Molecular Mechanisms and Therapeutics of Amyotrophic Lateral SclerosisEdited by K.AbeAmsterdam, NetherlandsELSEVIER2000 ISBN: 0-444-50613-6

Abstract

Book ReviewsMolecular Mechanisms and Therapeutics of Amyotrophic Lateral Sclerosis M. Zuheir Al-KawiMD, FACP, FAAN M. Zuheir Al-Kawi Senior Consultant Neurologist, Department of Neurosciences, King Faisal Specialist Hospital And Research Center, Riyadh, Saudi Arabi Search for more papers by this author Published Online:1 May 2003https://doi.org/10.5144/0256-4947.2003.227aSectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutIntroductionThis book covers proceedings of an international symposium held in Japan on 22-24 September 2000 under the same title. The target readership include neurologists and neuroscientists interested in the disease and related degenerative disorders.Amyotrophic Lateral Sclerosis (ALS) received publicity, and consequently funding for research, after the death of a celebrity baseball player (Lou Gehrig) in the United States over 60 years ago. ALS remains a rapidly progressive and ultimately fatal neurological disorder, caused by the selective loss of motor neurons in the brain and spinal cord. In spite of advances in research and availability of an approved treatment; no meaningful influence on the long-term prognosis has been achieved. The exact mechanism of disease onset and progression is still elusive. Several susceptibility factors, genetic and others, may interact with environmental risk factors to precipitate the neuronal degenerative process. Treatment with riluzole had a statistically significant but clinically marginal benefit in delaying respirator dependency by a mean of 3 months. Scientifically, however, the treatment lent support to the approach of excitotoxic pathogenesis. Other leads on pathogenesis appeared a decade ago with the discovery of mutations in the gene of Cu/Zn superoxide dismutase (SOD1) in some patients affected with an uncommon form of ALS, namely the familial one, and later in developing transgenic mice expressing mutant with SOD1 gene.Most of the reported work comes from Japan, the host country for the congress. The presentations are grouped in chapters according to the research areas covered in the work presented. Leading “keynote” lectures to set the tone for state-of-the-art knowledge in the area, which could have added to the usefulness of the volume, are not consistently present in all chapters. Selective vulnerability of motor neurons is addressed as well as topics related to the dismutase mutations and glutamate toxicity among other putative mechanisms.As is inherent in congress series, coverage of different aspects of the subject is heterogeneous and dependent on submissions of researchers. Some pathological aspects and therapeutic approaches undergoing testing, like neurotrophic factors, are covered. Others like epidemiology received only one article.The book in general is a useful reference for neurologists and researchers dealing with ALS in particular and neurodegenerative diseases in general. Previous article Next article FiguresReferencesRelatedDetails Volume 23, Issue 3-4May-July 2003 Metrics History Published online1 May 2003 InformationCopyright © 2003, Annals of Saudi MedicinePDF download