Date: Sat, 19 Nov 94 18:15:27 -0500 From: Bob Broedel To: als@huey.met.fsu.edu Subject: ALSD#151 ALS-ON-LINE =============================================================== == == == ----------- ALS Interest Group ----------- == == ALS Digest (#151, 19 November 1994) == == == == ------ Amyotrophic Lateral Sclerosis (ALS) == == ------ Motor Neurone Disease (MND) == == ------ Lou Gehrig's disease == == ------ Charcot'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. The ALS Digest is == == published (approximately) weekly. Currently there are == == 400+ 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 .. another promising growth factor 2 .. News Release 3 .. Support Groups Newsgroup Pointer 4 .. Dear Friend 5 .. CNTF Synergen/Amgen (1) ===== another promising growth factor ========== Date : Sat, 19 Nov 94 14:45:01 -0500 >From : "Dr. Kenneth Fischbeck" Subject: another promising growth factor An article which may be of interest to ALS Digest subscribers appeared in the November 11, 1994 issue of Science: Henderson CE, et al. GDNF: A potent survival factor for motoneurons present in peripheral nerve and muscle. Science 266:1062-1064, 1994. The authors (who are mostly from Marseille, France, and Genentech in South San Francisco) have studied a new neurotrophic factor and find it to be more effective at promoting motor neuron survival in cell culture and in rats than other factors such as CNTF and BDNF. K. Fischbeck, M.D. Neurology Dept., Univ. Pennsylvania Philadelphia, PA (fischbeck@a1.mscf.upenn.edu) (2) ===== News Release ========== Date : Sat, 19 Nov 1994 14:08:48 -0500 >From : JACKN74940@aol.com Subject: News Release Bob, I put this on Prodigy for Lynn Klein ALSA - dont know if you have seen it yet : NEWS RELEASE FROM SOCIETY OF NEUROSCIENCE -dated 16 November and provided by Lynn Klein - "Several recent advances promise to vastly improve the likelihood for understanding and developing new therapies for motor neuron disease, including ALS, also known as Lou Gehrig's disease. These developments, many of which involve new animal models of human disorders, provide a superb example of the ways in which clinical and basic neuroscience research can lead to significant new insights into human disease, including the search for causes, clarification of disease mechanisms and design of new treatments. This research shows how scientific thinking about a disease for which very little was known just a few years ago has changed dramatically with potentially profound implications for treatment of patients. The work on ALS has produced the best animal model so far for reproducing a human neurodegenerative disorder. This model allows investigators to establish the cause of some cases of ALS, examine the mechanisms of the disease, and test therapies. Motor neuron diseases, which are among the most devastating human neurological disorders, include classical ALS which is estimated to afflict 30,000 Americans, with 5000 new cases annually. Classical ALS appears in late life; familial ALS (FALS), which comprises 10 percent of all cases, usually appears in mid life; and several spinal muscular atrophies occur in infancy and childhood. Primary symptoms are muscle weakness and atrophy due to the degeneration of large motor nerve cells, or neurons, of the brainstem and spinal cord. Affected cells show Swelling of neurofilaments, structures that form the scafloid of neurons. These neurons, which control voluntary movement are destroyed; the loss of nerve inputs to muscles leaves patients fully paralyzed. There is no treatment. The first major advance occurred in 1993 when geneticists Robert Brown of Massachusetts General Hospital and Teepu Siddique of Northwestern Medical School and their colleagues demonstrated that some cases of FALS were linked to mutations in copper zinc superoxide dismutase (SOD1), a gene that codes for an enzyme that detoxifies free radicals. These radicals, which can damage and kill cells, have been implicated in a variety of disorders including stroke, Parkinson's disease, and ALS. The SOD1 mutation occurs in about 20 percent of FALS cases. The discovery that mutations in the SOD gene are linked to FALS suggests that transgenic strategies introducing SOD into the mice may produce models of human FALS and lead to a much better understanding of the disease. Since the clinical features of classical ALS and FALS are indistinguishable, it has been suggested that the abnormalities associated with the SOD1 mutation may be one of several mechanisms leading to a final common path of motor neuron degeneration