Evidence map›Paper›PMID 25733956›Full record

ReviewDialogues in clinical neuroscience2014

Intermediate phenotypes and biomarkers of treatment outcome in major depressive disorder.

Andrew F Leuchter, Aimee M Hunter, David E Krantz, Ian A Cook

Open access · diamondAbstract readReview
In one paragraph

Review in Dialogues in clinical neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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  12. Molecular neuropsychiatry · 2018
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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 at 1 institution in 1 country.

Andrew F LeuchterLaboratory of Brain, Behavior, and Pharmacology, and the Depression Research and Clinical Program, Semel Institute for Neuroscience and Human Behavior, UCLA; the Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Aimee M HunterLaboratory of Brain, Behavior, and Pharmacology, and the Depression Research and Clinical Program, Semel Institute for Neuroscience and Human Behavior, UCLA; the Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
David E KrantzLaboratory of Brain, Behavior, and Pharmacology, and the Depression Research and Clinical Program, Semel Institute for Neuroscience and Human Behavior, UCLA; the Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Ian A CookLaboratory of Brain, Behavior, and Pharmacology, and the Depression Research and Clinical Program, Semel Institute for Neuroscience and Human Behavior, UCLA; the Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, UCLA; the Department of Bioengineering, Henry Samueli School of Engineering and Applied Sciences, UCLA, Los Angeles, California, USA.
Samueli Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Major depressive disorder (MDD) is a pleomorphic illness originating from gene x environment interactions. Patients with differing symptom phenotypes receive the same diagnosis and similar treatment recommendations without regard to genomics, brain structure or function, or other physiologic or psychosocial factors. Using this present approach, only one third of patients enter remission with the first medication prescribed, and patients may take longer than 1 year to enter remission with repeated trials. Research to improve treatment effectiveness recently has focused on identification of intermediate phenotypes (IPs) that could parse the heterogeneous population of patients with MDD into subgroups with more homogeneous responses to treatment. Such IPs could be used to develop biomarkers that could be applied clinically to match patients with the treatment that would be most likely to lead to remission. Putative biomarkers include genetic polymorphisms, RNA and protein expression (transcriptome and proteome), neurotransmitter levels (metabolome), additional measures of signaling cascades, oscillatory synchrony, neuronal circuits and neural pathways (connectome), along with other possible physiologic measures. All of these measures represent components of a continuum that extends from proximity to the genome to proximity to the clinical phenotype of depression, and there are many levels along this continuum at which useful IPs may be defined. Because of the highly integrative nature of brain systems and the complex neurobiology of depression, the most useful biomarkers are likely to be those with intermediate proximity both to the genome and the clinical phenotype of MDD. Translation of findings across the spectrum from genotype to phenotype promises to better characterize the complex disruptions in signaling and neuroplasticity that accompany MDD, and ultimately to lead to greater understanding of the causes of depressive illness.

Indexed as

Treatment OutcomeAntidepressive AgentsBiomarkersHumansMajor Depressive DisorderPhenotypeAntidepressive AgentsBiomarkersbiomarkerbiosignaturecognitive and motivational domaincordancegenotypeHuntington's disease (HD)intermediate phenotypeMajor Depressive Disorder (MDD)oscillationoscillatory synchronypredictionqEEGRDoCthalamocortical dysrhythmiatreatment outcome

Identifiers

PMID25733956
PMCPMC4336921
OpenAlexW1505291704

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.