Key result
Symptomatic ICAS is linked to a 63% cognitive impairment prevalence, rising across the disease continuum.
Why the study?
While intracranial atherosclerosis is associated with cognitive impairment and dementia, the stage-specific contribution of the ICAS continuum remains undefined.
Is the severity stage of intracranial atherosclerosis associated with cognitive impairment and Alzheimer's disease biomarker profiles?
Is the severity stage of intracranial atherosclerosis associated with cognitive impairment and Alzheimer's disease biomarker profiles?
Intracranial atherosclerosis severity is independently associated with progressive cognitive impairment and distinct biomarker profiles, highlighting vascular contributions to cognitive decline.
ICAS stage independently linked to cognitive impairment after adjustment; extends observational data but leaves open causality and intervention targets.
Background: Intracranial atherosclerosis (ICAS) encompasses a severity continuum from subclinical plaque to flow-limiting stenosis and stroke. While associated with cognitive impairment and dementia, the stage-specific contribution of the ICAS continuum remains undefined. Methods: This cross-sectional analysis utilized baseline data from a multicenter cohort study. We enrolled patients with radiologically confirmed ICAS and ICAS-free controls. Participants underwent comprehensive assessments, including cognitive evaluation via a comprehensive neuropsychological battery, quantification of plasma Alzheimer’s disease(AD) biomarkers (Aβ42/40 ratio, pTau217, glial fibrillary acidic protein [GFAP], neurofilament light chain [NfL]) using Simoa technology, and evaluation of cerebral small vessel disease (CSVD) burden assessed by a standardized MRI visual rating scale. Results: Among 506 participants (mean age 60±11years; 53.4% male), stratified by ICAS stages: 99 were ICAS-free controls, 84 had asymptomatic ICAS (aICAS) with <50% stenosis, 156 had aICAS with ≥50% stenosis, and 167 had symptomatic ICAS (sICAS) with ≥50% stenosis. The prevalence of cognitive impairment increased progressively across groups: controls (22%), aICAS <50% (35%), aICAS ≥50% (44%), and sICAS (63%). GFAP levels were significantly higher than controls in both aICAS ≥50% (β=11.10; 95% CI, 1.09-21.10) and sICAS (β=14.67; 95% CI, 4.72-24.63). NfL elevation (β=13.51; 95% CI, 10.13-16.90) was observed only in sICAS. Aβ42/40 showed a borderline reduction in sICAS (β=-0.003; 95% CI, -0.005 to 0.00). pTau217 levels were unaltered. CSVD burden increased versus controls in all ICAS groups (aICAS <50%: β=0.53, 95% CI 0.11–0.95; aICAS ≥50%: β=0.56, 95% CI 0.20–0.92; sICAS: β=1.58, 95% CI 1.22–1.94). After adjusting for demographics, vascular risk factors, APOE ε4 carrier status, plasma biomarkers, and CSVD burden, ICAS stage remained independently associated with cognitive impairment (aICAS <50%: OR=2.36, 95% CI 1.13–4.91; aICAS ≥50%: OR=2.78, 95% CI 1.48–5.22; sICAS: OR=4.48, 95% CI 2.31–8.68). Conclusions: The ICAS continuum demonstrates progressive stage-specific associations with cognitive impairment and biomarker profiles, independent of AD pathology and CSVD burden. This supports the use of the ICAS continuum as a framework for defining vascular contributions to cognitive impairment and highlights ICAS severity stages as potential targets for therapeutic intervention.
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Liu et al. (2026) studied this question. Cognitive impairment prevalence increased from 22% in controls to 63% in symptomatic ICAS, with stage-specific associations evident across the ICAS continuum.
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