J
J.G. de Yebenes
Researcher at Carlos III Health Institute
Publications - 7
Citations - 334
J.G. de Yebenes is an academic researcher from Carlos III Health Institute. The author has contributed to research in topics: Parkin & Neuroprotection. The author has an hindex of 7, co-authored 7 publications receiving 316 citations.
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Toxic effects of L-DOPA on mesencephalic cell cultures: protection with antioxidants
TL;DR: The damage of DA neurons took place before the rising of quinones, suggesting thatQuinones are not essential in L-DOPA toxicity for DA neurons, and antioxidants completely prevented L- DOPA-induced quinone formation as well as the death of non-DA neurons.
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The accumulation of neurotoxic proteins, induced by proteasome inhibition, is reverted by trehalose, an enhancer of autophagy, in human neuroblastoma cells
María José Casarejos,Rosa M. Solano,Ana M. Gómez,Juan Perucho,J.G. de Yebenes,Maria Angeles Mena +5 more
TL;DR: Trehalose is a powerful modifier of abnormal protein accumulation in neurodegenerative diseases and inhibition of autophagy reverted the neuroprotective effects of trehalose in epoxomicin-induced cell death.
Journal ArticleDOI
Suppression of Parkin enhances nigrostriatal and motor neuron lesion in mice over-expressing human-mutated tau protein
J. Menéndez,Jose A. Rodriguez-Navarro,Rosa M. Solano,María José Casarejos,Izaskun Rodal,Rosa Guerrero,Marina P. Sánchez,Jesús Avila,Maria Angeles Mena,J.G. de Yebenes +9 more
TL;DR: There are interactions between tau and parkin that could be relevant for the pathogenesis and treatment of tauopathies, and it is hoped that the double transgenic parkin-/-+tau(VLW) mice could be useful for testing of compounds with putative therapeutic value in human t Tauopathies.
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On the Pathogenesis and Neuroprotective Treatment of Parkinson Disease: What have we Learned from the Genetic Forms of this Disease?
TL;DR: The in vitro and in vivo studies performed in genetic models of PD have shown that the proteins involved in the pathogenesis of PD interact with one another and have multiple mechanisms of cell toxicity, clear that the mechanisms leading to cell degeneration in PD are variable in the different subtypes of this disease.
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Effects of retinoic acid on NB 69 human neuroblastoma cells and fetal rat mid brain neurons.
TL;DR: RA may play a trophic positive role in the differentiation of immature cells to cholinergic neurons; this contrasts with the detrimental effects of RA on catecholamine neurons.