A neurotrophic model for stress-related mood disorders.
By R. Duman, L. Monteggia. Biological Psychiatry, 2006
3,358 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience
View Paper: https://www.semanticscholar.org/paper/632155eb515d485010aa160f57599620b3f7c523
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In Cellular and Molecular Neuroscience
In Developmental Neuroscience
Citations in the corpus
- A systematic review and meta-analysis of clinical studies on major depression and BDNF levels: implications for the role of neuroplasticity in depression. (2008, background): “, 2004; Videbech and Ravnkilde, 2004) – moreover, hippocampal and hypothalamic– pituitary–adrenal axis dysfunction is associated with significant depressive symptoms, such as memory deficit and cognitive impairment (Duman and Monteggia, 2006).”
- Psychoneuroimmunology Meets Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior (2012, background): “A number of antidepressants have been shown to increase neurogenesis in the brain, and some of the behavioral effects of these drugs are dependent on the stimulation of neurogenesis (Duman and Monteggia, 2006; David et al, 2009).”
- Depression: An Evolutionarily Conserved Mechanism to Terminate Separation Distress? A Review of Aminergic, Peptidergic, and Neural Network Perspectives (2009, background): “…that may promote cell death or at least atrophic change in the hippocampus (Dranovskya & Hen, 2006), potential deficits in neuronal growth factors (Duman & Monteggia, 2006), and associated alterations in corticotropin-releasing factor (CRF), brain-derived neurotrophic factor (BDNF), and…”
- Exercise promotes the expression of brain derived neurotrophic factor (BDNF) through the action of the ketone body β-hydroxybutyrate (2016, background): “A number of studies have indicated that decreased levels of BDNF are associated with depression and become enhanced following antidepressant treatment (Duman and Monteggia, 2006; Martinowich et al., 2007).”
- The mesolimbic dopamine reward circuit in depression. (2006, background): “…approaches to modeling key symptoms of depression in animals, and could enable the development of antidepressant edications with fundamentally new mechanisms of action. ey Words: Ventral striatum, nucleus accumbens, ventral tegmenal area, CREB, dynorphin, BDNF, MCH, orexin, melanocortin, Clock,”
- BDNF — a key transducer of antidepressant effects (2015, background): “In this context, BDNF has been linked to the mechanism of action of antidepressants (Duman et al., 1997; Ghosh et al., 1994; Monteggia et al., 2004; Duman and Monteggia, 2006).”
- Stress, Depression, and Neuroplasticity: A Convergence of Mechanisms (2008, background): “Indeed, the list may not end hereFthere is evidence that insulin-like growth factor1 and fibroblast growth factor-2 are involved in stress, depression, and antidepressant responses (Duman and Monteggia, 2006).”
- Immune System to Brain Signaling: Neuropsychopharmacological Implications (2011, background): “Neuogenesis is believed to play a fundamental role in the maintenance of neural integrity, and reduced neurogenesis especially in the hippocampus is a hallmark of chronic exposure to stress in laboratory animals (Duman and Monteggia, 2006).”
- Understanding resilience (2013, background): “Several studies have shown down-regulation of BDNF in the hippocampus after exposure of animals to various types of stress, and in postmortem studies of suicide-depression patients (Duman and Monteggia, 2006; Duman, 2009).”
- The role of neurotrophic factors in adult hippocampal neurogenesis, antidepressant treatments and animal models of depressive-like behavior (2007, background): “On the basis of escape or immobility behaviors, it is, however, difficult, if not impossible, to determine the state of mood or depression in a laboratory animal (Duman and Monteggia, 2006).”
- Altered connectivity in depression: GABA and glutamate neurotransmitter deficits and reversal by novel treatments (2019, background): “Decreased neurotrophic factor expression is another possible mechanism as the maintenance and survival of SST interneurons is dependent on BDNF, which is decreased by stress (Duman and Monteggia, 2006; Grosse et al., 2005; Martinowich et al., 2011).”