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SOLUBLE INTERCELLULAR ADHESION MOLECULE (SICAM-1) AS A BIOMARKER OF VASCULAR COGNITIVE IMPAIRMENT IN OLDER ADULTS

Background: Endothelial dysfunction and subsequent inflammation contribute to the development of vascular cognitive impairment (VCI). Soluble intercellular adhesion molecule-1 (sICAM-1) is upregulated in endothelial dysfunction and promotes an inflammatory response; however, the relationship between...

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Detalles Bibliográficos
Autores principales: Arenas, Rosalinda Sanchez, Gregory, Michael A, Manuel-Apolinar, Leticia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6844660/
http://dx.doi.org/10.1093/geroni/igz038.959
Descripción
Sumario:Background: Endothelial dysfunction and subsequent inflammation contribute to the development of vascular cognitive impairment (VCI). Soluble intercellular adhesion molecule-1 (sICAM-1) is upregulated in endothelial dysfunction and promotes an inflammatory response; however, the relationship between sICAM-1 and VCI remains equivocal. Objective: To determine whether sICAM-1 contributes to the prediction of VCI. Methods: Community-dwelling older adults (n=172) from the “Cohort of Obesity, Sarcopenia and Frailty of Older Mexican Adults” (COSFOMA) study were identified as VCI or controls using standard neuropsychological evaluations and neuroimaging. sICAM-1 was quantified using ELISA, and multivariate logistic regression determined the association between sICAM-1 and VCI. Results: 31 VCI cases were identified. sICAM-1 was higher in VCI [VCI: 450.7 (241.6) ng/ml vs. Control: 296.9 (140.9) ng/ml]. sICAM-1 concentrations above the 90th percentile (464.1 ng/mL) was associated with VCI group membership in all models [OR = 6.9 (95% CI: 1.1- 42.2)]. The final saturated model explained 64% of the variance in VCI group membership. Conclusion: High concentrations of sICAM-1 are independently associated with VCI group membership. Efforts to further characterize the relationship between indices of endothelial dysfunction and pathological changes to the aging brain should be further pursued.