Editorial: Excitotoxicity Turns 50. The Death That Never Dies

The review highlights three major findings: (1) the discovery of redox-dependent modulatory sites of NMDAR, (2) the oxidative-driven conversion of 3,4-dihydroxyphenylalanine (DOPA) to the neurotoxic compound 2,4,5-trihydroxyphenylalanine (TOPA) quinone, and (3) the contribution of oxidative stress t...

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Bibliographic Details
Published in:	Frontiers in neuroscience Vol. 15; p. 831809
Main Authors:	Granzotto, Alberto, Weiss, John H, Sensi, Stefano L
Format:	Journal Article
Language:	English
Published:	Switzerland Frontiers Research Foundation 17-01-2022 Frontiers Media S.A
Subjects:	Alzheimer's disease Brain research calcium Caspase Conflicts of interest Dihydroxyphenylalanine Editorials Excitotoxicity Glutamic acid receptors Hypotheses mitochondria N-Methyl-D-aspartic acid receptors Nervous system Neurological diseases neuronal death Neuroscience Neurosciences Neurotoxicity Oxidative stress Quinones reactive oxygen (nitrogen) species Science Stem cells stroke zinc United States > US Italy California calcium mitochondria neuronal death reactive oxygen (nitrogen) species stroke zinc glutamate ischemia
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Summary:	The review highlights three major findings: (1) the discovery of redox-dependent modulatory sites of NMDAR, (2) the oxidative-driven conversion of 3,4-dihydroxyphenylalanine (DOPA) to the neurotoxic compound 2,4,5-trihydroxyphenylalanine (TOPA) quinone, and (3) the contribution of oxidative stress to the mobilization of toxic amounts of intracellular zinc. [...]the paper dwells on the zinc-driven activation of AMPK, an event upstream of caspase activation and an exploitable pharmacological target. Am. 265, 56–63. doi: 10.1038/scientificamerican0791-56 Alberto Granzotto1,2,3, John H. Weiss4 and Stefano L. Sensi2,3,5* * 1Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, Irvine, CA, United States * 2Center for Advanced Sciences and Technology (CAST), University “G. d'Annunzio” of Chieti–Pescara, Chieti, Italy * 3Laboratory of Molecular Neurology, Department of Neuroscience, Imaging, and Clinical Sciences (DNISC), University “G. d'Annunzio” of Chieti–Pescara, Chieti, Italy * 4Department of Neurology, School of Medicine, University of California, Irvine, Irvine, CA, United States * 5Institute for Mind Impairments and Neurological Disorders (IMIND), University of California, Irvine, Irvine, CA, United States
Bibliography:	SourceType-Other Sources-1 content type line 63 ObjectType-Editorial-2 ObjectType-Commentary-1 Edited and reviewed by: Xiangping Chu, University of Missouri–Kansas City, United States This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience
ISSN:	1662-4548 1662-453X 1662-453X
DOI:	10.3389/fnins.2021.831809