Evidence map›Paper›PMID 37349844›Full record

ArticleAlzheimer's research & therapy2023

Acrolein adducts and responding autoantibodies correlate with metabolic disturbance in Alzheimer's disease.

Monika Renuka Sanotra, Shu-Huei Kao, Ching-Kuo Lee, Chun-Hsien Hsu, Wen-Chung Huang, Tsuei-Chuan Chang, Fang-Yu Tu, I-Uen Hsu, Yung-Feng Lin

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PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.3field-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

7 citing papers in PubMed, 19 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

Monika Renuka SanotraPh.D. Program in Medical Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, 110, Taiwan.
Shu-Huei KaoPh.D. Program in Medical Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, 110, Taiwan.
Ching-Kuo LeeSchool of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei, 110, Taiwan.
Chun-Hsien HsuDepartment of Family Medicine, Taipei City Hospital, Heping Fuyou Branch, Taipei, 100, Taiwan.
Wen-Chung HuangGraduate Institute of Health Industry Technology, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, 333, Taiwan.
Tsuei-Chuan ChangGraduate Institute of Health Industry Technology, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, 333, Taiwan.
Fang-Yu TuSchool of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, 110, Taiwan.
I-Uen HsuSchool of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, 110, Taiwan.
Yung-Feng LinPh.D. Program in Medical Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, 110, Taiwan. yflin@tmu.edu.tw.
Taipei Medical University · TWChang Gung University of Science and Technology · TWTaipei City Hospital · TW

Funding

Department of Health, Taipei City Government 11201-62-033Ministry of Science and Technology, Taiwan MOST 108-2622-B-038-001
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is caused by many intertwining pathologies involving metabolic aberrations. Patients with metabolic syndrome (MetS) generally show hyperglycemia and dyslipidemia, which can lead to the formation of aldehydic adducts such as acrolein on peptides in the brain and blood. However, the pathogenesis from MetS to AD remains elusive.

methodsAn AD cell model expressing Swedish and Indiana amyloid precursor protein (APP-Swe/Ind) in neuro-2a cells and a 3xTg-AD mouse model were used. Human serum samples (142 control and 117 AD) and related clinical data were collected. Due to the involvement of MetS in AD, human samples were grouped into healthy control (HC), MetS-like, AD with normal metabolism (AD-N), and AD with metabolic disturbance (AD-M). APP, amyloid-beta (Aß), and acrolein adducts in the samples were analyzed using immunofluorescent microscopy, histochemistry, immunoprecipitation, immunoblotting, and/or ELISA. Synthetic Aß

resultsAn increased level of acrolein adducts was detected in the AD model cells. Furthermore, acrolein adducts were observed on APP C-terminal fragments (APP-CTFs) containing Aß in 3xTg-AD mouse serum, brain lysates, and human serum. The level of acrolein adducts was correlated positively with fasting glucose and triglycerides and negatively with high-density lipoprotein-cholesterol, which correspond with MetS conditions. Among the four groups of human samples, the level of acrolein adducts was largely increased only in AD-M compared to all other groups. Notably, anti-acrolein-Aß autoantibodies, especially IgM, were largely reduced in AD-M compared to the MetS group, suggesting that the specific antibodies against acrolein adducts may be depleted during pathogenesis from MetS to AD.

conclusionsMetabolic disturbance may induce acrolein adduction, however, neutralized by responding autoantibodies. AD may be developed from MetS when these autoantibodies are depleted. Acrolein adducts and the responding autoantibodies may be potential biomarkers for not only diagnosis but also immunotherapy of AD, especially in complication with MetS.

Indexed as

Alzheimer DiseaseAcroleinAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAutoantibodiesBiomarkersChromatography, LiquidHumansImmunoglobulin MMiceTandem Mass SpectrometryAcroleinAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAutoantibodiesBiomarkersImmunoglobulin MAcrolein adductAlzheimer’s diseaseAmyloid-betaAutoantibodyMetabolic syndrome

Identifiers

PMID37349844
PMCPMC10286356
OpenAlexW4381684012

What OpenQuestion holds

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LicenceCC BY
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.