Evidence map›Paper›PMID 31612411›Full record

ReviewMolecular biology reports2020

The cellular and molecular basis of major depressive disorder: towards a unified model for understanding clinical depression.

Eleni Pitsillou, Sarah M Bresnehan, Evan A Kagarakis, Stevano J Wijoyo, Julia Liang, Andrew Hung, Tom C Karagiannis

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 4 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

106 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Cells · 2022
    Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Trial
  8. Peripheral S-(PGJBMC psychiatry · 2026
    Article
  9. Article
  10. Ecologically-Valid Emotion Signatures Enhance Mood Disorder Diagnostics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

46 more citing papers are in PubMed but not listed here.

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

7 authors.

Eleni PitsillouEpigenomic Medicine Program, Department of Diabetes, Central Clinical School, Monash University, Prahran, VIC, 3004, Australia.
Sarah M BresnehanEpigenomic Medicine Program, Department of Diabetes, Central Clinical School, Monash University, Prahran, VIC, 3004, Australia.
Evan A KagarakisEpigenomic Medicine Program, Department of Diabetes, Central Clinical School, Monash University, Prahran, VIC, 3004, Australia.
Stevano J WijoyoEpigenomic Medicine Program, Department of Diabetes, Central Clinical School, Monash University, Prahran, VIC, 3004, Australia.
Julia LiangEpigenomic Medicine Program, Department of Diabetes, Central Clinical School, Monash University, Prahran, VIC, 3004, Australia.
Andrew HungSchool of Science, RMIT University, Melbourne, VIC, 3001, Australia.
Tom C KaragiannisEpigenomic Medicine Program, Department of Diabetes, Central Clinical School, Monash University, Prahran, VIC, 3004, Australia. tom.karagiannis@monash.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Major depressive disorder (MDD) is considered a serious public health issue that adversely impacts an individual's quality of life and contributes significantly to the global burden of disease. The clinical heterogeneity that exists among patients limits the ability of MDD to be accurately diagnosed and currently, a symptom-based approach is utilized in many cases. Due to the complex nature of this disorder, and lack of precise knowledge regarding the pathophysiology, effective management is challenging. The aetiology and pathophysiology of MDD remain largely unknown given the complex genetic and environmental interactions that are involved. Nonetheless, the aetiology and pathophysiology of MDD have been the subject of extensive research, and there is a vast body of literature that exists. Here we overview the key hypotheses that have been proposed for the neurobiology of MDD and highlight the need for a unified model, as many of these pathways are integrated. Key pathways discussed include neurotransmission, neuroinflammation, clock gene machinery pathways, oxidative stress, role of neurotrophins, stress response pathways, the endocannabinoid and endovanilloid systems, and the endogenous opioid system. We also describe the current management of MDD, and emerging novel therapies, with particular focus on patients with treatment-resistant depression (TRD).

Indexed as

DepressionMajor Depressive DisorderModels, BiologicalAnimalsAntidepressive AgentsHumansInflammationMiceNeurotransmitter AgentsOxidative StressSignal TransductionSynapsesAntidepressive AgentsNeurotransmitter AgentsAntidepressantsMajor depressive disorderMonoamine oxidase enzymesNeuroinflammationNeurotransmittersNeurotrophinsOxidative stressTreatment-resistant depression

Identifiers

What OpenQuestion holds

Textmetadata
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.