Journal ArticleDOI
Neuroprotection by Imipramine against lipopolysaccharide-induced apoptosis in hippocampus-derived neural stem cells mediated by activation of BDNF and the MAPK pathway.
Chi-Hsien Peng,Chi-Hsien Peng,Shih Hwa Chiou,Shih Hwa Chiou,Shih-Jen Chen,Yueh Ching Chou,Hung-Hai Ku,Cheng-Kuo Cheng,Chih-Ju Yen,Tung Hu Tsai,Yuh-Lih Chang,Chun-Lan Kao +11 more
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TLDR
IM can increase the neuroprotective effects, suppress the LPS-induced inflammatory process, and promote serotoninergic differentiation in NSCs via the modulation of the BDNF/MAPK/ERK pathway/Bcl-2 cascades.About:
This article is published in European Neuropsychopharmacology.The article was published on 2008-02-01. It has received 144 citations till now. The article focuses on the topics: MAPK/ERK pathway & Neural stem cell.read more
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Inflammatory cytokines in depression: Neurobiological mechanisms and therapeutic implications
TL;DR: This review explores the idea that specific gene polymorphisms and neurotransmitter systems can confer protection from or vulnerability to specific symptom dimensions of cytokine-related depression and potential therapeutic strategies that target inflammatory cytokine signaling.
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Antidepressants increase neural progenitor cells in the human hippocampus
Maura Boldrini,Maura Boldrini,Mark D. Underwood,René Hen,Gorazd Rosoklija,Gorazd Rosoklija,Andrew J. Dwork,J. John Mann,Victoria Arango +8 more
TL;DR: The increase of NPCs and dividing cells in MDDT was localized to the rostral DG, and whether this finding is critical or necessary for the antidepressants effect remains to be determined.
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Brain-derived neurotrophic factor: a bridge between inflammation and neuroplasticity
Francesca Calabrese,Andrea C. Rossetti,Giorgio Racagni,Peter Gass,Marco A. Riva,Raffaella Molteni +5 more
TL;DR: One of the most interesting hypotheses: the involvement of the neurotrophin brain-derived neurotrophic factor (BDNF), which represents one of the major mediators of neuroplasticity, is discussed.
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In animal models, psychosocial stress-induced (neuro)inflammation, apoptosis and reduced neurogenesis are associated to the onset of depression.
TL;DR: It is concluded that external stressors may provoke depression-like behaviors through activation of inflammatory, oxidative, apoptotic and antineurogenic mechanisms and the clinical efficacity of antidepressants may be ascribed to their ability to reverse these different pathways.
Journal ArticleDOI
Neurotransmitter, peptide and cytokine processes in relation to depressive disorder: comorbidity between depression and neurodegenerative disorders.
TL;DR: The view is taken that synergy between stressors and inflammatory factors may promote pathological outcomes through their actions on neuropeptides and several neurotransmitters.
References
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Trk receptors: roles in neuronal signal transduction.
Eric J. Huang,Louis F. Reichardt +1 more
TL;DR: The most fascinating aspect of Trk receptor-mediated signaling is its interplay with signaling promoted by the pan-neurotrophin receptor p75NTR, which activates a distinct set of signaling pathways within cells that are in some instances synergistic and in other instances antagonistic to those activated by Trk receptors.
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Brain-Derived Neurotrophic Factor Produces Antidepressant Effects in Behavioral Models of Depression
TL;DR: The hypothesis that BDNF in the hippocampus produces an antidepressant effect in behavioral models of depression, the learned helplessness (LH) and forced swim test (FST) paradigms is tested and provides further support for the hypothesis thatBDNF contributes to the therapeutic action of antidepressant treatment.
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Cytokine-Associated Emotional and Cognitive Disturbances in Humans
Abraham Reichenberg,Raz Yirmiya,Andreas Schuld,Thomas Kraus,Monika Haack,Abraham Morag,Thomas Pollmächer +6 more
TL;DR: In humans, a mild stimulation of the primary host defense has negative effects on emotional and memory functions, which is probably caused by cytokine release, and cytokines represent a novel target for neuropsychopharmacological research.
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Antidepressant-Like Effect of Brain-derived Neurotrophic Factor (BDNF)
TL;DR: Findings demonstrate an antidepressant-like property of BDNF in two animal models of depression, which may be mediated by increased activity in monoaminergic systems.
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Prevention of programmed cell death of sympathetic neurons by the bcl-2 proto-oncogene.
TL;DR: Overexpression of the bcl-2 proto-oncogene in cultured sympathetic neurons has now been shown to prevent apoptosis normally induced by deprivation of nerve growth factor, suggesting that the B cl-2 protein may be a major mediator of the effects of neurotrophic factors on neuronal survival.