Neuro-inflammation as a therapeutic target in amyotrophic lateral sclerosis.
Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neuromuscular disease that destroys both upper and lower motor neurons, resulting in spasticity, diffuse muscular atrophy, weakness, and ultimately death from respiratory failure. It is presumed that in the vast majority of cases, ALS is acquired and occurs sporadically, although the exact etiology is unknown. Recent, emerging evidence suggests that neuro-inflammation may be a pathological characteristic of this disease; this could represent a potential therapeutic target for a pharmacological agent to help treat this severe disease. This article reviews the current research in this area and discusses theoretical and clinical ramifications of these recent findings.
Weydt
Patrick
P
Department of Neurology, University of Washington School of Medicine, 1959 Northeast Pacific Avenue, Seattle, WA 98195, USA.
Weiss
Michael D
MD
Möller
Thomas
T
Carter
Gregory T
GT
D000690:Amyotrophic Lateral Sclerosis / Q000188:drug therapy* / Q000276:immunology; D000818:Animals; D002986:Clinical Trials as Topic / Q000706:statistics & numerical data; D016503:Drug Delivery Systems / Q000379:methods*; D006801:Humans; D020078:Neurogenic Inflammation / Q000188:drug therapy* / Q000276:immunology; D013482:Superoxide Dismutase / Q000276:immunology; D000072105:Superoxide Dismutase-1
C000606290:SOD1 protein, human; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1