in humans. How the abnormal SOD enzyme causes disease, is still unknown. To discover how the mutation causes disease, Mark Gurney of Northwestern and his colleagues introduced a mutant human SOD gene into mice. First reported in the journal Science last June, the disease in one line of mice closely resembles the human systems. Gurney's co authors are Haifeng PU, Mauro Dal Canto and Sidiqque, all of Northwestern, and Arlene Chiu of City Hope Medical Center in Duarte. Calif. "Our work shows that mutations in SOD change a beneficial enzyme into a toxic one, known as "gain of function mutation" Gurney says, " The SOD enzyme has gained a new function that is toxic to motor neurons. We don't understand how that occurs, but now we can ask questions and find answers that directly relate to the therapy of human ALS." Other researchers, including Phil Wong, Donald Cleveland and Donald Price of Johns Hopkins and Nancy Jenkins at the National Cancer Institute have developed mice with another SOD1 mutation. The Hopkins team now reports four lines of mice which shows features of the human disease. This group has discovered evidence for abnormalities in the cytoskeleton of motor neurons as well as alterations in mitochondria, the energy source critical for the activity and survival of neurons. "Because the mutant SOD transgene used in these studies retains significant activity it seems likely that, in these two cases, the mechanisms of disease involves a gain in injurious properties by the mutant enzyme, " Price says. These animal models allow detailed examination in test tube, in cell culture and in living mammals of how the disease occurs. These studies in turn should provide clues to understanding the pathogenic processes that occur in sporadic ALS and be useful in the design of treatments. Studies conducted during the past few years indicate that motor neurons in ALS develop accumulations of neurofilaments in proximal axons. Moreover, Jack Griffin and Price showed that these abnormalities are due to the impairment in the intracellular delivery of neurofilament proteins. Building on these observations, Jean-Pierre Julien and his colleagues at McGill University and Cleveland and coworkers at Johns Hopkins generated other transgenic mouse models that exhibit some of the signs and pathological features of ALS. These two groups reported in the journal cell that transgenic mice overexpressing neurofilament genes showed disorganized neurofilament and a type of motor neuron disease. These mice which contain multiple copies of human neurofilament gene are normal at birth but progressively develop ALS like symptoms with age. Additional evidence for neuro filament involvement in ALS came from recent work in which Julien found specific mutations in the neurofilament heavy gene in five of 356 non related ALS patients. No mutations were detected in more than 306 normal individuals. " These mutations might predispose to ALS by causing subtle changes in neurofilament properties resulting in a tendency to develop accumulations. " Julien says, "The next step will be to generate transgenic mice with the mutated neurofilament gene found in these ALS cases." " A significant role of neurofilaments in motor neuron disease is compatible with the view that ALS is a disease involving multiple factors, genetic and environmental. ALS like mouse models will provide a means to identify those factors and a means to search for genes that confer resistance or susceptibility to the disease. The mice will be extremely useful for the testing of drugs aiming to slow down the progression of the disease." Researchers also are studying "wobbler " mice which develop an inherited motor neuron disease. Several neurotrophic factors - substances which nourish the growth of neurons during development and in some cases throughout life - have been tested in these mice as possible therapies for ALS. "Subcutaneous injection of either ciliary neurotrophic factor or brain derived neurotrophic factor delays disease progression and administration of both at the same time arrests deterioration." notes Hiroshi Mitsumoto of the Cleveland Clinic Foundation." These neurotrophic factors appear to delay neuronal degeneration and stimulate axonal regeneration. Thus an exogenous administration of neurotrophic factors appears to be beneficial in an experimental model of motor neuron degeneration." Mitsumoto adds: " Natural animal models and experimentally induced animal models are the crucial component of ALS research in further understanding the disease process and the potential therapeutic intervention for this devastating disease." - The Quest Continues! Jack Norton (3) ===== Support Groups Newsgroup Pointer ========== ________________________________________________________________________ Psychology & By: John M. 