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Background <p>Elucidating the altered spatiotemporal development of white matter (WM) axons during early childhood is essential for uncovering the neuropathology of autism spectrum disorder (ASD). However, previous studies have often failed to account for the heterogeneity of developmental trajectories or to adequately control for co-occurring developmental delay/intellectual disability (DD/ID), limiting our understanding of whether ASD-related alterations represent qualitative deviations or quantitative delays in otherwise preserved maturational patterns.</p> Methods <p>We analyzed multi-shell diffusion MRI and behavioral data from 364 children aged 1–7 years (156 individuals with ASD, 48 individuals with DD/ID, and 160 typically developing (TD) controls) using the Neurite Density Index (NDI)—an MRI-derived marker of axonal density. A subset of ASD children also underwent longitudinal MRI scans and provided blood metabolic and protein profiles.</p> Results <p>We identified the same three WM clusters in both typical and atypical development. These clusters exhibit distinct developmental stages with successively decreasing growth rates in ASD, similar to TD but delayed overall, especially for ASD with DD/ID, while DD/ID display little developmental effect. These findings are further validated across split-half, male-only and longitudinal subdatasets. Furthermore, we found NDIs of these WM clusters in ASD are: a) correlated with cognitive impairments at the stage with a fast developmental pace and social deficits at the stage with a moderate-slow developmental pace; b) linked with multiple metabolic and protein measurements.</p> Conclusions <p>ASD children exhibit the same coordinated spatial pattern of white matter development as TD, but with distinct developmental trajectories. These findings advance our understanding of the neuropathological underpinnings of ASD heterogeneity in early childhood, and highlight potential targets for future therapeutic design and evaluation.</p>

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Observational in vivo axon development during early childhood in autism spectrum disorder and developmental disability using MRI

  • 期刊论文

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  • 发表日期：

    2026年7月22日

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  • Yuqi Liu,
  • Jiaying Zhang,
  • Edmund T. Rolls,
  • Yuan Dai,
  • Shujie Geng,
  • Lin Deng,
  • Zilin Chen,
  • Yue Zhang,
  • Yunjun Sun,
  • Wei Zhou,
  • Lingli Zhang,
  • Tai Ren,
  • Jianfeng Feng,
  • Miao Cao,
  • Fei Li

摘要

Background

Elucidating the altered spatiotemporal development of white matter (WM) axons during early childhood is essential for uncovering the neuropathology of autism spectrum disorder (ASD). However, previous studies have often failed to account for the heterogeneity of developmental trajectories or to adequately control for co-occurring developmental delay/intellectual disability (DD/ID), limiting our understanding of whether ASD-related alterations represent qualitative deviations or quantitative delays in otherwise preserved maturational patterns.

Methods

We analyzed multi-shell diffusion MRI and behavioral data from 364 children aged 1–7 years (156 individuals with ASD, 48 individuals with DD/ID, and 160 typically developing (TD) controls) using the Neurite Density Index (NDI)—an MRI-derived marker of axonal density. A subset of ASD children also underwent longitudinal MRI scans and provided blood metabolic and protein profiles.

Results

We identified the same three WM clusters in both typical and atypical development. These clusters exhibit distinct developmental stages with successively decreasing growth rates in ASD, similar to TD but delayed overall, especially for ASD with DD/ID, while DD/ID display little developmental effect. These findings are further validated across split-half, male-only and longitudinal subdatasets. Furthermore, we found NDIs of these WM clusters in ASD are: a) correlated with cognitive impairments at the stage with a fast developmental pace and social deficits at the stage with a moderate-slow developmental pace; b) linked with multiple metabolic and protein measurements.

Conclusions

ASD children exhibit the same coordinated spatial pattern of white matter development as TD, but with distinct developmental trajectories. These findings advance our understanding of the neuropathological underpinnings of ASD heterogeneity in early childhood, and highlight potential targets for future therapeutic design and evaluation.