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Peer-reviewedCC BY-NC-ND 4.0Alzheimer's & Dementia

Blood transcriptomic signatures of vascular risk in Alzheimer's disease

  • Sang‐Won Han1,2
  • Young Ho Park3
  • Jung‐Min Pyun3
  • Jiyun Hwang3
  • Jeong Su Park4
  • SangYun Kim3
  • Kwangsik Nho5
5 affiliations
  1. 1Department of Neurology Soonchunhyang University Seoul Hospital, Soonchunhyang University College of Medicine Seoul Republic of Korea
  2. 2Department of Neurology Seoul Metropolitan Government–Seoul National University Boramae Medical Center Seoul National University College of Medicine Seoul Republic of Korea
  3. 3Department of Neurology Seoul National University Bundang Hospital and Seoul National University College of Medicine Seongnam Republic of Korea
  4. 4Department of Laboratory Medicine Seoul National University Bundang Hospital and Seoul National University College of Medicine Seongnam Republic of Korea
  5. 5Center for Neuroimaging Department of Radiology and Imaging Sciences Indiana Alzheimer's Disease Research Center Indiana University School of Medicine Indianapolis Indiana USA
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Abstract

INTRODUCTION: Lifestyle and environmental factors contributing to cardiovascular risk are components of the exposome, yet molecular signatures associated with cumulative cardiovascular risk in Alzheimer's disease (AD) remain incompletely understood.

METHODS: We analyzed blood‐based transcriptomics data from two independent cohorts: Seoul National University Bundang Hospital (SNUBH; N = 148, Korean) and Alzheimer's Disease Neuroimaging Initiative (ADNI; N = 743, predominantly European ancestry). Framingham cardiovascular risk score (FRS)–associated co‐expression network modules were identified, followed by pathway‐based enrichment, hub gene–based participant stratification, and bidirectional cross‐cohort discovery–replication analyses.

RESULTS: Two co‐expression modules were associated with FRS in SNUBH, and six in ADNI. Bidirectional analyses identified two preserved modules with consistent module–FRS associations across cohorts, enriched in pathways implicated in cellular responses to exposure, including RNA–protein homeostasis, mitochondrial function, and hematopoietic processes. Hub genes in the two modules stratified participants into molecularly distinct subgroups concordant with clinical FRS categories.

DISCUSSION: FRS‐associated molecular pathways were identified and warrant further investigation as potential targets for risk modification.

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Cite

BibTeXRIS
BibTeX
@article{han2026blood,
  title = {{Blood transcriptomic signatures of vascular risk in Alzheimer's disease}},
  author = {Sang‐Won Han and Young Ho Park and Jung‐Min Pyun and Jiyun Hwang and Jeong Su Park and SangYun Kim and Kwangsik Nho},
  journal = {Alzheimer's \& Dementia},
  year = {2026},
  month = oct,
  doi = {10.1002/alz.71930},
  url = {https://doi.org/10.1002/alz.71930},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Blood transcriptomic signatures of vascular risk in Alzheimer's disease
AU  - Sang‐Won Han
AU  - Young Ho Park
AU  - Jung‐Min Pyun
AU  - Jiyun Hwang
AU  - Jeong Su Park
AU  - SangYun Kim
AU  - Kwangsik Nho
PY  - 2026
DA  - 2026/10/01
JO  - Alzheimer's & Dementia
DO  - 10.1002/alz.71930
UR  - https://doi.org/10.1002/alz.71930
AB  - INTRODUCTION: Lifestyle and environmental factors contributing to cardiovascular risk are components of the exposome, yet molecular signatures associated with cumulative cardiovascular risk in Alzheimer's disease (AD) remain incompletely understood.  METHODS: We analyzed blood‐based transcriptomics data from two independent cohorts: Seoul National University Bundang Hospital (SNUBH; N = 148, Korean) and Alzheimer's Disease Neuroimaging Initiative (ADNI; N = 743, predominantly European ancestry). Framingham cardiovascular risk score (FRS)–associated co‐expression network modules were identified, followed by pathway‐based enrichment, hub gene–based participant stratification, and bidirectional cross‐cohort discovery–replication analyses.  RESULTS: Two co‐expression modules were associated with FRS in SNUBH, and six in ADNI. Bidirectional analyses identified two preserved modules with consistent module–FRS associations across cohorts, enriched in pathways implicated in cellular responses to exposure, including RNA–protein homeostasis, mitochondrial function, and hematopoietic processes. Hub genes in the two modules stratified participants into molecularly distinct subgroups concordant with clinical FRS categories.  DISCUSSION: FRS‐associated molecular pathways were identified and warrant further investigation as potential targets for risk modification.
SN  - 1552-5260
SN  - 1552-5279
ER  -