SOD1 and amyotrophic lateral sclerosis: The pathological processes linked to ALS are formation of intraneuronal aggregates of neurofilament [1]; microglia mediated neurotoxicity as a result of enhanced inflammatory response [2–5]; glutamatergic neurotoxicity as a result of deficit in glutamate transporter or receptor function [6–11]; and mitochondrial dysfunction as a result of failure in oxidative metabolism [12, 13] and superoxide dismutase-1 (SOD1) mediated neurotoxicity, which is associated to gene mutation and found in familiar form of ALS [14, 15].