Evidence mapPaperPMID 38405149Full record

ArticleFrontiers in endocrinology2024

Serum amyloid beta 42 levels correlated with metabolic syndrome and its components.

Kecheng Li, Xiaoli Zhou, Youren Liu, Dongyu Li, Yinyin Li, Ting Zhang, Chunyan Fu, Lin Li, Yang Hu, Li Jiang

Abstract read
In one paragraph

Article in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Amyloid-beta (1-40) peptide is associated with systemic metabolic health.European journal of clinical investigation · 2026
    Article
  4. Article
  5. Review
  6. 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

10 authors.

Kecheng Li *Department of Laboratory Medicine, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Xiaoli Zhou *Department of Laboratory Medicine, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Youren LiuDepartment of Health Management, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Dongyu LiDepartment of Health Management, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Yinyin LiDepartment of Health Management, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Ting ZhangDepartment of Laboratory Medicine, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Chunyan FuDepartment of Laboratory Medicine, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Lin LiDepartment of Laboratory Medicine, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Yang HuDepartment of Gastrointestinal Surgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Li JiangDepartment of Laboratory Medicine, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Beta-amyloid accumulation in the brain appears to be a key initiating event in Alzheimer's disease (AD), and factors associated with increased deposition of beta-amyloid are of great interest. Enhanced deposition of amyloid-β peptides is due to an imbalance between their production and elimination. Previous studies show that diminished levels of CSF amyloid beta 42 (Aβ42) is a biomarker in AD; however, the role of serum Aβ42 in AD is contradictory. BMI and obesity have been reported to be related to increased serum Aβ42 levels. Therefore, we aimed to investigate the relation between metabolic syndrome (MetS), its clinical measures (abdominal obesity, high glucose, high triglyceride, low high-density lipoprotein cholesterol level, and hypertension), and serum Aβ42 levels. Methods: A total of 1261 subjects, aged 18-89 years in Chengdu, China, were enrolled from January 2020 to January 2021 to explore the correlation of serum Aβ42 levels with body mass index (BMI), blood lipids, and blood pressure. Furthermore, as the risk of MetS is closely related to age, 1,212 participants ( Results: The results showed that log-transformed serum Aβ42 level was positively correlated with BMI ( Discussion: These observations indicate that MetS and its components are associated with higher levels of serum Aβ42 and hence limit the potential of serum Aβ42 as a suitable diagnostic biomarker for AD. As such, we recommend serum Aβ42 serve as a direct risk biomarker for MetS rather than for AD.

Indexed as

Alzheimer DiseaseMetabolic SyndromeAged, 80 and overAmyloid beta-PeptidesBiomarkersGlucoseHumansLipoproteins, HDLObesityTriglyceridesAmyloid beta-PeptidesBiomarkersGlucoseLipoproteins, HDLTriglyceridesAlzheimer’s disease (AD)blood lipidsblood pressurebody mass index (BMI)metabolic syndromeserum amyloid beta 42 (Aβ42)

Identifiers

PMID38405149
PMCPMC10893966

What Socratic holds

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Registered trials

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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 Socratic graph.