Alzheimer's disease (AD) is a chronic neurodegenerative disease featured by progressive memory loss and cognitive dysfunction. Long non-coding RNAs are recently demonstrated as important regulatory molecules in neurodegenerative diseases. This study explored regulatory role of lncRNA small nucleolar RNA host gene 1 (SNHG1) in the neuronal cell injury induced by A beta(2)(5-35). Our results showed that A beta(2)(5-35 )inhibited cell viability, induced cell apoptosis and increased the expression of SNHG1 in SH-SY5Y and human primary neuron (HPN) cells. Knockdown of SNHG1 partially reversed the effects of A beta(2)(5-35) treatment on cell viability, cell apoptosis, mitochondrial membrane potential (MMP), caspase-3 activity, and apoptosis signaling-related protein levels in SH-SY5Y and HPN cells. The bioinformatics analysis and luciferase reporter assay showed that SNHG1 functioned as competing endogenous RNA (ceRNA) for miR-137, and pre-treatment with SNHG1 siRNA increased cell viability, suppressed cell apoptosis, increased MMP, decreased caspase-3 activity and caused a decrease in the protein levels of cytochrome C and cleaved caspase-3 and an increase in Bcl-2 protein level in the A beta(2)(5-35)-treated SH-SY5Y and HPN cells, which was significantly attenuated by the presence of miR-137 mimics. Moreover, miR-137 negatively regulated the expression of kringle containing transmembrane protein 1 (KREMENI) via targeting its 3' untranslated region, and knockdown of SNHG1 also suppressed KREMENI in SH-SY5Y and HPN cells. Overexpression of KREMENI impaired the neuronal protective effects of SNHG1 knockdown in the A beta(2)(5-35)-treated SH-SY5Y and HPN cells. In summary, our result indicated that knockdown of SNHG1 exerted its neuronal protective effects via repressing KRENENI by acting as a ceRNA for miR-137 in the in vitro cell model of AD. (C) 2019 Elsevier Inc. All rights reserved.