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Case-control study finds higher calprotectin levels linked to cognitive impairment after stroke, suggesting predictive potential.
Background and aims Inflammation is a key component of ischemic stroke pathophysiology, and it is known to contribute to the development of other stroke-associated complications such as post-stroke cognitive impairment (PSCI). Higher calprotectin levels have been associated with worse stroke evolution, but there are no studies that evaluate its role in PSCI. Methods We conducted a nested case-control study within a prospective cohort of 476 patients with acute ischemic stroke. Patients with no pre-existing cognitive impairment who developed PSCI were defined as cases. Plasma calprotectin levels were measured by ELISA in blood samples within the first 24 hours post-stroke. We analyzed the association between plasma calprotectin levels and subsequent development of PSCI, adjusting for clinical variables. Results 81 subjects were included (40 cases, 41 controls), with no significant differences in sex, age or inflammation parameters (neutrophil-to-lymphocyte ratio or C-reactive protein). Cases showed higher calprotectin levels than controls [median (IQR) =1,865 ng/mL (1,270-3,248) vs 1,475 ng/mL (902.5-2,210); p-value<0.05]. Logistic regression demonstrated that calprotectin levels were independently associated with the presence of PSCI [OR=1; CI95%=1.000-1.001 (p-value<0.05)]. The area under the curve (AUC) was 0.639 (p-value<0.05) Conclusions Calprotectin levels were significantly higher in patients who developed PSCI compared to those who did not and emerged as a modest independent predictor of PSCI development. These findings suggest that plasma calprotectin could serve as an early biomarker for identifying stroke patients at higher risk of cognitive decline. Further studies are required to confirm these results and explore the integration of calprotectin with other biomarkers to predict PSCI.
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Molina et al. (2026) studied this question.
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