=============================================================== == == == ----------- ALS INTEREST GROUP ----------- == == ALS Digest (#45, 27 MAY 1993) == == == == To subscribe, to unsubscribe, to contribute notes, etc. == == to ALS Digest, please send e-mail to: == == bro@huey.met.fsu.edu (Bob Broedel) == == == == All interested people may "broadcast" messages to == == ALS Digest subscribers by sending to: == == als@huey.met.fsu.edu == == == =============================================================== In order to get the back issues, one should send e-mail to: LISTSERV@mailer.fsu.edu Then in the body of your message say (it ignores the subject line) GET ALS ALSD01 GET ALS ALSD02 GET ALS ALSD03 etc. To join the ALS-related discussion on that LISTSERV, send e-mail to: LISTSERV@mailer.fsu.edu In the body of the message say ... SUBSCRIBE ALS yourfirstname yourlastname Here are two ALS-related articles from Cornell. (1) ===== Cornell Chronicle (02/04/93) CUMC establishes center to fight ALS By Jonathan Weil The New York Hospital-Cornell Medical Center's Department of Neurology has established a new center for amyotrophic lateral sclerosis (ALS), or Lou Gehrig's Disease. The ALS Center - located at The Hospital for Special Surgery, a close affiliate of New York-Cornell - will be among the first in the United States to test one of several new promising drugs for this degenerative disease. The ALS Center will also provide physical therapy and other essential rehabilitation services for ALS patients. ALS is a progressive neurological disease which attacks the motor nerves that control voluntary muscle movement. This results in muscle weakness, wasting and eventually complete paralysis. The muscles involved in breathing also usually are affected, a complication that can be fatal. Affected individuals are usually elderly, but the disease can also strike those in their 20s and 30s. Presently, there is no cure for ALS. However, exciting and promising work is currently under way with substances known as nerve growth (or neurotrophic) factors. These substances are naturally occurring proteins that are present in living tissue and increase in concentration in response to injury. They promote early childhood development and, in the adult, may accelerate healing and prevent degeneration of injured tissues, including nerves. Pharmaceutical companies are presently manufacturing some of these nerve growth factors. Based on successful studies halting motor nerve disease in experimental animals, physicians believe that these factors may slow down or halt the progression of ALS - thereby prolonging survival and improving quality of life. The ALS Center will shortly begin a trial for one of these nerve growth factors known as CNTF (ciliary neurotrophic factor). Patients with ALS, between the ages of 21 and 85, and with no other neurological or serious medical illnesses, will be eligible. Patients will be evaluated by a neurologist at the ALS Center to determine their eligibility. Once enrolled in the trial, there will be no cost to the patient for medication or procedures directly related to the trial. ALS is an uncommon but devastating disease (with a prevalence of 5 persons per 100,000). However, because of some of its famous victims, it has received widespread notoriety. One famous victim, Lou Gehrig, has the disease eternally connected with his name. Other affected celebrities have included actor David Niven and Sen. Jacob Javits. The ALS Center is directed by Dr. Michael Rubin, assistant professor of neurology at the Medical College and assistant attending neurologist at both New York-Cornell and The Hospital for Special Surgery. The center is a component of the New York-Cornell Department of Neurology's Peripheral Nerve Program, also directed by Rubin. The drug trial is sponsored by Synergen, which manufactures and supplies the synthetic version of CNTF. For more information about the drug trial or for referral of patients, call Barbara Laurenzi, R.N., ALS nurse clinician, at (212) 606-1046. (2) ===== Cornell Chronicle (05/06/93) Vitamin deficiency considered in equine ALS By Roger Segelken Cornell veterinary medical researchers who study equine motor neuron disease (EMND), which closely resembles a form of amyotrophic lateral sclerosis (ALS) or Lou Gehrig's disease in humans, see vitamin deficiency as one possible clue to debilitating nerve damage. There is evidence in EMND horses that an "oxidative insult" may be involved in motor neuron death, and that a deficiency in protective antioxidants may be at least partially responsible for the disease, according to Dr. Thomas J. Divers of the College of Veterinary Medicine. Blood tests in EMND cases referred to Cornell found "incredibly low, even undetectable levels" of vitamin E, said Divers, an associate professor of medicine. Vitamin E is an antioxidant that counteracts the harmful free radicals that are naturally produced during metabolism in animals and humans. Coupled with the discovery by researchers at the Massachusetts Institute of Technology and Massachusetts General Hospital of the defective human gene that fails to initiate production of anti- radical enzymes in ALS patients, the Cornell finding "could indicate an interplay of antioxidant vitamins and enzymes, all working together in healthy bodies, and a similar mechanism for the neurode- generative disorder in humans and horses." The underlying changes in EMND were first recognized in 1989 by Dr. John F. Cummings, professor of anatomy and member of a team that published the finding in 1990, and the horse is now an animal model for ALS research. The Cornell veterinary clinic became a national "magnet" for suspected EMND cases, as an interdisciplinary research team was assembled with funding from the ALS Association, National Institutes of Health, American Horse Shows Association and college alumni. Like human ALS patients, EMND horses experience progressive muscle wasting as dying motor neurons fail to transmit signals to muscles, Cummings noted. Motor neuron changes in the spinal cords of human and equine victims of the diseases "are virtually identical - the same cranial nerves are affected, and the same ones are spared," Divers reported. Weight loss, difficulty standing and fasciculations (quivering of the leg and shoulder muscles) are others signs of EMND. The epidemiologist on the Cornell EMND team, Dr. Hussni O. Mohammed, is sorting through 123 putative risk factors in the search for disease causes. Among the variables under consideration are management practices, breed, horse vices (such as chewing wooden stall materials) and nutrition. Nutrition may be a factor, he speculates, after noting that many EMND horses are not pastured where they eat can fresh grass but rather are fed commercial feed and cut hay. == end of als 45 ==