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• W4367179918 abstract "Abstract Background Alzheimer's Disease (AD) is a progressive complex neurodegenerative disorder clinical characterized by demolishing cognitive functions and behavioral abilities. Until recently, molecular mechanisms of AD have not been clarified yet. Alterations in biochemical and molecular pathways in patients suffering from AD may not only emerge in the brain but also could affect blood cells and vessels. Platelets are the blood cells that have a crucial function in the regulation of hemostasis and also play an important role in pathophysiological conditions such as neurodegenerative diseases, including AD. Methods In the current study, analyzed platelet function by optical density in 43 AD patients and 45 controls. White-Matter changes evaluated by MRI Axial FLAIR images (Fazekas scale). We measured the serum levels of vWF and GP1b proteins by ELISA and hsa-miR-26a-5p and hsa-mir24-3p by qRT-PCR analysis. Results ADP-induced platelet aggregation decreased in AD (p = 0.016). We evaluated aspirin (ASA) usage and detected that AD patients free of ASA have a significantly higher platelet function. Serum GP1b levels are a significant increase in AD (p = 0.018). The relative expression levels of hsa-miR-26a-5p are significantly low in AD (p = 0.001). A positive significant correlation was found between the relative expression values of hsa-miR-24-3p and hsa-miR-26a-5p in both control groups and AD ( p = 0.0051, r = 0.4149, 95% CI = 0.1256–0.6392; p = 0.0023, r = 0.6820, 95% CI 0.4728–0.8184) Conclusion The present study implicates that increased expression of serum GP1b and decreased relative expression levels of hsa-miR-26a-5p in AD. As a conclusion, we suggest that GP1b and hsa-miR-26a-5p essential roles of platelet function in AD." @default.
• W4367179918 created "2023-04-28" @default.
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• W4367179918 date "2023-04-27" @default.
• W4367179918 modified "2023-10-01" @default.
• W4367179918 title "Glycoprotein 1b (GP1b) protein, miR-26a-5p levels and platelet function in Alzheimer’s Disease" @default.
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• W4367179918 doi "https://doi.org/10.21203/rs.3.rs-2831899/v1" @default.
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