ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2026
APOE ε4 accelerates plasma p-tau217 trajectory: a Bayesian joint longitudinal analysis of ADNI.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivePlasma GFAP and p-tau217 are leading blood biomarkers for Alzheimer's disease (AD), but whether APOE ε4 modulates their longitudinal rates of change - directly or via amyloid burden - is unresolved. We tested APOE ε4 modulation of plasma GFAP and p-tau217 trajectories and their coupling with cognitive/structural decline in ADNI participants.
methodsA total of 325 ADNI participants aged ≥ 65 (CN 181/MCI 106/AD 38) with ≥ 2 plasma GFAP and ≥ 2 p-tau217 (UPENN-Fujirebio) measurements over ≤ 10 years were analyzed. Linear mixed-effects models tested APOE ε4 × time interactions; Bayesian joint models (brms) estimated random-slope correlations ρ between biomarker and outcome trajectories. A formal counterfactual mediation analysis quantified direct versus amyloid-mediated pathways.
resultsAPOE ε4 was associated with a steeper p-tau217 slope (β = 0.0307/year, p = 0.002) but not GFAP slope (p = 0.149); p-tau217 co-varied with ADAS-Cog 13 (ρ = +0.67), MMSE (ρ = -0.69), and hippocampal ratio (ρ = - 0.39), while GFAP correlations were null, though the GFAP-paired joint models had convergence limitations. A formal mediation analysis found the APOE ε4 effect on p-tau217 slope was predominantly direct (ADE = 0.029, p < 0.001), with a small, only partially robust indirect pathway through baseline amyloid positivity (proportion mediated 6.4%, p = 0.045; attenuating to marginal significance with amyloid modeled continuously, p = 0.088).
conclusionsAPOE ε4 carriage predicts a steeper plasma p-tau217 trajectory over up to ten years, an effect that is predominantly direct rather than amyloid-mediated. Individual-level p-tau217 trajectory tracks cognitive decline; GFAP does not. Plasma p-tau217 trajectory is informative of cognitive trajectory, although whether it predicts or parallels decline cannot be determined from these data.
Indexed as
Identifiers
42909513What OpenQuestion holds
Registered trials
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.