OSCR

Systemic proteomic and organ aging signatures associated with plasma Aβ oligomerization in a Korean cohort: a cross-sectional study.

Overview

Authors: Hyunjung Oh1, Hongju Kim1, Hojin Kang1, Dohyeon Kwon1, Leon French2, Young Ho Park3, Young Chul Youn4, Seong Soo An5, SangYun Kim3, Sungmin Kang1
  1. PeopleBio Inc., Seongnam-si, Gyeonggi-do, Republic of Korea
  2. Physiology Department and Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, Toronto, ON, Canada
  3. Department of Neurology, Seoul National University Bundang Hospital and Seoul National University College of Medicine, Seongnam-si, Gyeonggi-do, Republic of Korea
  4. Department of Neurology, Chung-Ang University College of Medicine, Seoul, Republic of Korea
  5. Department of BionanoTechnology, Gachon University, Seongnam-si, Gyeonggi-do, Republic of Korea
Institutions: PeopleBio (South Korea) (South Korea); University of Toronto (Canada); Seoul National University (South Korea); Seoul National University Bundang Hospital (South Korea); Chung-Ang University (South Korea); Gachon University (South Korea)
Journal: Frontiers in aging neuroscience, volume 18, article 1620991
Dates: received 30 April 2025; accepted 18 February 2026; published online 23 March 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.3389/fnagi.2026.1620991 · PMID 41948065 · PMCID PMC13051358 · OpenAlex W7140115029
Open access: gold, a free copy (OpenAlex)
Categories: genetics / omics (modality), PET / SPECT (modality), human (organism), Alzheimer's / dementia (population)
Methods: Connectivity, Statistics, Smoothing, state filtering, decompositions, Machine learning, Preprocessing, Spectral & time-frequency
Keywords: Alzheimer’s disease, blood proteome, dementia, oligomerization tendency, β-amyloid
Topic: Alzheimer's disease research and treatments (Cellular and Molecular Neuroscience, Neuroscience), according to OpenAlex
Funding: National Research Foundation; National Research Foundation of Korea (RS-2021-NR060117); Ministry of SMEs and Startups
Citations: cited by 1 paper (Europe PMC); 66 references in the paper

Abstract

Background: Alzheimer’s disease (AD) is characterized by the accumulation of amyloid-beta (Aβ) in the brain, which begins decades before the appearance of clinical symptoms. Blood from AD patients, when spiked with synthetic Aβ, exhibited a higher Aβ oligomerization tendency (OAβT) than the non-AD subjects. OAβT reflected early pathological changes of AD and is considered as a promising blood-based biomarker. However, the mechanism underlying OAβT remained elusive. This study aimed to identify proteomic signatures associated with OAβT and explore its role in AD diagnosis.

Methods: Forty AD and non-AD subjects from a Korean cohort were divided into four groups based on the disease diagnosis, OAβT values (thresholded at 0.78 ng/mL), and amyloid PET status (A-PET): A-PET-positive AD patients with high or low OAβT values, A-PET-negative non-AD subjects with high or low OAβT values. Using aptamer-based proteomics, 7,288 proteins from plasma samples were quantified, and the group differences were assessed in protein levels and the enrichment of gene sets associated with annotations from the Gene Ontology database. Further, we assessed whether OAβT-PET mismatched cases (A-PET-positive but OAβT-low or A-PET-negative but OAβT-high) exhibited distinct blood proteome signatures in comparison to typical AD cases. Aging signatures for 11 organs were analyzed to explore systemic factors linked to OAβT-PET discrepancies. Additionally, the pharmacological influences on the OAβT-related proteome were investigated by comparing OAβT-correlated proteins with a database of drug-induced proteomic changes.

Results: Elevated OAβT values, regardless of AD diagnosis, correlated with increased immune response and decreased cellular metabolism. Dementia-predicting proteins were enriched in non-AD individuals with high OAβT. Accelerated muscle aging was associated with high OAβT values and worse cognitive function. Furthermore, several potential pharmacological modulators of OAβT, including Minocycline and Anamorelin, were identified.

Conclusion: Our findings demonstrated OAβT as a reflection of systemic changes linked to early AD pathology. Moreover, the influence of medications and systemic aging on OAβT values pointed to the potential avenues for intervention and emphasized the importance of considering systemic factors in AD pathogenesis and treatment.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

The paper links to its data and to no code of its authors: see the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

Data availability statement

The datasets generated and analyzed in this study are publicly available in the FigShare repository and can be accessed at https://doi.org/10.6084/m9.figshare.31428272 (https://figshare.com/articles/dataset/Systemic_proteomic_and_organ_aging_signatures_associated_with_plasma_A_oligomerization_in_a_Korean_cohort_a_cross-sectional_study/31428272).

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 30 September 2026: the first record

Recorded: type, language, journal, volume, pages, dates, 10 authors, 5 keywords, 3 funders, 66 references.

