TY - JOUR
T1 - Age-Related Brain Atrophy Mediates a Composite Outcome of One-Year Ischemic Stroke Recurrence and All-Cause Mortality Through YKL-40–Related Inflammatory Pathways
T2 - A Structural Equation Model
AU - Chang, Xu
AU - Liu, Hao
AU - Liu, Ziyang
AU - Zhou, Yijun
AU - Zhou, Hongyu
AU - Yang, Kaixuan
AU - Jia, Jiajing
AU - Jing, Jing
AU - Wang, Chunjuan
AU - Meng, Xia
AU - Liu, Liping
AU - Wang, Yilong
AU - Zhao, Xingquan
AU - Li, Zixiao
AU - Liu, Tao
AU - Wang, Yongjun
N1 - Publisher Copyright:
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2026.
PY - 2026/8
Y1 - 2026/8
N2 - Chronological age is a strong predictor of poor outcomes after ischemic stroke but may not fully capture underlying biological vulnerability. This study investigated whether age-related brain atrophy and plasma YKL-40, a marker of astroglial inflammation, mediate the association between age and the one-year risk of ischemic stroke recurrence or all-cause mortality. Data were obtained from 4,305 participants enrolled in the Third China National Stroke Registry. Baseline brain atrophy was quantified from structural T1-weighted MRI using an automated deep learning–based pipeline (FastSurfer), yielding hemispheric cortical and white matter volumes that were modeled as indicators of a latent atrophy construct. Structural equation modeling was applied to estimate direct and indirect pathways linking age, brain atrophy, YKL-40, and one-year composite outcomes, adjusting for sex, atrial fibrillation or flutter, hypertension, and diabetes, with indirect effects evaluated using 5,000 bootstrap resamples. The total effect of age on one-year outcomes was not significant (β = −0.011; 95% CI, − 0.060 to 0.038), whereas the total indirect effect was significant (β = 0.028; 95% CI, 0.005–0.050). Mediation was primarily attributable to YKL-40 (β = 0.026; 95% CI, 0.010–0.041), while the independent contribution of brain atrophy was minimal. The indirect effects accounted for approximately 255% of the total effect, indicating a suppressor-type mediation pattern in which direct and indirect effects operated in opposite directions. These findings suggest that advancing age confers increased long-term risk of stroke recurrence or death predominantly through astroglial inflammation rather than through a direct age effect, with brain atrophy modestly amplifying this risk, supporting the integration of neuroimaging and inflammatory biomarkers into translational stroke risk stratification.
AB - Chronological age is a strong predictor of poor outcomes after ischemic stroke but may not fully capture underlying biological vulnerability. This study investigated whether age-related brain atrophy and plasma YKL-40, a marker of astroglial inflammation, mediate the association between age and the one-year risk of ischemic stroke recurrence or all-cause mortality. Data were obtained from 4,305 participants enrolled in the Third China National Stroke Registry. Baseline brain atrophy was quantified from structural T1-weighted MRI using an automated deep learning–based pipeline (FastSurfer), yielding hemispheric cortical and white matter volumes that were modeled as indicators of a latent atrophy construct. Structural equation modeling was applied to estimate direct and indirect pathways linking age, brain atrophy, YKL-40, and one-year composite outcomes, adjusting for sex, atrial fibrillation or flutter, hypertension, and diabetes, with indirect effects evaluated using 5,000 bootstrap resamples. The total effect of age on one-year outcomes was not significant (β = −0.011; 95% CI, − 0.060 to 0.038), whereas the total indirect effect was significant (β = 0.028; 95% CI, 0.005–0.050). Mediation was primarily attributable to YKL-40 (β = 0.026; 95% CI, 0.010–0.041), while the independent contribution of brain atrophy was minimal. The indirect effects accounted for approximately 255% of the total effect, indicating a suppressor-type mediation pattern in which direct and indirect effects operated in opposite directions. These findings suggest that advancing age confers increased long-term risk of stroke recurrence or death predominantly through astroglial inflammation rather than through a direct age effect, with brain atrophy modestly amplifying this risk, supporting the integration of neuroimaging and inflammatory biomarkers into translational stroke risk stratification.
KW - Aging
KW - Astroglial inflammation
KW - Brain atrophy
KW - Ischemic stroke
KW - Structural equation modeling
KW - YKL-40
UR - https://www.scopus.com/pages/publications/105045081072
U2 - 10.1007/s12975-026-01464-3
DO - 10.1007/s12975-026-01464-3
M3 - 文章
C2 - 42470512
AN - SCOPUS:105045081072
SN - 1868-4483
VL - 17
JO - Translational Stroke Research
JF - Translational Stroke Research
IS - 4
M1 - 81
ER -