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- W96314905 abstract "In Parkinson's and other neurodegenerative diseases, a therapeutic strategy has been proposed to halt progressive cell death. Propargylamine derivatives, rasagiline and (-)deprenyl (selegiline), have been confirmed to protect neurons against cell death induced by various insults in cellular and animal models of neurodegenerative disorders. In this paper, the mechanism and the markers of the neuroprotection are reviewed. Propargylamines prevent the mitochondrial permeabilization, membrane potential decline, cytochrome c release, caspase activation and nuclear translocation of glyceraldehyde 3-phosphate dehydrogenase. At the same time, rasagiline induces anti-apoptotic pro-survival proteins, Bcl-2 and glial cell-line derived neurotrophic factor, which is mediated by activated ERK-NF-kappaB signal pathway. DNA array studies indicate that rasagiline increases the expression of the genes coding mitochondrial energy synthesis, inhibitors of apoptosis, transcription factors, kinases and ubiquitin-proteasome system, sequentially in a time-dependent way. Products of cell survival-related gene induced by propargylamines may be applied as markers of neuroprotection in clinical samples." @default.
- W96314905 created "2016-06-24" @default.
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- W96314905 date "2007-01-01" @default.
- W96314905 modified "2023-09-27" @default.
- W96314905 title "Neuroprotection by propargylamines in Parkinson’s disease: intracellular mechanism underlying the anti-apoptotic function and search for clinical markers" @default.
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- W96314905 doi "https://doi.org/10.1007/978-3-211-73574-9_15" @default.
- W96314905 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17982885" @default.
- W96314905 hasPublicationYear "2007" @default.
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