Cite

This paper

Oh, H., Kim, H., Kang, H., Kwon, D., French, L., Park, Y. H., Youn, Y. C., An, S. S., Kim, S., & Kang, S. (2026). Systemic proteomic and organ aging signatures associated with plasma Aβ oligomerization in a Korean cohort: a cross-sectional study. Frontiers in aging neuroscience, 18, 1620991. https://doi.org/10.3389/fnagi.2026.1620991

BibTeX

@article{oh2026systemic,
author = {Oh, Hyunjung and Kim, Hongju and Kang, Hojin and Kwon, Dohyeon and French, Leon and Park, Young Ho and Youn, Young Chul and An, Seong Soo and Kim, SangYun and Kang, Sungmin},
title = {{Systemic proteomic and organ aging signatures associated with plasma Aβ oligomerization in a Korean cohort: a cross-sectional study}},
journal = {Frontiers in aging neuroscience},
year = {2026},
month = mar,
volume = {18},
pages = {1620991},
publisher = {Frontiers Media SA},
issn = {1663-4365},
doi = {10.3389/fnagi.2026.1620991},
url = {https://doi.org/10.3389/fnagi.2026.1620991},
pmid = {41948065},
pmcid = {PMC13051358}
}

RIS

TY - JOUR
AU - Oh, Hyunjung
AU - Kim, Hongju
AU - Kang, Hojin
AU - Kwon, Dohyeon
AU - French, Leon
AU - Park, Young Ho
AU - Youn, Young Chul
AU - An, Seong Soo
AU - Kim, SangYun
AU - Kang, Sungmin
TI - Systemic proteomic and organ aging signatures associated with plasma Aβ oligomerization in a Korean cohort: a cross-sectional study
T2 - Frontiers in aging neuroscience
J2 - Front Aging Neurosci
PY - 2026
DA - 2026/03/23
VL - 18
SP - 1620991
SN - 1663-4365
PB - Frontiers Media SA
DO - 10.3389/fnagi.2026.1620991
UR - https://doi.org/10.3389/fnagi.2026.1620991
LA - en
ER -

CSL-JSON

{
"id": "10.3389/fnagi.2026.1620991",
"type": "article-journal",
"title": "Systemic proteomic and organ aging signatures associated with plasma Aβ oligomerization in a Korean cohort: a cross-sectional study",
"container-title": "Frontiers in aging neuroscience",
"author": [
{
"family": "Oh",
"given": "Hyunjung"
},
{
"family": "Kim",
"given": "Hongju"
},
{
"family": "Kang",
"given": "Hojin"
},
{
"family": "Kwon",
"given": "Dohyeon"
},
{
"family": "French",
"given": "Leon"
},
{
"family": "Park",
"given": "Young Ho"
},
{
"family": "Youn",
"given": "Young Chul"
},
{
"family": "An",
"given": "Seong Soo"
},
{
"family": "Kim",
"given": "SangYun"
},
{
"family": "Kang",
"given": "Sungmin"
}
],
"container-title-short": "Front Aging Neurosci",
"volume": "18",
"page": "1620991",
"DOI": "10.3389/fnagi.2026.1620991",
"PMID": "41948065",
"PMCID": "PMC13051358",
"ISSN": "1663-4365",
"publisher": "Frontiers Media SA",
"URL": "https://doi.org/10.3389/fnagi.2026.1620991",
"language": "en",
"issued": {
"date-parts": [
[
2026,
3,
23
]
]
}
}

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.1002/acn3.52250
APOE genotype and brain amyloid are associated with changes in the plasma proteome in elderly subjects without dementia.
Journal: Annals of clinical and translational neurology
In common: Alzheimer's / dementia, genetics / omics, 4 references
[2] doi:10.1073/pnas.2402117122
Inhibition of amyloid beta oligomer accumulation by NU-9: A unifying mechanism for the treatment of neurodegenerative diseases.
Journal: Proceedings of the National Academy of Sciences of the United States of America
In common: Alzheimer's / dementia, 3 references
[3] doi:10.1002/alz.14142
Proteomic analyses reveal plasma EFEMP1 and CXCL12 as biomarkers and determinants of neurodegeneration.
Journal: Alzheimer's & dementia : the journal of the Alzheimer's Association
In common: Alzheimer's / dementia, genetics / omics, 3 references
[4] doi:10.1038/s43587-025-00965-4 [code]
Plasma proteomic associations with Alzheimer's disease endophenotypes.
Journal: Nature aging
In common: Alzheimer's / dementia, genetics / omics, 3 references
[5] doi:10.1021/acscentsci.3c00592 [code]
Antibodies Raised Against an Aβ Oligomer Mimic Recognize Pathological Features in Alzheimer's Disease and Associated Amyloid-Disease Brain Tissue.
Journal: ACS central science
In common: Alzheimer's / dementia, 3 references
[6] doi:10.1186/s13195-023-01302-w
Head-to-head comparison between plasma p-tau217 and flortaucipir-PET in amyloid-positive patients with cognitive impairment.
Journal: Alzheimer's research & therapy
In common: PET / SPECT, Alzheimer's / dementia, 2 references
[7] doi:10.1590/0004-282x-anp-2022-s138
From clinical phenotype to proteinopathy: molecular neuroimaging in neurodegenerative dementias.
Journal: Arquivos de neuro-psiquiatria
In common: PET / SPECT, Alzheimer's / dementia, 2 references
[8] doi:10.1093/braincomms/fcag287 [code]
Plasma proteomics reveals molecular overlap between physical activity and dementia risk.
Journal: Brain communications
In common: Alzheimer's / dementia, genetics / omics, 2 references
[9] doi:10.1038/s43587-023-00373-6 [code]
Heterochronic parabiosis reprograms the mouse brain transcriptome by shifting aging signatures in multiple cell types.
Journal: Nature aging
In common: Alzheimer's / dementia, genetics / omics, 2 references
[10] doi:10.1371/journal.pbio.3002607 [code]
Brain high-throughput multi-omics data reveal molecular heterogeneity in Alzheimer's disease.
Journal: PLoS biology
In common: Alzheimer's / dementia, genetics / omics, 2 references

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion, reproductions, activity

Discussion: code errors and mismatches between the code and the paper about this paper and its code, from readers and its authors, beside the paper and its tracing map.

Reproductions: reports from readers who ran the authors' code and did not get the paper's result, what they ran, with which environment, commit and data.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.