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Excitotoxicity, calcium and mitochondria: a triad in synaptic neurodegeneration

translational Neurodegeneration 2022年第1期11卷 917-930页

作者： Manish Verma Britney N.Lizama charleen t.chu Department of Pathology University of Pittsburgh School of MedicinePittsburghPA 15261USA Department of Ophthalmology University of Pittsburgh School of MedicinePittsburghPA 15261USA Pittsburgh Institute for Neurodegenerative Diseases University of Pittsburgh School of MedicinePittsburghPA 15261USA McGowan Institute for Regenerative Medicine University of Pittsburgh School of MedicinePittsburghPA 15261USA Center for Protein Conformational Diseases University of PittsburghPittsburghPA 15261USA Center for Neuroscience University of PittsburghPittsburghPA 15261USA Present Address:Astellas Pharma Inc. 9 Technology DriveWestboroughMA 01581USA.

Glutamate is the most commonly engaged neurotransmitter in the mammalian central nervous system,acting to mediate excitatory ***,high levels of glutamatergic input elicit excitotoxicity,contribut-ing to neuronal cell death following acute brain injuries such as stroke and *** excitotoxic cell death has also been implicated in some neurodegenerative disease models,the role of acute apoptotic cell death remains controversial in the setting of chronic ***,it is clear that excitatory synaptic dysregula-tion contributes to neurodegeneration,as evidenced by protective effects of partial N-methyl-D-aspartate receptor ***,we review evidence for sublethal excitatory injuries in relation to neurodegeneration associated with Parkinson’s disease,Alzheimer’s disease,amyotrophic lateral sclerosis and Huntington’s *** contrast to classic excitotoxicity,emerging evidence implicates dysregulation of mitochondrial calcium handling in excitatory post-synaptic *** discuss mechanisms that regulate mitochondrial calcium uptake and release,the impact of LRRK2,PINK1,Parkin,beta-amyloid and glucocerebrosidase on mitochondrial calcium transporters,and the role of autophagic mitochondrial loss in axodendritic ***,we discuss strategies for normalizing the flux of calcium into and out of the mitochondrial matrix,thereby preventing mitochondrial calcium toxicity and excitotoxic dendritic *** the mechanisms that underlie increased uptake or decreased release of mitochondrial calcium vary in different model systems,a common set of strategies to normalize mitochondrial calcium flux can prevent excitatory mitochondrial toxicity and may be neuroprotective in multiple disease contexts.

关键词： Mitochondrial calcium Mitochondrial calcium uniporter NCLX antiporter Parkinson’s disease Alzheimer’s disease LRRK2 PINK1 Beta-amyloid Mitophagy Excitotoxicity Amyotrophic lateral sclerosis Huntington’s disease Glucocerebrosidase

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