Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5739118 | Progress in Neurobiology | 2016 | 77 Pages |
Abstract
Oxidative stress reflects an imbalance between the overproduction and incorporation of free radicals and the dynamic ability of a biosystem to detoxify reactive intermediates. Free radicals produced by oxidative stress are one of the common features in several experimental models of diseases. Free radicals affect both the structure and function of neural cells, and contribute to a wide range of neurodegenerative diseases, including Parkinson's disease and Alzheimer's disease. Although the precise mechanisms that result in the degeneration of neurons and the relevant pathological changes remain unclear, the crucial role of oxidative stress in the pathogenesis of neurodegenerative diseases is associated with several proteins (such as α-synuclein, DJ-1, Amyloid β and tau protein) and some signaling pathways (such as extracellular regulated protein kinases, phosphoinositide 3-kinase/Protein Kinase B pathway and extracellular signal-regulated kinases 1/2) that are tightly associated with the neural damage. In this review, we present evidence, gathered over the last decade, concerning a variety of pathogenic proteins, their important signaling pathways and pathogenic mechanisms associated with oxidative stress in Parkinson's disease and Alzheimer's disease. Proper control and regulation of these proteins' functions and the related signaling pathways may be a promising therapeutic approach to the patients. We also emphasizes antioxidative options, including some new neuroprotective agents that eliminate excess reactive oxygen species efficiently and have a certain therapeutic effect; however, controversy surrounds some of them in terms of the dose and length of therapy. These agents require further investigation by clinical application in patients suffering Parkinson's disease and Alzheimer's disease.
Keywords
PI3K6-OHDAJnkMSRCMACATNrf2Aβ6-HydroxydopamineDATα-SynAPPIκBLRRK2MPTPFOXO3aAChEIsSOD1PKBP2X7RSOD2RAGERegulator of Calcineurin 1Rcan1sRAGEchaperone mediated autophagyNOX1IKKsSporadic ADSoluble RAGEPRDX3PYCR11-methyl-4-phenyl-1,2,3,6-tetrahydropyridinec-Jun N-terminal kinaseERK1/2MAPKMPP+NADPH oxidase 1O2−P-TauROSTrx1α-synucleinHydrogen peroxideamyloid-betaIronApoeapolipoprotein ENADPH oxidaseLoadFADAlzheimer’s diseaseNeurodegenerative diseaseParkinson’s diseasephosphorylated tauOxidative stressleucine-rich repeat kinase 2Thioredoxin 1forkhead box O3DA transporterHappCNSDopamineHydroxyl radicalSODsuperoxide dismutase 1Superoxide dismutaseSuperoxide dismutase 2central nervous systemUbiquitin proteasome systemantioxidant response elementSADFamilial ADnuclear factor erythroid 2-related factor 2Phoxphosphoinositide 3-kinaseZincinterstitial fluidmethionine sulfoxide reductaseCopperSignaling pathwayManganeseinhibitory κBacetylcholinesterase inhibitorsMitochondriaknockoutISFNickelAREH2O2peroxiredoxin 3amyloid precursor proteinprotein kinase Bmitogen-activated protein kinaseCatalaseSHIP-1Extracellular signal-regulated kinases 1/2Reactive oxygen speciesP2X7 receptorreceptor for advanced glycation endproductsUPS
Related Topics
Life Sciences
Neuroscience
Neuroscience (General)
Authors
Tianfang Jiang, Qian Sun, Shengdi Chen,