Advanced glycation end products induce Aβ1–42 deposition and cognitive decline through H19/miR-15b/BACE1 axis in diabetic encephalopathy

Lei Jiang,Nannan Yuan,Na Zhao,Pei Tian,Di Zhang,Yushi Qin,Zhongli Shi,Zhaoyu Gao,Nan Zhang,Huimin Zhou,Rui Zhang,Shunjiang Xu

Brain Research Bulletin（2022）

Cited 5|Views8

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Abstract

•MiR-15b was downregulated while BACE1 was upregulated in the hippocampus of DE rats.•The expression of BACE1 protein was negatively regulated by miR-15b in HT-22 cells.•Administration of miR-15b mimics markedly improved the cognitive decline in DE rats.•LncRNA H19 regulated Aβ1–42 deposition through the miR-15b/BACE1 axis in DE.

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Key words

Diabetic encephalopathy,Advanced glycation end products (AGEs),miR-15b,BACE1,Long non-coding RNA H19

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