Evidence map›Paper›PMID 39889254›Full record

ArticleNeurology2025

Association of Plasma Biomarkers of Alzheimer Disease and Neurodegeneration With Longitudinal Intra-Network Functional Brain Connectivity.

Heather E Dark, Andrea T Shafer, Jenifer Cordon, Yang An, Alexandria Lewis, Abhay Moghekar, Bennett Landman, Susan M Resnick, Keenan A Walker

Abstract read
In one paragraph

Article in Neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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.

Heather E DarkLaboratory of Behavioral Neuroscience, National Institute on Aging, Bethesda, MD.ORCID 0000-0001-7194-3637
Andrea T ShaferLaboratory of Behavioral Neuroscience, National Institute on Aging, Bethesda, MD.ORCID 0000-0003-4599-5980
Jenifer CordonLaboratory of Behavioral Neuroscience, National Institute on Aging, Bethesda, MD.
Yang AnLaboratory of Behavioral Neuroscience, National Institute on Aging, Bethesda, MD.ORCID 0000-0002-3312-7265
Alexandria LewisDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD; and.
Abhay MoghekarDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD; and.ORCID 0000-0001-9464-1551
Bennett LandmanDepartment of Electrical and Computer Engineering, Department of Computer Science, Vanderbilt University, Nashville, TN.
Susan M ResnickLaboratory of Behavioral Neuroscience, National Institute on Aging, Bethesda, MD.
Keenan A WalkerLaboratory of Behavioral Neuroscience, National Institute on Aging, Bethesda, MD.ORCID 0000-0002-5989-9853

Funding

Research Education ComponentP30AG066507 · NIA · JOHNS HOPKINS UNIVERSITY · PI Corinne Pettigrew · 2020 to 2026
$29.3M
NIA NIH HHS P30 AG066507
6 · The paper itself

Abstract

BACKGROUND AND

objectivesAlzheimer disease (AD) is defined by cortical β-amyloid (Aβ), tau, and neurodegeneration, which contribute to cognitive decline, in part, by altering large-scale functional brain networks. While cortical Aβ and tau have been associated with changes in functional brain connectivity, it is unknown whether plasma biomarkers relate to such changes. In a healthy community sample of cognitively unimpaired adults free from major CNS disease from the Baltimore Longitudinal Study of Aging, we examined whether plasma biomarkers of AD pathology (Aβ

methodsPlasma biomarkers were measured using the Quanterix SIMOA assays. Intranetwork connectivity (3T resting-state fMRI) from 7 functional networks was derived using a predefined cortical parcellation mask for each participant visit. Cognitive performance was assessed concurrently with fMRI scan. Covariate-adjusted linear mixed-effect models were used to determine (1) whether plasma biomarkers were associated with longitudinal changes in connectivity, (2) whether the magnitude of the biomarker-connectivity relationships differed by amyloid status, and (3) whether changes in connectivity co-occurred with longitudinal changes in cognition.

resultsOur primary findings (n = 486; age = 65.5 ± 16.2 years; 54% female; mean follow-up time = 4.3 ± 1.7 years) showed that higher baseline GFAP was associated with faster declines in somatomotor (β = -0.04, DISCUSSION: Among cognitively unimpaired participants, plasma biomarkers of amyloidosis, astrogliosis, and neuronal injury are associated with declines in network connectivity, particularly among amyloid-positive participants. Major limitations include the lack of inclusion of the sensitive pTau-217 and pTau-231 isoforms and comparative PET biomarkers.

Indexed as

Alzheimer DiseaseBrainAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersFemaleGlial Fibrillary Acidic ProteinHumansLongitudinal StudiesMagnetic Resonance ImagingMaleMiddle AgedNeurofilament ProteinsPeptide Fragmentstau ProteinsAmyloid beta-PeptidesBiomarkersGFAP protein, humanGlial Fibrillary Acidic Proteinneurofilament protein LNeurofilament ProteinsPeptide Fragmentstau Proteins

Identifiers

PMID39889254
PMCPMC11784718

What OpenQuestion holds

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Read underepoch 390

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 OpenQuestion graph.