Abstract

Alzheimer’s disease (AD) is a neurodegenerative disease with progressive cognitive impairment as the main clinical manifestation. Long non-coding RNAs (lncRNAs) are crucial regulators of diverse cellular processes. This study examined the clinical significance and underlying mechanisms of LINC00641 in AD diagnosis. qRT-PCR was used to measure plasma LINC00641 levels in AD patients, and its diagnostic value was assessed using ROC curve. Cell proliferation was measured via the CCK-8 assay. Apoptosis and AD-related proteins were detected by ELISA. The interaction between LINC00641 and its downstream target miR-501-3p was validated through online network prediction and dual-luciferase reporter assay. Plasma LINC00641 expression was lower in AD patients than in controls. It correlated positively with Aβ42 and negatively with p-Tau181 and p-Tau217. Combining of LINC00641 with clinical markers obviously improved diagnostic accuracy for distinguishing AD patients. Overexpression of LINC00641 restored the viability of H19-7 cells after Aβ42 treatment, and reduced levels of cleaved Caspase-3, Aβ42, p-Tau181/Tau, and p-Tau217/Tau. Functionally, miR-501-3p acts downstream of LINC00641. The cellular effects of LINC00641 overexpression were reversed by co-transfection with miR-501-3p mimic. Overexpression of LINC00641 downregulated miR-501-3p expression, restoring neuronal cell viability and reducing cell damage. Targeting LINC00641 holds potential as a diagnostic biomarker and therapeutic candidate for AD, which requires further validation in animal models.