Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1832, Issue 2, Pages 312-322Publisher
ELSEVIER
DOI: 10.1016/j.bbadis.2012.11.013
Keywords
Amyotrophic lateral sclerosis; N-methyl-D-aspartate receptor; Excitotoxicity; Glutamate; Neurodegeneration
Funding
- Compagnia San Paolo [4932, 20082395]
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Amyotrophic lateral sclerosis (ALS) is an adult onset neurodegenerative disease pathologically characterized by the massive loss of motor neurons in the spinal cord, brain stem and cerebral cortex. There is a consensus in the field that ALS is a multifactorial pathology and a number of possible mechanisms have been suggested. Among the proposed hypothesis, glutamate toxicity has been one of the most investigated. Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor mediated cell death and impairment of the glutamate-transport system have been suggested to play a central role in the glutamate-mediated motor neuron degeneration. In this context, the role played by the N-methyl-D-aspartate (NMDA) receptor has received considerable less attention notwithstanding its high Ca2+ permeability, expression in motor neurons and its importance in excitotoxicity. This review overviews the critical role of NMDA-mediated toxicity in ALS, with a particular emphasis on the endogenous modulators of the NMDAR. (C) 2012 Elsevier B.V. All rights reserved.
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