Evidence map›Paper›PMID 40701901›Full record

ArticleThe journal of prevention of Alzheimer's disease2025

Organ-specific proteomic aging and cognitive performance: Implications for risk prediction of Alzheimer's disease and related dementias in older adults.

Sujin Kang, Susan Baker, Benedict Hayhoe, Geraint Price, Gerald Novak, Janice Wong, Lefkos Middleton, Oliver Robinson

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Article in The journal of prevention of Alzheimer's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
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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

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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

4 citing papers in PubMed.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

8 authors.

Sujin KangAgeing & Epidemiology (AGE) Research Unit, School of Public Health, Imperial College London, London, UK. Electronic address: sujin.kang@imperial.ac.uk.
Susan BakerAgeing & Epidemiology (AGE) Research Unit, School of Public Health, Imperial College London, London, UK.
Benedict HayhoeDivision of Primary Care and Public Health, School of Public Health, Imperial College London, London, UK.
Geraint PriceAgeing & Epidemiology (AGE) Research Unit, School of Public Health, Imperial College London, London, UK.
Gerald NovakFormerly Janssen Research & Development, USA.
Janice WongJohnson & Johnson, Cambridge, MA 02142, USA.
Lefkos MiddletonAgeing & Epidemiology (AGE) Research Unit, School of Public Health, Imperial College London, London, UK.
Oliver RobinsonAgeing & Epidemiology (AGE) Research Unit, School of Public Health, Imperial College London, London, UK; MRC Centre for Environment & Health, Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesBiological aging, characterized by cellular and molecular changes, may play a key role in neurodegenerative diseases. While recent proteomic advancements have introduced new aging clocks, widespread validation remains necessary. This study evaluated organ-specific and cognition-enriched proteomic clocks in relation to chronological age and cognitive change.

methodsWe analyzed plasma proteomic data from the CHARIOT PRO SubStudy (N = 409), measured using the SomaScan assay (version 4.1) at four time points over three years (months 0, 12, 24, and 36). Using published proteomic organ age weights, we calculated conventional, organ-specific, and cognition-enriched biological ages and compared them with chronological age. Adjusted multilevel regression analyses assessed associations between baseline proteomic AgeGaps (biological-chronological age differences) and cognitive performance over 54 months.

resultsThe cohort (mean age: 71.8 ± 5.5 years; 50.1 % female) showed moderate to strong correlations between proteomic ages and chronological age (r = 0.37-0.80; MAE = 4.2-2.7). Over three years, AgeGaps increased across the conventional, organismal, muscle, liver, artery, and immune systems, ranging from 2.1 ± 1.9 to 1.0 ± 2.3 years. The artery AgeGap was most strongly associated with cognitive decline, with conventional and organismal AgeGaps showing similar patterns. Higher baseline AgeGap z-scores (i.e., greater biological age) in the artery and brain were associated with poorer cognition, as measured by the Repeatable Battery for the Assessment of Neuropsychological Status Total Scores (Coeff. -3.0, 95 % CI: -3.4, -2.5; and -1.1, 95 % CI: -1.5, -0.6) and the Preclinical Alzheimer's Cognitive Composite (Coeff. -0.5, 95 % CI: -0.6, -0.4; and -0.14, 95 % CI: -0.3, -0.03).

conclusionsThese findings highlight the interplay between neurological function and cardiovascular aging in cognitive decline. Organ-specific biological age assessments may aid in the early detection of age-related changes, informing personalized interventions. Our study underscores the importance of proteomic aging signatures in elucidating Alzheimer's disease mechanisms and other neurodegenerative conditions, advocating for an integrated approach to brain and cardiovascular health.

Indexed as

AgingAlzheimer DiseaseCognitionDementiaProteomicsAgedAged, 80 and overFemaleHumansMaleNeuropsychological TestsBiological ageCognitive changesLongitudinal validationMultilevel modelsOrgan-specific agingProteomics

Identifiers

PMID40701901
PMCPMC12501340

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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.