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Copyright 1994 John M. Grohol. All rights reserved. Send comments/questions/suggestions regarding this newsgroup Pointer to the author (replying to this message should work). Do *not* include this Pointer in your reply, or it may not be read. -- John M. Grohol Co-moderator sci.psychology.research Assistant Editor, InterPsych Newsletter Center for Psychological Studies, Nova Southeastern University, Florida Dutchess County Department of Mental Hygiene, Poughkeepsie, New York (4) ===== Dear Friend ========== Date : Sat, 19 Nov 1994 06:47:08 -0500 Sender : Parkinson's Disease - Information Exchange Network : >From : Bonander@AOL.COM Subject: Dear Friend Sometime ago, Jerry Finch wrote a letter to a friend. Jerry is a writer and has a wonderful way of expressing himself. I published this letter sometime ago, but would like to share it with you. Dear Friend, You haven't been by to see me in quite some time. I wondered about what happened. Did I say something that offended you? I started asking around. Word finally got back that you were uncomfortable around me because of the Parkinson's thing. That's why, instead of calling, I thought I might write you a note. Maybe I can explain a little better to you about the way I feel. The last time you came over, I was having a lot of physical problems. Parkinson's is like that; good for two days, bad for three. Before you come, call. I'll tell you honestly if I'm up or down. That way you know what to expect. But don't avoid me. Inside, I am still the same person I always was. I can still beat you at chess, still out-talk you over religion and politics. I can still laugh at all your jokes, still feel sad when we talk about some of our lost friends. I'm still me. Don't be afraid to talk about the things you see. My hands shake, my walk is unsteady. I know that. It isn't a secret. I'll tell you about what I'm going through, about the medications and stuff. You need to know so you will feel comfortable when you see something happen. Parkinson's isn't contagious, it isn't even life-threatening. Chances are, I'll live just as long as you, although I'm trying for one day longer, just to prove the point. Just because I've accepted Parkinson's doesn't mean I've accepted defeat. I'm still fighting. But the fighting would be so much easier if you were around. Why? Because we used to talk about everything and I miss that. We used to laugh at stupid stuff and I miss that. We used to punch one another in the arm, work on our cars together, tell lies, talk about kids - and I miss all of that. We used to get sad together, remembering the things in the past. We made a vow never to talk about those things outside of our friendship and I need to talk about them with you. I'm still the same. Nothing inside has changed, only the outside. That's why you don't need to feel uncomfortable around me. We've traveled too many miles together to let something like Parkinson's come between us. So I'm asking you - call me. Come visit. Let's talk about today, tomorrow, ten years from now, because the future will be so much richer if you're around, and so much poorer without you. I might have Parkinson's, but you snore. So I'd say we all have problems. I've missed you. As always, I'll be here for you, waiting for you to call. Sincerely, Your friend Thanks to Jerry for opening his heart to us. Jerry has PD also. He can be reached at JFinch@AOL.COM. There are great writers out there. Please use your talent. Regards, Alan Bonander Bonander@aol.com (5) ===== CNTF Synergen/Amgen ========== REUTER BUSINESS REPORT via NewsNet Friday November 18, 1994 AMGEN BUYING SYNERGEN IN $240 MILLION DEAL THOUSAND OAKS, Calif. (Reuter) - Biotechnology leader Amgen Inc. said Friday it agreed to buy Synergen Inc., a struggling biotech company, in a $240 million deal. Under the agreement, which the two companies described as a merger, Amgen will pay $9.25 each for Synergen's approximately 25.9 million shares. < parts deleted because of copyright > Synergen's work focuses on inflammatory diseases such as rheumatoid arthritis and neurological disorders such as Parkinson's Disease, Alzheimer's and amyotrophic lateral sclerosis, or ``Lou Gehrig's'' disease. < the rest of the article has been deleted > REUTER.END === end of als 151 ===