Evidence map›Paper›PMID 28261061›Full record

ReviewFrontiers in cellular neuroscience2017

Molecular Mechanisms of Bipolar Disorder: Progress Made and Future Challenges.

Yeni Kim, Renata Santos, Fred H Gage, Maria C Marchetto

Abstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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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.

Yeni KimLaboratory of Genetics, The Salk Institute for Biological StudiesLa Jolla, CA, USA; Department of Child and Adolescent Psychiatry, National Center for Mental HealthSeoul, South Korea.
Renata SantosLaboratory of Genetics, The Salk Institute for Biological StudiesLa Jolla, CA, USA; Ecole Normale Supérieure, PSL Research University, Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de Biologie de l'Ecole Normale Supérieure (IBENS)Paris, France.
Fred H GageLaboratory of Genetics, The Salk Institute for Biological Studies La Jolla, CA, USA.
Maria C MarchettoLaboratory of Genetics, The Salk Institute for Biological Studies La Jolla, CA, USA.

Funding

Role of CACNA1C - a shared risk gene in neuropsychiatric disordersU19MH106434 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI GAGE, FRED H · 2016 to 2020
$13.8M
Single-Cell Approaches to Reveal How Jumping Genes Individualize Neural CircuitsR01MH095741 · NIMH · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI GAGE, FRED H · 2011 to 2015
$6.5M
NIMH NIH HHS R01 MH095741NIMH NIH HHS U19 MH106434
6 · The paper itself

Abstract

Bipolar disorder (BD) is a chronic and progressive psychiatric illness characterized by mood oscillations, with episodes of mania and depression. The impact of BD on patients can be devastating, with up to 15% of patients committing suicide. This disorder is associated with psychiatric and medical comorbidities and patients with a high risk of drug abuse, metabolic and endocrine disorders and vascular disease. Current knowledge of the pathophysiology and molecular mechanisms causing BD is still modest. With no clear biological markers available, early diagnosis is a great challenge to clinicians without previous knowledge of the longitudinal progress of illness. Moreover, despite recommendations from evidence-based guidelines, polypharmacy is still common in clinical treatment of BD, reflecting the gap between research and clinical practice. A major challenge in BD is the development of effective drugs with low toxicity for the patients. In this review article, we focus on the progress made and future challenges we face in determining the pathophysiology and molecular pathways involved in BD, such as circadian and metabolic perturbations, mitochondrial and endoplasmic reticulum (ER) dysfunction, autophagy and glutamatergic neurotransmission; which may lead to the development of new drugs.

Indexed as

bipolar disorderdisease modelingendoplasmic reticulum stressglutamatehyperexcitabilitymitochondrial dysfunctionoxidative stress

Identifiers

PMID28261061
PMCPMC5306135

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.