Plasma S100A8/A9 and Post-Stroke Cognitive Impairment

10 Mar 20264 min read0 viewsJournal Feed

GIST

Journal of the American Heart Association, Volume 15, Issue 6 , March 17, 2026. BackgroundS100A8/A9 (S100 calcium‐binding protein A8/A9) was suggested to play pathophysiological roles in the amyloid–neuroinflammatory cascade, contributing to cognitive impairment.

However, little is known about the impacts of S100A8/A9 on poststroke cognitive impairment. We aimed to prospectively investigate the relationships between baseline plasma S100A8/A9 levels with cognitive impairment among patients with acute ischemic stroke.MethodsOur prospective cohort study included patients with acute ischemic stroke from an ancillary study of CATIS (China Antihypertensive Trial in Acute Ischemic Stroke).

At the 3‐month follow‐up, cognitive impairment was evaluated using the Montreal Cognitive Assessment and the Mini‐Mental State Examination. Logistic regression analysis was conducted to estimate the association between S100A8/A9 and the risk of poststroke cognitive impairment (PSCI).ResultsA total of 618 participants were included, of whom 405 (65.5%) met the criteria for PSCI on the basis of the Montreal Cognitive Assessment, and 323 (52.3%) on the basis of the Mini‐Mental State Examination.

Clinical Editorial

Baseline context and study purpose

Investigated whether initial plasma levels of S100A8/A9 (S100 calcium-binding protein A8/A9) relate to cognitive outcomes after acute ischemic stroke.
Grounded within an ancillary study of the China Antihypertensive Trial in Acute Ischemic Stroke (CATIS).
Aimed to illuminate potential pathophysiologic or predictive links between S100A8/A9 and poststroke cognitive impairment (PSCI).

Design, population, and measurements

Prospective cohort of patients with acute ischemic stroke.
Cognitive assessment conducted at 3 months post-event using two instruments: Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE).
Baseline plasma S100A8/A9 measured and analyzed in relation to later PSCI.
Statistical approach employed logistic regression to estimate associations between S100A8/A9 tertiles and PSCI, adjusting for potential confounders with emphasis on high-sensitivity C-reactive protein (hs-CRP).

Key findings and dose–response signal

PSCI prevalence at 3 months: 65.5% by MoCA criteria and 52.3% by MMSE criteria in the overall sample.
After adjustment for confounders, participants in the highest S100A8/A9 tertile exhibited higher odds of PSCI:
MoCA-defined PSCI: OR 2.27 (95% CI 1.37–3.75) versus the lowest tertile.
MMSE-defined PSCI: OR 1.62 (95% CI 1.01–2.60) versus the lowest tertile.
Evidence of a linear dose–response relationship between baseline S100A8/A9 and PSCI risk:
MoCA: P for linearity = 0.030
MMSE: P for linearity = 0.018

Contextual interpretation and limitations

Findings indicate higher baseline S100A8/A9 levels are associated with increased PSCI risk, suggesting potential utility as a predictive biomarker.
The analysis explicitly accounted for hs-CRP, but residual confounding and causality cannot be established from observational data alone.
The report does not include numeric outcomes beyond the odds ratios and confidence intervals, nor does it present subgroups or secondary analyses beyond the primary PSCI definitions.