LncRNA FBXL19-AS1 regulates the miR-650/ITGB3 axis to drive pathological progression in Alzheimer’s Disease
Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder characterized by complex and not yet fully understood pathological mechanisms. This study was designed to explore the molecular mechanisms of long non-coding RNA (lncRNA) FBXL19-AS1 in the pathological progression of AD. 110 AD patients and 110 healthy controls were recruited for this study. Relevant gene expression was measured using reverse transcription quantitative real-time PCR (RT-qPCR), and the diagnostic performance was assessed through receiver operating characteristic (ROC) curve analysis. AD cell models were established by treating SH-SY5Y and BV2 cells with amyloid β (Aβ)25–35. Cell proliferation was evaluated using the cell counting kit-8 (CCK-8) assay, cell apoptosis was analyzed by flow cytometry, and the secretion levels of inflammatory factors were determined via enzyme-linked immunosorbent assay (ELISA). A dual-luciferase reporter assay was performed to confirm the direct regulatory interactions. In AD patients, the FBXL19-AS1 and integrin subunit beta 3 (ITGB3) expression were significantly elevated, whereas microRNA-650 (miR-650) expression was markedly reduced. FBXL19-AS1 showed certain diagnostic potential for AD, and its expression was negatively correlated with Montreal Cognitive Assessment (MoCA) scores. Following treatment with Aβ25–35, SH-SY5Y cells exhibited reduced proliferative capacity and increased apoptosis, while BV2 cells showed elevated levels of inflammatory factors. Additionally, Aβ25–35 treatment led to upregulated expression of FBXL19-AS1 and ITGB3, along with downregulated expression of miR-650. Knockdown of FBXL19-AS1 effectively reversed these effects. However, inhibition of miR-650 partially attenuated the changes induced by FBXL19-AS1 knockdown. Furthermore, knockdown of FBXL19-AS1 markedly reduced ITGB3 expression, whereas concurrent inhibition of miR-650 partially reversed this downregulatory effect. FBXL19-AS1 appears to interact with and modulate miR-650, thereby affecting ITGB3 expression and potentially participating in the pathological progression of AD.