ArticlebioRxiv : the preprint server for biology2025
Patient-specific functional brain architecture explains cortical patterns of tau PET in Alzheimer's disease.
Article in bioRxiv : the preprint server for biology, 2025. 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
18 authors.
Funding
Abstract
The spatial distribution of tau pathology, the core driver of neurodegeneration in Alzheimer's disease (AD), varies markedly across individuals. While tau is thought to spread along brain networks, the role of inter-individual variability in shaping these patterns remains underexplored. Using resting-state fMRI and tau-PET from 805 participants across the AD continuum, we studied whether subject-specific functional connectivity (FC) profiles enhance the characterization of tau deposition patterns. A hybrid approach integrating individual and group-average FC outperformed both alone, particularly in symptomatic individuals and at finer spatial resolutions, the latter underscoring a critical but often overlooked role of spatial scale. Individualized FC also better captured individual tau topographies than canonical tau-PET maps derived from cohort-level data. These effects were specific to tau, and not seen for β-amyloid, and their predictive power increased with spatial granularity. Furthermore, baseline FC also predicted future tau accumulation at the individual level, supporting its prognostic value. Together, these findings provide strong evidence that individual functional brain architecture shapes tau propagation in humans, supporting the network spread hypothesis by showing that variability in connectivity translates into heterogeneity in tau distribution. This work advances biological understanding of tau propagation in AD, highlighting functional connectivity as a mechanistic substrate that supports prognostic assessment of tau trajectories.
Identifiers
What Socratic 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 Socratic graph.