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Overexpression of miR-132-3p contributes to neuronal protection in in vitro and in vivo models of Alzheimer’s disease

Zeng, Chong, Meng, Xingjun, Mai, Dongmei, Xu, Kai, Qu, Shaogang·2022·Behavioural Brain Research
DOI 10.1016/j.bbr.2021.113584
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Abstract

One of the neuropathological hallmarks of Alzheimer's disease (AD) is accumulation and deposition of amyloid-beta (Aβ 1-42 ) plaques in the hippocampus. Recently, microRNAs (miRNAs), have been demonstrated to play an essential role in AD. We have previously demonstrated that miR-132-3p exerts neuroprotection via regulating histone deacetylase 3 (HDAC3) in a mouse model of AD. In the present study, we further unveiled neuroprotective roles of miR-132-3p in transgenic amyloid precursor protein/presenilin 1 (APP/PS1) mice compared with those in age-matched wild-type C57BL/6 mice. Lentiviral-mediated inhibition or overexpression of miR-132-3p in the hippocampus of APP/PS1 mice was used to explore the contributions of hippocampal miR-132-3p in spatial memory, amyloid burden, apoptosis, and the number of hippocampal cells in a mouse model of AD. Overexpression of hippocampal miR-132-3p ameliorated spatial memory deficits in the Morris water maze, reduced both Aβ 1-42 accumulation and apoptosis, and promoted the numbers of hippocampal cells in the brains of APP/PS1 mice. Furthermore, trichostatin A (TSA) promoted the expression of miR-132-3p in Aβ 1-42 -burdened neurons while increasing the expression levels of synaptic proteins. Taken together, our results suggest that miR-132-3p may represent a promising therapeutic target for the treatment of AD.

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Metadata

Authors
Zeng, C., Meng, X., Mai, D., Xu, K., & Qu, S.
Venue
Behavioural Brain Research
Publisher
Elsevier BV
Published
2022-01
Volume
417
Pages
113584
ISSN
0166-4328
DOI
10.1016/j.bbr.2021.113584
Cited by
32
References
5
Language
en
Licence
Funders
National Natural Science Foundation of China (81870991, U1603281)

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