Evidence map›Paper›PMID 42100483›Full record

ArticleFrontiers in aging neuroscience2026

Limbic-predominant neuroimaging correlates of plasma p-Tau217 in preclinical and clinical Alzheimer's disease.

Ankit Patel, William Guiler, Sam Pepper, Riley E Kemna, Paul J Kueck, Ian W Weidling, Hana D Mayfield, Casey S John, Dinesh Pal Mudaranthakam, Heather M Wilkins and 4 more

Abstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Ankit PatelUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
William GuilerUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Sam PepperUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Riley E KemnaUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Paul J KueckUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Ian W WeidlingUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Hana D MayfieldUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Casey S JohnUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Dinesh Pal MudaranthakamUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Heather M WilkinsUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Russell H SwerdlowUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Jeffrey M BurnsUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Jill K MorrisUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.
Robyn A HoneaUniversity of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, United States.

Funding

Bioenergetic Contributions to Tau Phosphorylation in Aging and Alzheimer DiseaseF31AG091982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Riley Kemna · 2025 to 2026
$78k
NIA NIH HHS F31 AG091982
6 · The paper itself

Abstract

Background: Plasma phosphorylated tau at threonine 217 (p-Tau217) has emerged as a highly sensitive and specific blood-based biomarker for Alzheimer's Disease (AD). However, its regional brain correlates with multimodal neuroimaging, beyond tau-PET, remain underexplored, particularly in early disease phases where limbic involvement may predominate. This study aimed to map the associations of plasma p-Tau217 with amyloid-PET burden, FDG-PET metabolism, and structural brain morphometry in a well-characterized cohort spanning cognitively unimpaired (CU) and cognitively impaired (CI) individuals across AD dementia stages, hypothesizing increased AD neuroimaging biomarkers in individuals with elevated p-Tau217. Methods: We analyzed data from 259 participants from the University of Kansas Alzheimer's Disease Research Center (KU ADRC) Clinical Cohort. Imaging outcomes included amyloid-PET, FDG-PET, gray matter volumetric regions of interest as well as whole brain voxel-based morphometry (VBM), and surface-based morphometry (SBM) for cortical thickness (CT), sulcal depth (SD), gyrification index (GI), fractal dimension (FD). Analyses were stratified by diagnostic and pTau-217 positivity (CU pTau + , CU pTau -, CI pTau + and CI pTau-). Spearman's correlations and voxel/surface-wise regressions evaluated p-Tau217 associations with imaging metrics, accounting for age and sex. Results: Plasma p-Tau217 was elevated in CI versus CU. Individuals with elevated plasma p-Tau217 had increased amyloid-PET deposition across the cortex, as well as significantly higher centiloids, both in CU and CI individuals. In CI individuals, elevated p-Tau217 was associated with reduced voxel-wise gray matter volume and cortical thickness in limbic, temporal, parietal, and frontal regions, plus increased cingulate FD. In both CU and CI pTau + individuals, p-Tau217 correlated with AD Signature gray matter decreases. Conclusion: These findings show that CU and CI individuals with elevated plasma p-Tau217 have both increased amyloid-PET burden but also temporolimbic gray matter atrophy and hypometabolism. This supports p-Tau217 as a minimally invasive, scalable biomarker for early AD detection, risk stratification, and prognostic monitoring in preclinical stages, potentially guiding trial enrichment and personalized interventions.

Indexed as

centiloidcortical thicknessFDG-PEThippocampusp-tau217voxel-based morphometry

Identifiers

PMID42100483
PMCPMC13144096

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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.