---- Date : 26 Jan 1993 08:37:10 -0500 (EST) From : LINDA@northeastern.edu Subject: Re: als 12 To : bro@huey.met.fsu.edu Bob, Here is the text of an article published in Science News recently regarding ALS. Although I suspect that most of the clinical/researchers find this to be old news I thought it might be of general intersest to others. Please post as you see fit. Doug Hanson (linda@nuhub.acs.northeastern.edu) ------------------------------------- From: SCIENCE NEWS, January 2, 1993, Vol 143, No. 1 CLOSING IN ON THE LOU GEHRIG'S DISEASE GENE A team of neuroscientists has identified a gene that when damaged may cause the inherited form of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease -- a devastating, ultimately fatal neuro-degenerative disorder with no effective treatment. If confirmed by further studies, the finding may pave the way for the development of therapeutic drugs for both the inherited and the non-inherited -- or sporadic forms of ALS, which together strike roughly one in every 100,000 individuals worldwide. The research team, lead by James O. McNamara of the Duke University Medical Center in Durham, N.C., has found that a gene which codes for part of a key nerve-cell receptor lies within the same region of chromosome 21 as that known to become damaged in the inherited form of ALS. Taken together with previous research findings related to ALS, McNamara asserts, the new evidence suggests that mutations in the gene cause the inherited form of the disorder. ALS results from the gradual death of nerves in the lower brain and spinal cord that control movement. Most ALS patients develop the initial symptoms, including muscle stiffness and weakness, in their forties or fifties. Eventually, the disorder disables the body's muscles, and patients usually die within five years from respiratory failure. From studies of families with multiple members affected by the disorder, researchers estimate that between 5 and 10 percent of ALS cases have a genetic cause. In the mid- 1980s, some scientists began to suspect that the nerve-cell death in ALS arises from mutations imparing the cells' ability to properly use glutamate, one of the chemicals that transfers messages between nerve cells. Laboratory studies showed that high concentrations of glutamate can kill nerve cells by causing them to take up toxic levels of calcium. Moreover, epidemiologists identified a glutamate-like compound as the cause of the high-incidence of an ALS-like disease in Guam. Other scientists discovered that the same compound can prompt calcium-related nerve damage when fed to monkeys. McNamara -- who also holds an appointment at the Department of Veterans Affairs Medical Center in Durham -- and his colleagues have now added to these previous finding by isolating the gene that codes for one subunit of the receptor that responds to glutamate by allowing calcium to enter a nerve cell. In the Jan. 1 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES, the researchers suggest that mutations in the gene lead to the production of faulty receptors, which permit too much calcium to enter the cell when triggered by glutamate. McNamara asserts that the faulty-receptor theory might explain why the symptoms of ALS develop only later in life. Each defective receptor might take up just a bit too much calcium, he suggests, leading to a slow but steady calcium buildup that eventually proves fatal to a nerve cell years later. The same nerve-destroying process might occur after the gene for the glutamate receptor subunit becomes damaged by envionmental insults, McNamara says, leading to the sporadic form of ALS. "By understanding the genetics...we may shed light on the mechanisms involved in the sporadic form," he says. "This is a very good candidate gene for ALS," comments Allen D. Roses, a neuroscientist at Duke who did not participate in the new study. However, he says that researchers must perform further experiments to determine the role of the glutamate receptor subunit gene in the disorder, such as splicing a defective copy of the gene into nerve cells to see if it makes them accumulate calcium and die. Both McNamara and Roses agree that the advance, if confirmed, could lead to a treatment for ALS by providing a target for drug therapy. "If this is the gene, drugs to block the [defective] receptors would be a rational approach to therapy," Roses says. ---- end of als 13 ----