PMID: 8580551Sep 1, 1995Paper

Amyotrophic lateral sclerosis

Internal Medicine
A Eisen

Abstract

The final cascade of amyotrophic lateral sclerosis (ALS) coincides with the onset of clinical neurological deficits and involves multifactorial interactive mechanisms. These terminal events include excitotoxicity, free radical accumulation and possibly immunological disturbances. They are probably predated by months or years by thus far unidentified triggers. Selective vulnerability of the corticomotneuronal system in ALS is likely due to degradation of several gene products essential to transmitter, receptor and nerve growth factor maintenance specific to this functional system. Therapeutic strategies involve neuroprotection, symptomatic and combination neuronal therapy targeted to the final cascade of ALS.

Citations

Feb 11, 2004·Progress in Biophysics and Molecular Biology·Matthew C Zimmerman, Robin L Davisson
Jan 19, 2000·Neurobiology of Aging·V I KlichkoW C Orr
Dec 19, 1998·Magnetic Resonance Imaging·J L TanabeW D Rooney
Apr 30, 2002·Free Radical Biology & Medicine·Silke WendtOle A Andreassen
Dec 18, 2007·Toxicological Sciences : an Official Journal of the Society of Toxicology·Richard M LoPachinTerrence Gavin
Aug 2, 2013·Internal Medicine·Natsumi FurutaKoichi Okamoto
Sep 13, 2014·Neurological Research·MuDan CaiEun Jin Yang
Oct 2, 2015·Internal Medicine·Natsumi FurutaYoshio Ikeda
Nov 14, 2020·ELife·Shanaya Shital ShahWolf-Dietrich Heyer
Jun 28, 2008·Neurotoxicology·Richard M LopachinDavid S Barber

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