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        Etidronate rescues cognitive deficits through improving synaptic transmission and suppressing apoptosis in 2-vessel occlusion model rats

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        Author
        Li, Wen
        Yuan, Huijuan
        Yu, Yao
        Cheong, Yuen-Ki
        Ren, Guogang
        Yang, Zhuo
        Attention
        2299/17655
        Abstract
        Vascular dementia (VD) is a neurodegenerative disorder caused by the reduction of cerebral blood flow. It shows a progressive cognitive impairment. In our previous study, we found that etidronate (ET) showed neuroprotective effects against glutamate-injured PC12 cells. Thus in this study, we aimed to observe the effects of ET on learning and memory impairment and the related mechanism in 2-vessel occlusion (2VO) model rats. Rats were administered a permanent bilateral common carotid artery occlusion to induce VD model. Two weeks later, 2VO model rats were treated with ET (10ml/kg/day i.p.) for one week. Results showed that ET improved the spatial learning and memory function in 2VO rats detected by Morris water maze experiment. A reduced long-term potentiation (LTP) was also rescued by ET treatment in 2VO rats. Moreover, the LTP related proteins calcium/calmodulin-dependent protein kinase II (CaMKII), NMDAR 2B and PSD95 were up-regulated after treatment with ET. By testing the levels of malondialdehyde and superoxide dismutase in 2VO rats, we discovered that ET lowered oxidative stress. Furthermore, ET displayed a better anti-apoptosis ability through detecting the levels of Bcl-2 and Bax protein and TUNEL-positive cells. In conclusion, ET shows neuroprotective effects on 2VO rats through rescuing spatial working memory deficits, and a possible mechanism may be related to the increased synaptic transmission and the inhibition of oxidative stress and apoptosis. This article is protected by copyright. All rights reserved.
        Publication date
        2017-01-20
        Published in
        Journal of Neurochemistry
        Published version
        https://doi.org/10.1111/jnc.13904
        License
        http://creativecommons.org/licenses/by-nc/4.0/
        Other links
        http://hdl.handle.net/2299/17655
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