Abstract

BackgroundTo explore the diagnostic role and potential mechanism of serum lncRNA UCA1 in Alzheimer's disease (AD). MethodsUCA1 concentration was determined using quantitative PCR. The receiver operating characteristic curve was plotted to assess the diagnostic value. Cell viability and apoptotic capacity were assessed by Cell counting kit-8 (CCK-8) and flow cytometry. Water maze experiments were used to test cognitive function in mice. The target genes of UCA1 were identified with a dual luciferase reporter. Functional and pathway analysis of miR-342-3p target genes was determined using enrichment analysis. ResultsThe concentration of UCA1 was elevated in the AD group and represented a diagnostic possibility of AD. The silenced UCA1 reduced the roles of Aβ on viability and apoptosis of SH⁃SY5Y cells by sponging miR-342-3p. The impaired cognitive impairment was partly recovered by the knockdown of the UCA1/miR-342-3p axis. Potential targets of miR-342-3p were enriched in function and pathways related to AD progression. ConclusionThe UCA1/miR-342-3p axis contributed to the occurrence of AD by regulating cognitive ability.

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