Evidence map›Paper›PMID 39424870›Full record

ArticleScientific reports2024

Serum proteomic changes related to residual impairment in remittent depression are associated with immune and inflammatory processes.

Seungyeon Lee, Sora Mun, Eun-Jeong Joo, Yeeun Yun, Hee-Gyoo Kang, Jiyeong Lee

Abstract readValidation Study
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. SAA4: An Underdog Within the Serum Amyloid a Superfamily?International journal of molecular sciences · 2026
    Review
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

6 authors.

Seungyeon LeeDepartment of Senior Healthcare, Graduate School, Eulji University, Uijeongbu, 11759, Republic of Korea.
Sora MunDepartment of Biomedical Laboratory Science, College of Health Sciences, Eulji University, Seongnam, 13135, Republic of Korea.
Eun-Jeong JooDepartment of Neuropsychiatry, School of Medicine, Eulji University, Daejeon, 35233, Republic of Korea.
Yeeun YunDepartment of Biomedical Laboratory Science, Graduate School, Eulji University, Uijeongbu, 11759, Republic of Korea.
Hee-Gyoo KangDepartment of Senior Healthcare, Graduate School, Eulji University, Uijeongbu, 11759, Republic of Korea. kanghg@eulji.ac.kr.
Jiyeong LeeDepartment of Biomedical Laboratory Science, Graduate School, Eulji University, Uijeongbu, 11759, Republic of Korea. leejiyeong@eulji.ac.kr.

Funding

National Research Foundation of Korea 2020R1C1C1009196
6 · The paper itself

Abstract

In patients with major depressive disorder, various functional areas are impaired, negatively impacting the quality of life. Remission can restore pre-depression functions; however, some patients may still have residual impairments. Distinguishing between near-normal recovery and residual impairment helps identify those at a high risk of relapse risk and helps tailor treatment. Accordingly, we aimed to discover and validate biomarkers that distinguish between near-normal recovery and residual impairment in remission states through serum proteome analysis. Pooled serum and individual serum samples from three groups (depression status, remission status with residual impairment, and remission status with normal recovery) were analyzed using liquid chromatography-tandem mass spectrometry. The combination of four proteins-antithrombin-III, serum amyloid A4 protein, C1q subcomponent subunit B, and serum amyloid P-component-was selected as a candidate biomarker. The trend of protein changes suggests complement C1q subcomponent subunit B and serum amyloid P-component as potential biomarkers for distinguishing remission from residual impairment. Changes in complement C1q subcomponent subunit B and serum amyloid P-component suggest that the complement system and inflammation-related immune mechanisms are associated with residual impairment in remittent major depressive disorder.

Indexed as

Amyloid beta-PeptidesAntithrombin IIIComplement C1qMajor Depressive DisorderSerum Amyloid P-ComponentAdultAgedBiomarkersCohort StudiesComplement System ProteinsFemaleHumansMaleProteomeRecovery of FunctionRemission InductionAmyloid beta-PeptidesAntithrombin IIIBiomarkersC1QB protein, humanComplement C1qComplement System ProteinsProteomeSAA4 protein, humanSerum Amyloid A ProteinSerum Amyloid P-ComponentInflammationMajor depressive disorderProteomicsRemissionResidual impairment

Identifiers

PMID39424870
PMCPMC11489708

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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.