Association of glycoprotein 1b and miR-26a-5p levels with platelet function in Alzheimer's disease.

Abstract

BackgroundAlterations in biochemical and molecular pathways in Alzheimer's disease (AD) may be evident in the brain, blood cells, and vessels. Platelets regulate blood hemostasis and play key roles in neurodegenerative diseases like AD. miR-26a-5p and GP1b may affect platelet functions (PF), with miR-26a-5p as a diagnostic/therapeutic target and GP1b linking vascular and neurological disorders in AD progression.ObjectiveThis study explores the roles of GP1b and hsa-miR-26a-5p in regulating PF in AD.Methods85 participants, including 43 AD, and 45 controls, were included. PF induced by ADP were assessed by optical density and white matter changes by MRI Axial FLAIR. Serum levels of von Willebrand Factor and GP1b were measured by ELISA. Platelet receptor expressions of CD62P and CD42b (GPIb) were measured by flow cytometry, and levels of hsa-miR-26a-5p and hsa-miR-24-3p by qRT-PCR.ResultsADP-induced PF was significantly reduced in AD (p = 0.016). Flow cytometry showed significantly low CD42b and high CD62P expression in AD, respectively (p < 0.0001, p = 0.014). Serum GP1b levels were significantly higher in AD (p = 0.018). Additionally, hsa-miR-26a-5p expression was significantly low in AD (p = 0.001), and a positive correlation was found between the expression levels of hsa-miR-24-3p and hsa-miR-26a-5p in both controls; and AD (r = 0.4149, p = 0.0051, 95% CI = 0.1256-0.6392; r = 0.6820, p = 0.0023, 95% CI 0.4728-0.8184).ConclusionsThis study highlights increased serum GP1b levels with decreased both platelet surface GP1b levels and hsa-miR-26a-5p expressions in AD. GP1b and hsa-miR-26a-5p might have essential roles on PF in AD.