Evidence map›Paper›PMID 25056514›Full record

ReviewExpert opinion on therapeutic targets2014

Targeting mitochondrially mediated plasticity to develop improved therapeutics for bipolar disorder.

Rafael T de Sousa, Rodrigo Machado-Vieira, Carlos A Zarate, Husseini K Manji

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Targeting Mitochondrial Dysfunction for Bipolar Disorder.Current topics in behavioral neurosciences · 2021
    Review
  11. Review
  12. Review
  13. Article
  14. Interaction of the Psychiatric Risk GeneFrontiers in cellular neuroscience · 2019
    Article
  15. Opportunities and challenges in psychopharmacology
.Dialogues in clinical neuroscience · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 3 institutions in 2 countries.

Rafael T de SousaUniversity of Sao Paulo, Institute and Department of Psychiatry, Laboratory of Neuroscience, LIM-27, Faculty of Medicine , Paulo Rua Ovidio Pires de Campos 785, São Paulo, SP , Brazil.
Rodrigo Machado-Vieira
Carlos A Zarate
Husseini K Manji
National Institute of Mental Health · USUniversidade de São Paulo · BRWeatherford College · US

Funding

Target validation of novel therapeutic agents in mood disordersZIAMH002927 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI ZARATE, CARLOS · 2010 to 2025
$37.1M
Intramural NIH HHS Z99 MH999999
6 · The paper itself

Abstract

introductionBipolar disorder (BPD) is a severe illness with few treatments available. Understanding BPD pathophysiology and identifying potential relevant targets could prove useful for developing new treatments. Remarkably, subtle impairments of mitochondrial function may play an important role in BPD pathophysiology. AREAS COVERED: This article focuses on human studies and reviews evidence of mitochondrial dysfunction in BPD as a promising target for the development of new, improved treatments. Mitochondria are crucial for energy production, generated mainly through the electron transport chain (ETC) and play an important role in regulating apoptosis and calcium (Ca²⁺) signaling as well as synaptic plasticity. Mitochondria move throughout the neurons to provide energy for intracellular signaling. Studies showed polymorphisms of mitochondria-related genes as risk factors for BPD. Postmortem studies in BPD also show decreased ETC activity/expression and increased nitrosative and oxidative stress (OxS) in patient brains. BPD has been also associated with increased OxS, Ca²⁺ dysregulation and increased proapoptotic signaling in peripheral blood. Neuroimaging studies consistently show decreased energy levels and pH in brains of BPD patients. EXPERT OPINION: Targeting mitochondrial function, and their role in energy metabolism, synaptic plasticity and cell survival, may be an important avenue for development of new mood-stabilizing agents.

Indexed as

Molecular Targeted TherapyAntimanic AgentsApoptosisBipolar DisorderCalciumCell SurvivalDrug DesignEnergy MetabolismHumansMitochondriaNeuronal PlasticityPolymorphism, GeneticRisk FactorsAntimanic AgentsCalciumapoptosisbipolar disordercalciummitochondriamood stabilizeroxidative stress

Identifiers

PMID25056514
PMCPMC4180305
OpenAlexW2153674729

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.