bioRxiv paper· developmental cognitive neuroscience· empirical study

Intrinsic timescale develops hierarchically from sensorimotor to association cortex in youth and stabilizes in adulthood

Shafiei, G., Bagautdinova, J., Sydnor, V. J., Bassett, D. S., Barch, D. M., Cieslak, M., Fan, Y., Flook, E., et al.

neuroscience

Quick verdict

Claims fMRI timescale develops along the S-A axis in youth and stabilizes in adulthood; rigorous study, but replication is partial and metric-dependent.

Summary

This bioRxiv preprint maps developmental change in fMRI-derived intrinsic timescale — quantified as the sum of positive autocorrelation function values up to the first zero-crossing, scaled by TR — in youth. Using resting-state fMRI from HCPD (n=565, ages 8-22), HBN (n=729, ages 8-22), and HCPYA (n=973, ages 22-37), processed with fMRIPrep/XCP-D and parcellated with Schaefer-400, the authors fit GAMs with age smooths (k=3) controlling sex and motion. Whole-brain timescale increased with age in HCPD (partial R²=0.047) and HBN (0.037); regional age effects were larger in association cortex, stable in sensorimotor cortex, and correlated with the sensorimotor-association (S-A) axis (HCPD rs=0.41; HBN rs=0.19). Age-effect maps correlated across cohorts (rs=0.30; Dice=0.42). In young adults, age effects were largely absent (11.7% of regions significant), supporting youth specificity. Extensive sensitivity analyses covered eTIV, parcel size, tSNR, site harmonization (CovBat-GAM), atlas resolution, and alternative metrics; a short/long-lag decomposition showed ACF-sum findings were driven by long-lag autocorrelation, distinct from lag-1 TA (which was not S-A aligned). Limitations: cross-sectional design, attenuated replication statistics in HBN, metric- and band-pass-dependence of the hierarchical pattern, and untested conflict with EEG/ECoG studies reporting decreasing timescales with age.

Review complete

Assessment at a glance

developmental cognitive neuroscience

5

risk flags identified

● high 0

● medium 3

● low 2

Reproducibility readinesshigh
Code & data availableyes
Review confidencehigh
AI text signal1/20 passages flagged
Deep research viableCode-reproducible

5 strengths · 5 weaknesses · 5 author questions

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Key claims under review

  • In youth (8-22 years), fMRI intrinsic timescale (ACF-sum) is longer in association than sensorimotor cortex in two independent cohorts.
  • Age-related increases in timescale concentrate in association cortex and align with the sensorimotor-association axis (HCPD rs=0.41; HBN rs=0.19), while sensorimotor timescales remain stable.
  • The developmental pattern is specific to youth: young adults (22-37 years) show largely absent age effects (11.7% of regions significant).
  • ACF-sum and lag-1 temporal autocorrelation capture partially distinct autocorrelation features (long-lag vs short-lag), explaining discrepancies with Bero et al. (2026) and with EEG/ECoG developmental studies.

Strengths

  • Multi-cohort design with independent replication and an adult specificity control

    Discovery (HCPD, n=565), replication (HBN, n=729), and specificity (HCPYA, n=973, ages 22-37) samples; cross-cohort age-effect maps correlate at rs=0.30 (pspin=0.0002) with Dice=0.42 for significant regions (Figure 5).

  • Unusually thorough sensitivity battery

    eTIV (S3), parcel size, HBN low-motion and low-p-factor subsets (S4), Schaefer-200 atlas (S5), tSNR (S6), CovBat-GAM site harmonization (S7), and alternative ACF definitions — exponential fit and first zero-crossing (S8) — all consistent with main findings.

  • Honest metric dissection

  • Rigorous spatial statistics

  • Full reproducibility infrastructure

Weaknesses

  • HBN replication is attenuated on every hierarchy statistic

  • The adulthood 'stabilization' claim glosses over a nominally significant result

  • Hierarchical pattern is metric-dependent

  • Cross-sectional design with residual physiological confound risk

  • Modality conflict remains an argument, not a test

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Preliminary Review: Intrinsic timescale develops hierarchically from sensorimotor to association cortex in youth (Shafiei et al., bioRxiv)

The remaining sections cover Methodology Assessment, Statistical Evidence, Results & Reproducibility, Limitations & Risks, and Verdict & Recommendations.

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Frequently asked questions

What is intrinsic timescale in fMRI and how was it measured in this study?

Intrinsic timescale indexes how long a brain region's spontaneous activity persists. Here it was quantified per cortical parcel as the sum of positive autocorrelation function (ACF) values up to the first zero-crossing, multiplied by the scanner's repetition time (TR), computed on resting-state fMRI band-pass filtered to 0.01-0.08 Hz.

Does intrinsic timescale increase or decrease with age during development?

In this fMRI study of 8-22 year olds, timescale increased with age, driven mainly by association cortex while sensorimotor cortex stayed stable, and the pattern aligned with the sensorimotor-association cortical axis; effects were largely absent in young adults (22-37). EEG and ECoG studies report decreases, which the authors attribute to modality differences such as BOLD filtering.

What data and code are available for this paper?

All analyses used public datasets (HCP-Development, Healthy Brain Network, HCP Young Adult). Analysis code and ready-to-plot data are released on GitHub (pennlinc.github.io/shafiei_timescale) and Zenodo (doi:10.5281/zenodo.22799416).

Is this study longitudinal?

No. All three samples are cross-sectional, so development is inferred from age differences between participants rather than within-person change. The authors acknowledge this and call for longitudinal follow-up to confirm individual trajectories.

About this review

This is an AI-generated preliminary review by Evolve.Pub, produced from the openly available text of the paper. It is not peer review and does not represent the authors' views. The canonical record of the paper is at the publisher link above.

  • Figures could not be analyzed visually; numeric values are taken from the text and figure captions.
  • Supplementary figures are known only via captions; underlying distributions and scatter plots were not inspected.
  • This is a bioRxiv preprint and has not completed peer review.
  • The extracted text appears complete through references, but interpretation of figure panels (e.g., trajectory plots in Figures 3d/4d) relies solely on captions.

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