Evidence map›Paper›PMID 19442176›Full record

ReviewCurrent pharmaceutical design2009

Targeting glutamatergic signaling for the development of novel therapeutics for mood disorders.

Rodrigo Machado-Vieira, Giacomo Salvadore, Lobna A Ibrahim, Nancy Diaz-Granados, Carlos A Zarate

Open access · greenAbstract readReview
In one paragraph

Review in Current pharmaceutical design, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
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  7. Review
  8. Riluzole Impairs Cocaine Reinstatement and Restores Adaptations in Intrinsic Excitability and GLT-1 Expression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  9. Article
  10. New targets for rapid antidepressant action.Progress in neurobiology · 2017
    Review
  11. Review
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  13. Article
  14. Article
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  20. Bcl-2 rs956572 polymorphism is associated with increased anterior cingulate cortical glutamate in euthymic bipolar I disorder.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Rodrigo Machado-VieiraExperimental Therapeutics, Mood and Anxiety Disorders Research Program, National Institute of Mental Health/NIH, 10 Center Drive, Bethesda, MD 20892, USA.
Giacomo Salvadore
Lobna A Ibrahim
Nancy Diaz-Granados
Carlos A Zarate
National Institute of Mental Health · US

Funding

Glutamatergic Modulators for Rapid & Sustained Antidepressant EffectZIAMH002857 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI ZARATE, CARLOS · 2009 to 2025
$55.0M
Efficacy of an Antiglutamatergic Agents in Treatment-Resistant DepressionZIAMH002828 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI ZARATE, CARLOS · 2009 to 2014
$1.6M
Glutamatergic Modulators--Rapid Sustained AntidepressantZ01MH002857 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI MANJI, HUSSEINI K · 2005 to 2008
$621k
Investigation of Antidepressant Efficacy in BPDZ01MH002828 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI ZARATE, CARLOS · 2003 to 2008
$568k
Intramural NIH HHS Z01 MH002828Intramural NIH HHS Z01 MH002857
6 · The paper itself

Abstract

There have been no recent advances in drug development for mood disorders in terms of identifying drug targets that are mechanistically distinct from existing ones. As a result, existing antidepressants are based on decades-old notions of which targets are relevant to the mechanisms of antidepressant action. Low rates of remission, a delay of onset of therapeutic effects, continual residual depressive symptoms, relapses, and poor quality of life are unfortunately common in patients with mood disorders. Offering alternative options is requisite in order to reduce the individual and societal burden of these diseases. The glutamatergic system is a promising area of research in mood disorders, and likely to offer new possibilities in therapeutics. There is increasing evidence that mood disorders are associated with impairments in neuroplasticity and cellular resilience, and alterations of the glutamatergic system are known to play a major role in cellular plasticity and resilience. Existing antidepressants and mood stabilizers have prominent effects on the glutamate system, and modulating glutamatergic ionotropic or metabotropic receptors results in antidepressant-like properties in animal models. Several glutamatergic modulators targeting various glutamate components are currently being studied in the treatment of mood disorders, including release inhibitors of glutamate, N-methyl-D-aspartate (NMDA) antagonists, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) throughput enhancers, and glutamate transporter enhancers. This paper reviews the currently available knowledge regarding the role of the glutamatergic system in the etiopathogenesis of mood disorders and putative glutamate modulators.

Indexed as

Drug Delivery SystemsAnimalsAntidepressive AgentsAntimanic AgentsExcitatory Amino Acid AntagonistsGlutamatesHumansMood DisordersReceptors, N-Methyl-D-AspartateSignal TransductionAntidepressive AgentsAntimanic AgentsExcitatory Amino Acid AntagonistsGlutamatesReceptors, N-Methyl-D-Aspartate

Identifiers

PMID19442176
PMCPMC2795357
OpenAlexW2020948229

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.