Yanbo Wang, Min Shi, Zhenmei Hong, Junling Kang, Haiyan Pan, Ci Yan
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引用次数: 0
Abstract
The present study investigated the role and potential mechanisms of miR-130a-3p in AD. SH-SY5Y cells were treated with Aβ 1-42 to construct AD cell models. APP/PS1 mice were used for the animal experiments. MiR-130a-3p was downregulated in Aβ-induced SH-SY5Y cells. Overexpression of miR-130a-3p attenuates Aβ induced SH-SY5Y cell apoptosis. Low miR-130a-3p expression was detected in the hippocampus tissues of AD mice. The Morris water maze (MWM) results indicated that miR-130a-3p upregulation reduced the escape latency time and increased the time of AD mice spent in the target quadrant. DAPK1 was the target gene of miR-130a-3p. High DAPK1 mRNA level was detected in Aβ treated PC 12 cells and in the hippocampus tissues of AD mice. It was concluded that overexpression of miR-130a-3p may attenuate Aβ-induced neurotoxicity and improve the cognitive function of AD mice via targeting DAPK1.
期刊介绍:
American Journal of Alzheimer''s Disease and other Dementias® (AJADD) is for professionals on the frontlines of Alzheimer''s care, dementia, and clinical depression--especially physicians, nurses, psychiatrists, administrators, and other healthcare specialists who manage patients with dementias and their families. This journal is a member of the Committee on Publication Ethics (COPE).