Literature DB >> 11200700

Treatment of amyotrophic lateral sclerosis--what is the next step?

A C Ludolph1.   

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease which was thought to be untreatable. However, recent evidence in both experimental animals and men indicates that antiglutamatergic strategies are the first to have an influence on its pathogenesis and slow down the disease process. Since the effect of drugs is still small, this progress cannot only be seen as a success of the present but must also be acknowledged as a basis for future developments. How will future studies be designed? They will have to take into account that the disease presumably has a long preclinical period and they will use a number of novel compounds and treatment strategies which have been shown to be effective in transgenic animal models. This also implies that we are likely to use a combination of therapies and we will try to treat patients early. The latter will be associated with the demand for a novel clinical attitude toward the diagnosis of the disease and the development of novel markers for both the preclinical period and the longitudinal course of the disease.

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Year:  2000        PMID: 11200700     DOI: 10.1007/bf03161074

Source DB:  PubMed          Journal:  J Neurol        ISSN: 0340-5354            Impact factor:   4.849


  49 in total

1.  Inhibition of ICE slows ALS in mice.

Authors:  R M Friedlander; R H Brown; V Gagliardini; J Wang; J Yuan
Journal:  Nature       Date:  1997-07-03       Impact factor: 49.962

2.  Progressive motor neuron impairment in an animal model of familial amyotrophic lateral sclerosis.

Authors:  M Azzouz; N Leclerc; M Gurney; J M Warter; P Poindron; J Borg
Journal:  Muscle Nerve       Date:  1997-01       Impact factor: 3.217

3.  Increased 3-nitrotyrosine and oxidative damage in mice with a human copper/zinc superoxide dismutase mutation.

Authors:  R J Ferrante; L A Shinobu; J B Schulz; R T Matthews; C E Thomas; N W Kowall; M E Gurney; M F Beal
Journal:  Ann Neurol       Date:  1997-09       Impact factor: 10.422

4.  An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria.

Authors:  P C Wong; C A Pardo; D R Borchelt; M K Lee; N G Copeland; N A Jenkins; S S Sisodia; D W Cleveland; D L Price
Journal:  Neuron       Date:  1995-06       Impact factor: 17.173

5.  Motor neuron degeneration induced by excitotoxin agonists has features in common with those seen in the SOD-1 transgenic mouse model of amyotrophic lateral sclerosis.

Authors:  C Ikonomidou; Y Qin Qin; J Labruyere; J W Olney
Journal:  J Neuropathol Exp Neurol       Date:  1996-02       Impact factor: 3.685

6.  Elevated "hydroxyl radical" generation in vivo in an animal model of amyotrophic lateral sclerosis.

Authors:  M B Bogdanov; L E Ramos; Z Xu; M F Beal
Journal:  J Neurochem       Date:  1998-09       Impact factor: 5.372

7.  Clinical and [18F] dopa PET findings in early Parkinson's disease.

Authors:  P K Morrish; G V Sawle; D J Brooks
Journal:  J Neurol Neurosurg Psychiatry       Date:  1995-12       Impact factor: 10.154

8.  Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1.

Authors:  L I Bruijn; M K Houseweart; S Kato; K L Anderson; S D Anderson; E Ohama; A G Reaume; R W Scott; D W Cleveland
Journal:  Science       Date:  1998-09-18       Impact factor: 47.728

9.  Proton magnetic resonance spectroscopy of the primary motor cortex in patients with motor neuron disease: subgroup analysis and follow-up measurements.

Authors:  W Block; J Karitzky; F Träber; C Pohl; E Keller; R R Mundegar; R Lamerichs; H Rink; F Ries; H H Schild; F Jerusalem
Journal:  Arch Neurol       Date:  1998-07

10.  Reduced cerebral glucose metabolism in asymptomatic subjects at risk for Huntington's disease.

Authors:  J C Mazziotta; M E Phelps; J J Pahl; S C Huang; L R Baxter; W H Riege; J M Hoffman; D E Kuhl; A B Lanto; J A Wapenski
Journal:  N Engl J Med       Date:  1987-02-12       Impact factor: 91.245

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