Evidence map›Paper›PMID 39236111›Full record

ArticleBrain and behavior2024

Relationships among tumor necrosis factor-alpha levels, beta-amyloid accumulation, and hippocampal atrophy in patients with late-life major depressive disorder.

Szu-Kai Ho, Ing-Tsung Hsiao, Kun-Ju Lin, Yi-Ming Wu, Kuan-Yi Wu

Abstract read
In one paragraph

Article in Brain and behavior, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

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

  1. 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

5 authors.

Szu-Kai HoDepartment of Psychiatry, Chang Gung Memorial Hospital and College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Ing-Tsung HsiaoDepartment of Nuclear Medicine and Center for Advanced Molecular Imaging and Translation, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Kun-Ju LinDepartment of Nuclear Medicine and Center for Advanced Molecular Imaging and Translation, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Yi-Ming WuDepartment of Radiology, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Kuan-Yi WuDepartment of Psychiatry, Chang Gung Memorial Hospital and College of Medicine, Chang Gung University, Taoyuan, Taiwan.ORCID 0000-0003-3030-9706

Funding

The Ministry of Science and Technology, Taiwan
6 · The paper itself

Abstract

backgroundMajor depressive disorder (MDD) is characterized by hippocampal volume reduction, impacting cognitive function. Inflammation, particularly elevated tumor necrosis factor-alpha (TNF-α) levels, is consistently implicated in MDD pathophysiology. This study investigates the relationships between TNF-α levels, hippocampal volume, beta-amyloid (Aβ) burden, and cognitive abilities in MDD patients, aiming to illuminate the complex interplay among inflammatory markers, pathology indicators, structural brain alterations, and cognitive performance in non-demented MDD individuals.

methodFifty-two non-demented MDD patients, comprising 25 with mild cognitive impairment (MCI), were recruited along with 10 control subjects. Each participant underwent a thorough assessment encompassing TNF-α blood testing,

resultsMCI MDD patients displayed elevated TNF-α levels and reduced HVa relative to controls. Correlation analyses demonstrated inverse relationships between TNF-α level and HVa in MCI MDD, all MDD, and all subjects groups. Both TNF-α level and HVa exhibited significant correlations with processing speed across all MDD and all subjects. Notably, global

conclusionThis study highlights elevated TNF-α levels and reduced hippocampal volume in MCI MDD patients, indicating a potential association between peripheral inflammation and structural brain alterations in depression. Furthermore, our results suggest that certain cases of MDD may be affected by non-amyloid-mediated process, which impacts their TNF-α and hippocampal volume. These findings emphasize the importance of further investigating the complex interplay among inflammation, neurodegeneration, and cognitive function in MDD.

Indexed as

Amyloid beta-PeptidesAtrophyCognitive DysfunctionHippocampusMagnetic Resonance ImagingMajor Depressive DisorderPositron-Emission TomographyTumor Necrosis Factor-alphaAgedAniline CompoundsEthylene GlycolsFemaleHumansMaleMiddle AgedNeuropsychological TestsAmyloid beta-PeptidesAniline CompoundsEthylene GlycolsflorbetapirTumor Necrosis Factor-alpha18F‐florbetapir (AV‐45/Amyvid)amyloidhippocampal atrophymajor depressive disorderTNF‐α

Identifiers

PMID39236111
PMCPMC11376440

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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.