Biochemical and Biophysical Research Communications
Regular ArticleSelegiline and Desmethylselegiline Stimulate NGF, BDNF, and GDNF Synthesis in Cultured Mouse Astrocytes
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Astrocytes in Parkinson's disease: from preclinical assays to in vivo imaging and therapeutic probes
2020, Neurobiology of AgingSelegiline ameliorates depression-like behaviors in rodents and modulates hippocampal dopaminergic transmission and synaptic plasticity
2019, Behavioural Brain ResearchCitation Excerpt :Some monoaminergic antidepressants enhance synaptic plasticity at several levels, including hippocampal neurogenesis, brain-derived neurotrophic factor (BDNF) expression, and modulation of synaptic formation [18,19]. Several studies have shown that selegiline enhances BDNF expression in cultured mouse astrocytes and the anterior cingulate cortex of mice [20,21], and facilitates differentiation of neural stem cells isolated from the adult mouse subventricular zone into neurons, through induction of neurotrophic factors [22]. Thus, the antidepressant-like effects of selegiline might be attributable to some mechanisms other than enhancement of serotonergic and noradrenergic transmission, through MAO-A inhibition.
Gene expression profiling coupled with Connectivity Map database mining reveals potential therapeutic drugs for Hirschsprung disease
2018, Journal of Pediatric SurgeryBinge ethanol exposure increases the Krüppel-like factor 11-monoamine oxidase (MAO) pathway in rats: Examining the use of MAO inhibitors to prevent ethanol-induced brain injury
2016, NeuropharmacologyCitation Excerpt :Moreover, ethanol not only reduces BDNF levels, it also inhibits BDNF-mediated signaling (Li et al., 2004), which could influence pro-apoptotic routes of cell death and converge with KLF11-mediated cell death signaling. Conversely, MAOIs reduce apoptosis and increase BDNF in cell culture and in rodents (Kontkanen and Castren, 1999; Mizuta et al., 2000; Youdim et al., 2014; Bar-Am et al., 2015). In the current study, binge ethanol exposure nearly doubled caspase-3 levels and reduced BDNF by half, strongly suggesting that cell death processes are enhanced by binge ethanol.
Rationale for an experimental treatment of retinitis pigmentosa: 140-Month test of hypothesis with one patient
2013, Medical HypothesesCitation Excerpt :Trophic factor withdrawal is a widely recognized cause of neuron apoptosis. It is therefore important to note that deprenyl, in addition to inhibiting apoptosis, may also exert protective effects on cones by the upregulation of eight neurotrophic factors: basic fibroblast growth factor, bFGF [28]; nerve growth factor, NGF [29]; ciliary neurotrophic factor, CNTF [30]; glial cell line-derived neutrophic factor, GDNF [31]; brain-derived neurotrophic factor and GDNF [32]; insulin-like growthfactor-1, IGF-1 [33]; superoxide dismutase via NGF [34]; and fibroblast growthfactor-2, FGF-2, and bFGF [35]. The delivery of one of these trophic factors, CNTF by Neurotech’s encapsulated cell technology, is currently undergoing clinical trials for RP and age-related macular degeneration [36].
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