MicroRNA-26b is upregulated in a double transgenic mouse model of Alzheimer's disease and promotes the expression of amyloid-β by targeting insulin-like growth factor 1

Abstract

Alzheimer's disease (AD) is the most common form of dementia among the aging population. It is pathologically characterized by synaptic impairment, accumulation of neurofibrillary tangles and amyloid-β (Aβ) deposition. MicroRNA-26b (miR-26b) has been observed to be upregulated in the human temporal cortex in AD, however, the function of miR-26b has not been verified. Reverse transcription-quantitative polymerase chain reaction was conducted to investigate the expression levels of miR-26b in a double transgenic mouse model of AD. Following transfection of miR-26b or an miR-26b inhibitor, western blot analysis, enzyme-linked immunosorbent assay and luciferase assays were performed. The present study demonstrated that the expression levels of miR-26b were upregulated in a double transgenic mouse model of AD. It was also demonstrated that upregulation of miR-26b in N2a/APP cells downregulated the insulin-like growth factor 1 (IGF-1) protein expression level and promoted Aβ production, whereas inhibition of miR-26b in N2a/APP cells upregulated the IGF-1 protein level and suppressed Aβ production. Furthermore, miR-26b target sites in IGF-1 were confirmed using a luciferase assay in HEK293 cells. The present study may be useful in the development of effective therapeutic strategies against AD.