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Original languageEnglish
Number of pages9
Pages (from-to)476-484
JournalJournal of Neurochemistry
Journal publication date20 Jan 2017
Volume140
Issue3
Early online date6 Jan 2017
DOIs
Publication statusPublished - 20 Jan 2017

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.

Notes

This is the peer-reviewed version of the following article: Li, W., Yuan, H., Yu, Y., Cheong, Y.-K., Ren, G. and Yang, Z., ‘Etidronate rescues cognitive deficits through improving synaptic transmission and suppressing apoptosis in 2-vessel occlusion model rats’. Journal of Neurochemistry, Vol 140(3): 476–484, February 2017, which has been published in final form at http://dx.doi.org/10.1111/jnc.13904. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.

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