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Excitotoxicity as a target against neurodegenerative processes

dc.contributor.authorBinvignat O.
dc.contributor.authorOlloquequi J.
dc.date.accessioned2020-09-02T22:13:11Z
dc.date.available2020-09-02T22:13:11Z
dc.date.issued2020
dc.identifier10.2174/1381612826666200113162641
dc.identifier.citation26, 12, 1251-1262
dc.identifier.issn13816128
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3764
dc.descriptionThe global burden of neurodegenerative diseases is alarmingly increasing in parallel to the aging of population. Although the molecular mechanisms leading to neurodegeneration are not completely understood, excitotoxicity, defined as the injury and death of neurons due to excessive or prolonged exposure to excitatory amino acids, has been shown to play a pivotal role. The increased release and/or decreased uptake of glutamate results in dysregulation of neuronal calcium homeostasis, leading to oxidative stress, mitochondrial dysfunctions, disturbances in protein turn-over and neuroinflammation. Despite the anti-excitotoxic drug memantine has shown modest beneficial effects in some patients with dementia, to date, there is no effective treatment capable of halting or curing neurodegenerative diseases such as Alz-heimer’s disease, Parkinson disease, Huntington’s disease or amyotrophic lateral sclerosis. This has led to a grow-ing body of research focusing on understanding the mechanisms associated with the excitotoxic insult and on uncovering potential therapeutic strategies targeting these mechanisms. In the present review, we examine the molecular mechanisms related to excitotoxic cell death. Moreover, we provide a comprehensive and updated state of the art of preclinical and clinical investigations targeting excito-toxic-related mechanisms in order to provide an effective treatment against neurodegeneration. © 2020 Bentham Science Publishers.
dc.language.isoen
dc.publisherBentham Science Publishers
dc.subjectAlzheimer’s disease
dc.subjectCalcium
dc.subjectER stress
dc.subjectGlutamate
dc.subjectNeurodegeneration
dc.subjectNeuroinflammation
dc.subjectOxidative stress
dc.subjectParkinson’s disease
dc.subjectadenosine triphosphatase
dc.subjectamino acid
dc.subjectapoptosome
dc.subjectapoptotic protease activating factor 1
dc.subjectBH3 protein
dc.subjectcalcium
dc.subjectcalcium channel blocking agent
dc.subjectcalpain
dc.subjectcaspase 9
dc.subjectcinnarizine
dc.subjectDNA
dc.subjectflunarizine
dc.subjectglutamic acid
dc.subjectglyceraldehyde 3 phosphate dehydrogenase
dc.subjectinositol 1,4,5 trisphosphate receptor
dc.subjection channel
dc.subjectionotropic receptor
dc.subjectisoflurane
dc.subjectlomerizine
dc.subjectmemantine
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectnimodipine
dc.subjectnitric oxide
dc.subjectpropofol
dc.subjectreactive oxygen metabolite
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase
dc.subjectsodium calcium exchange protein
dc.subjectunindexed drug
dc.subjectverapamil
dc.subjectzonisamide
dc.subjectAlzheimer disease
dc.subjectamyotrophic lateral sclerosis
dc.subjectapoptosis
dc.subjectcalcium homeostasis
dc.subjectcell death
dc.subjectcytotoxicity
dc.subjectdegenerative disease
dc.subjectdementia
dc.subjectdisease exacerbation
dc.subjectdisorders of mitochondrial functions
dc.subjectDNA fragmentation
dc.subjectdopaminergic nerve cell
dc.subjectendoplasmic reticulum stress
dc.subjectexcitotoxicity
dc.subjectfrontotemporal dementia
dc.subjecthuman
dc.subjectHuntington chorea
dc.subjectin vitro study
dc.subjectin vivo study
dc.subjectinflammation
dc.subjectmitochondrial permeability
dc.subjectmolecular mechanics
dc.subjectmotor performance
dc.subjectnerve degeneration
dc.subjectnervous system inflammation
dc.subjectnitrosylation
dc.subjectoxidative stress
dc.subjectParkinson disease
dc.subjectpathophysiology
dc.subjectpriority journal
dc.subjectprotein processing
dc.subjectReview
dc.subjecttraumatic brain injury
dc.subjectunfolded protein response
dc.titleExcitotoxicity as a target against neurodegenerative processes
dc.typeReview


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