Molecular basis of treatment in motor neurone disease.
The pathways leading to motorneuron degeneration in amyotrophic lateral sclerosis (ALS) are complex. Excitotoxicity, oxidative damage and, maybe, abnormal aggregation of neurofilaments are key events on which therapeutical strategies can be designed. This paper reviews current knowledge on these strategies. Even though we should be aware that appropriate management of disease symptoms remains the most effective therapeutical intervention, understanding the pathophysiology of ALS is essential for developing new therapies.
Anneser
J
J
Department of Neurology, Klinikum Grosshadern, Marchioninistrasse 15, 81377 Munich, Germany.
D000690:Amyotrophic Lateral Sclerosis / Q000188:drug therapy / Q000503:physiopathology* / Q000821:virology; D000818:Animals; D020805:Central Nervous System Viral Diseases / Q000150:complications / Q000235:genetics / Q000503:physiopathology; D018698:Glutamic Acid / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D009414:Nerve Growth Factors / Q000627:therapeutic use*; D016900:Neurofilament Proteins / Q000235:genetics* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000235:genetics*; D017470:Receptors, Glutamate / Q000235:genetics / Q000378:metabolism; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D000072105:Superoxide Dismutase-1
D009414:Nerve Growth Factors; D016900:Neurofilament Proteins; D017470:Receptors, Glutamate; C000606290:SOD1 protein, human; D018698:Glutamic Acid; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1