MicroRNA-107 prevents amyloid-[beta]-induced neurotoxicity and memory impairment in mice

• Published in: International journal of molecular medicine 2018-03, Vol.41 (3), p.1665
• Main Authors: Shu, Bohui, Zhang, Xiaoyan, Du, Ganqin, Fu, Qizhi, Huang, Lina
• Format: Article
• Language: English
• Subjects: Alzheimer's disease; Amyloid beta-protein; Care and treatment; Development and progression; Gene expression; Genetic aspects; Health aspects; MicroRNA
• ISSN: 1107-3756
• DOI: 10.3892/ijmm.2017.3339

The pathogenesis of Alzheimer's disease (AD) has still not been fully elucidated, however it is thought that the build up of amyloid plaque at least partially causes the symptoms of AD. MicroRNAs (miRNAs) are endogenous non-coding small RNA molecules that regulate the expression and degradation of proteins. The present study induced symptoms of AD in mice via intraventricular injection of amyloid-[beta] 1-42 (A[beta]1-42), which decreased levels of miR-107. However, miR-107 levels increased following administration of miR-107 mimic, a double-stranded RNA molecule designed to imitate the native miRNA. Intraventricular injection of A[beta]1-42 aggregates led to spatial memory impairments, inhibited hippocampal long-term potentiation (LTP) and resulted in the loss of pyramidal cells in the CA1 region of the hippocampus. The miR-107 mimic reversed the impairments of spatial memory and LTP and the loss of pyramidal neurons caused by A[beta] neurotoxicity. Furthermore, the miR-107 mimic reversed the A[beta]-induced increase in A[beta]1-42 and phosphorylated Tau levels. critically, A[beta]1-42 injection decreased levels of brain-derived neurotrophic factor and reduced the phosphorylation of tyrosine receptor kinase B and protein kinase B; these changes were reversed following treatment with the miR-107 mimic. collectively, these results demonstrated that miR-107 may be a potential target for the treatment of AD. Key words: microRNA-107, Alzheimer's disease, amyloid-[beta], memory