Alzheimer's disease (AD) is the primary cause of dementia. There is no effective treatment. Amyloid-β peptide (Aβ) plays an important role in the pathogenesis and thus strategies suppressing Aβ production and accumulation seem promising. Citalopram is an antidepressant drug and can decrease Aβ production and amyloid plaques in transgenic mice of AD and humans. Whether citalopram can ameliorate memory deficit was not known yet. We tested the effects of citalopram on behavioral performance and synaptic plasticity in female 3xTgAD mice, a well-characterized model of AD. Mice were treated with citalopram or water from 5 months of age for 3 months. Citalopram treatment at approximately 10 mg/kg/day significantly improved spatial memory in the Morris water maze (MWM) test, while not affecting anxiety-like and depression-like behavior in 3xTgAD mice. Further, hippocampal long-term potentiation (LTP) impairment in 3xTgAD mice was reversed by citalopram treatment. Citalopram treatment also significantly decreased the levels of insoluble Aβ40 in hippocampal and cortical tissues in 3xTgAD mice, accompanied with a reduced amyloid precursor protein (APP). Together, citalopram treatment may be a promising strategy for AD and further clinical trials should be conducted to verify the effect of citalopram on cognition in patients with AD or mild cognitive impairment.

译文

阿尔茨海默氏病 (AD) 是痴呆症的主要原因。没有有效的治疗方法。淀粉样 β 肽 (a β) 在发病机理中起着重要作用,因此抑制a β 产生和积累的策略似乎很有希望。西酞普兰是一种抗抑郁药,可以减少AD和人类转基因小鼠中a β 的产生和淀粉样斑块。西酞普兰是否能改善记忆缺陷尚不清楚。我们测试了西酞普兰对雌性3xtgad小鼠 (一种特征良好的AD模型) 的行为表现和突触可塑性的影响。从5个月大的小鼠用西酞普兰或水治疗3个月。在Morris水迷宫 (MWM) 测试中,约10 mg/kg/天的西酞普兰治疗可显着改善空间记忆,而不影响3xtgad小鼠的焦虑样和抑郁样行为。此外,西酞普兰治疗可逆转3xtgad小鼠的海马长时程增强 (LTP) 损伤。西酞普兰治疗还显着降低了3xtgad小鼠海马和皮质组织中不溶性Aβ40的水平,并伴有淀粉样蛋白前体蛋白 (APP) 降低。总之,西酞普兰治疗可能是AD的一种有前途的策略,应进行进一步的临床试验以验证西酞普兰对AD或轻度认知障碍患者认知功能的影响。

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