Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10958101 | Neurochemistry International | 2013 | 8 Pages |
Abstract
⺠Oxidative stress evokes oligomerisation and secretion of synuclein (ASN). ⺠Secreted ASN can be transferred between neurons causing the death of the recipient cells. ⺠ASN evokes alterations in neurotransmission, mitochondrial dysfunction and oxidative stress. ⺠Secreted ASN increases the release of other amyloidogenic peptides and interact with them. ⺠The molecular events activated by secreted ASN lead to inflammation and selective neuronal death.
Keywords
CREBASNTNTsnNOSICAM-1AβNACMmpsPARP-1NF-κBIL-6O2−ONOO−ROSα-synucleinHydrogen peroxideamyloid βsuperoxide anionMitochondria dysfunctioninterleukin-6Lewy bodiesAlzheimer’s diseaseNeurodegenerative diseasesParkinson’s diseaseOxidative stressDopamineHydroxyl radicalsneuronal nitric oxide synthasenuclear factor kappa BMatrix metalloproteasesCSFCerebrospinal fluidintercellular adhesion molecule-1CANNitric oxideH2O2cAMP response element-binding proteinPeroxynitritePoly(ADP-ribose) polymerase-1CalcineurinReactive oxygen species
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Authors
Anna Wilkaniec, Joanna B. Strosznajder, Agata Adamczyk,