Effect of Synthetic Cannabinoid HU210 on Memory Deficits and Neuropathology in Alzheimer's Disease Mouse Model

被引:29
作者
Chen, B. [1 ]
Bromley-Brits, K. [1 ,2 ]
He, G. [1 ]
Cai, F. [1 ]
Zhang, X. [3 ]
Song, W. [1 ,2 ]
机构
[1] Univ British Columbia, Dept Psychiat, Townsend Family Labs, Brain Res Ctr, Vancouver, BC V6T 1Z3, Canada
[2] Univ British Columbia, Grad Program Neurosci, Vancouver, BC V6T 1Z3, Canada
[3] Univ Ottawa, Mental Hlth Res Inst, Ottawa, ON K1Z 7K4, Canada
基金
加拿大健康研究院;
关键词
Cannabinoids; HU210; memory deficits; A beta; neurogenesis; Alzheimer; IN-VIVO; CEREBRAL-ISCHEMIA; BRAIN; NEUROPROTECTION; ANANDAMIDE; NEURONS; RECEPTORS; PROTECTS; INJURY; VITRO;
D O I
10.2174/156720510791050948
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Cannabinoids have been shown to increase neurogenesis in adult brain, as well as protect neurons from excitotoxicity, calcium influx, inflammation, and ischemia. Recent studies have shown that synthetic cannabinoids can alleviate water maze impairments in rats treated with intracranial amyloid beta protein (A beta); however it is unknown whether this effect is due to the cannabinoids' anti-inflammatory properties or whether it affects A beta processing. Here we investigate whether cannabinoids have any effect on Alzheimer's disease in vivo. We found that HU210, a potent synthetic cannabinoid, did not improve water maze performance or a contextual fear conditioning task in an APP23/PS45 double transgenic mouse model of AD. HU210 had no effect on APP processing and A beta generation, as well as neuritic plaque formation in the brains of AD transgenic mice. Our study showed that synthetic cannabinoid HU210 had no beneficial effects on AD neuropathology and behavioral deficits of AD model mice, which advises caution of such drug's application in AD therapies.
引用
收藏
页码:255 / 261
页数:7
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