Molecular mechanisms of excitotoxicity and their relevance to pathogenesis of neurodegenerative diseases

By Xiao-xia Dong, Yan Wang, Zheng-Hong Qin. Acta Pharmacologica Sinica, 2009

1,200 citations recorded by the source corpus.

A pivotal role for excitotoxicity in neurodegenerative diseases is gaining increasingly more acceptance, but the underlying mechanisms through which it participates in neurodegeneration still need further investigation. Excessive activation of glutamate receptors by excitatory amino acids leads to a number of deleterious consequences, including impairment of calcium buffering, generation of free radicals, activation of the mitochondrial permeability transition and secondary excitotoxicity. Recent studies implicate excitotoxicity in a variety of neuropathological conditions, suggesting that neurodegenerative diseases with distinct genetic etiologies may share excitotoxicity as a common pathogenic pathway. Thus, understanding the pathways involved in excitotoxicity is of critical importance for the future clinical treatment of many neurodegenerative diseases. This review discusses the current understanding of excitotoxic mechanisms and how they are involved in the pathogenesis of neurodegenerative diseases.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/1d9e24d00b67e31504783204979469a17676bd60

Citations in the corpus

• Selective Neuronal Vulnerability to Oxidative Stress in the Brain (2010, neutral): “Mechanistically, OS plays an important role in the selective loss of neurons or synapses from glutamate excitotoxicity (Michaelis, 1998; Dong et al., 2009).”