Antidepressive effects of targeting ELK-1 signal transduction

@article{Apazoglou2018AntidepressiveEO,
  title={Antidepressive effects of targeting ELK-1 signal transduction},
  author={Kallia Apazoglou and S{\'e}verine Farley and Victor Gorgievski and Raoul Belzeaux and Juan Pablo Lopez and Julien Grenier and El Ch{\'e}rif Ibrahim and Marie-Anne El Khoury and Yiu Chung Tse and Rapha{\"e}le Mongr{\'e}dien and Alexandre Barb{\'e} and Carlos E. A. de Macedo and Wojciech Jaworski and Ariane Bochereau and Alejandro Orrico and Elsa Isingrini and Chlo{\'e} Guinaudie and Lenka Mikasov{\'a} and Franck Louis and Sophie Gautron and Laurent Groc and Charbel Massaad and Ferah Yildirim and Vincent Vialou and Sylvie Dumas and Fabio Marti and Naguib Mechawar and Elise Morice and Tak Pan Wong and Jocelyne Caboche and Gustavo Turecki and Bruno Giros and Eleni T. Tzavara},
  journal={Nature Medicine},
  year={2018},
  volume={24},
  pages={591-597}
}
Depression, a devastating psychiatric disorder, is a leading cause of disability worldwide. Current antidepressants address specific symptoms of the disease, but there is vast room for improvement1. In this respect, new compounds that act beyond classical antidepressants to target signal transduction pathways governing synaptic plasticity and cellular resilience are highly warranted2–4. The extracellular signal–regulated kinase (ERK) pathway is implicated in mood regulation5–7, but its… 
Chronically altered NMDAR signaling in epilepsy mediates comorbid depression
TLDR
The findings suggest NMDAR signaling alterations are a major contributor to EAD development and a potential target for treating conditions associated with underlying excitotoxic neuronal damage.
The Eph receptor A4 plays a role in demyelination and depression-related behavior
TLDR
The results provide insights into the etiology of depressive symptoms in some patients and suggest that inhibition of EphA4 or the promotion of myelination could be a promising strategy for treating depression.
GPR56/ADGRG1 is associated with response to antidepressant treatment
TLDR
In the blood of individuals with depression, GPR56 expression increases in responders to antidepressant treatment, but not in non-responders, uncovering a potential role of G PR56 in antidepressant response.
SRF in Neurochemistry: Overview of Recent Advances in Research on the Nervous System.
TLDR
The phenotypes of mice with nervous system-specific KO of SRF or its cofactors are presented by depicting recent findings associated with brain development, plasticity, epilepsy, stress response, and drug addiction, all of which result from function or dysfunction of the SRF axis.
Antidepressive Effects of Taraxacum Officinale in a Mouse Model of Depression Are Due to Inhibition of Corticosterone Levels and Modulation of Mitogen-Activated Protein Kinase Phosphatase-1 (Mkp-1) and Brain-Derived Neurotrophic Factor (Bdnf) Expression
TLDR
Investigation of the underlying mechanism revealed that the T. officinale extract exerts significant antidepressant effects in a mouse model of depression by inhibition of corticosterone levels and modulation of Mkp-1 and Bdnf expression.
Cinnamaldehyde prevents intergenerational effect of paternal depression in mice via regulating GR/miR-190b/BDNF pathway.
TLDR
Cinnamaldehyde is a potential intervening agent for intergenerational inheritance of depression, probably by regulating GR/miR-190b/BDNF pathway.
SWI/SNF chromatin remodeler complex within the reward pathway is required for behavioral adaptations to stress
TLDR
It is shown that repeated social defeat induces changes in BRG1 nuclear distribution, and the pivotal function of SWI/SNF complexes in behavioral and transcriptional adaptations to salient environmental challenges is demonstrated.
RNA therapeutics for mood disorders: current evidence toward clinical trials
TLDR
A systematic review of RNA therapeutics for the treatment of mood disorders studied in pre-clinical animal models listed in PubMed, in clinical trials registered in ClinicalTrials.gov and available on the market by combining literature search and Food and Drug Administration and European Medicine Agency online databases.
ELK-1: A molecular substrate of depression
  • C. Liston
  • Psychology, Biology
    Science Translational Medicine
  • 2018
Converging data from depressed patients and rodent chronic stress models implicate ELK-1, a stress-related transcription factor, in the pathophysiology of depression. Converging data from depressed
...
...

References

SHOWING 1-10 OF 71 REFERENCES
A negative regulator of MAP kinase causes depressive behavior.
TLDR
It is found that increased hippocampal MKP-1 expression, as a result of stress or viral-mediated gene transfer, causes depressive behaviors, and chronic antidepressant treatment normalizes stress-induced MKP -1 expression and behavior, and mice lacking MKp-1 are resilient to stress.
The Role of the Extracellular Signal-Regulated Kinase Signaling Pathway in Mood Modulation
TLDR
Lithium- and valproate-induced behavioral changes are qualitatively similar to the changes induced by amphetamine, a compound that induces relapse in remitted manic patients and mood elevation in normal subjects, suggesting that the ERK pathway may mediate the antimanic effects of mood stabilizers.
miR-1202: A Primate Specific and Brain Enriched miRNA Involved in Major Depression and Antidepressant Treatment
TLDR
It is shown that miR-1202, a miRNA specific to primates and enriched in the human brain, is differentially expressed in individuals with depression and is a potential target for new antidepressant treatments.
Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants
TLDR
Treatment with new agents results in an improvement in mood ratings within hours of dosing patients who are resistant to typical antidepressants, and these new agents have also been shown to reverse the synaptic deficits caused by stress.
Sustained hippocampal chromatin regulation in a mouse model of depression and antidepressant action
TLDR
An important role for histone remodeling in the pathophysiology and treatment of depression is underscored and the therapeutic potential for hist one methylation and deacetylation inhibitors in depression is highlighted.
Kinase-mediated signaling cascades in mood disorders and antidepressant treatment
TLDR
Fast developing kinome profiling approaches that allow identification of multiple kinases and kinase network connections simultaneously are reviewed, technical limitation and challenges are analyzed, and their future applications to mood disorders and antidepressant treatment are discussed.
Molecular Neurobiology and Promising New Treatment in Depression
TLDR
Beyond neuroanatomy and monoamine theory, cells and molecules, neural plasticity, neurotrophisms, endocrine mechanisms, immunological mechanisms, genetics, circadian rhythms, and metabolic regulation in depression are discussed.
...
...