Hossain Md Shamim, Tajima Ayako, Kotoura Satoshi, Katafuchi Toshihiko
Department of Neuroinflammation and Brain Fatigue Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Department of Neuroinflammation and Brain Fatigue Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Biochem Biophys Res Commun. 2018 Feb 19;496(4):1033-1039. doi: 10.1016/j.bbrc.2018.01.078. Epub 2018 Jan 11.
Plasmalogens (Pls) are the special phospholipids which were reported to be reduced in brain and blood samples of Alzheimer's disease (AD) patients, suggested a possibility that an oral ingestion of Pls may prevent the disease progression. Interestingly, the clinical study showed that the daily oral ingestion of Pls among the mild AD patients improved cognition. However, it is unknown of whether the oral ingestion of Pls inhibits the AD like changes in brain e.g., glial activation and accumulation of amyloid beta (Aβ) proteins. To elucidate the beneficial effects of the Pls oral ingestion, we have used the chronic lipopolysaccharide (LPS) injection model mice where the glial activation and Aβ accumulation were well reported. In the present study, we have found that the Pls drinking at the doses of 0.1 μg/ml and 10 μg/ml for 3 months attenuated the glial activation and accumulation of amyloid beta (Aβ) proteins in the murine brain. Interestingly, the LPS injection reduced the hippocampal dependent memory in the control mice but the groups of Pls drinking mice showed a better performance in the memory test, suggesting that oral intake of Pls can inhibit LPS-mediated memory loss associated with a reduction of glial activation and Aβ accumulation in the brain. We, therefore, suggest that the oral ingestion of Pls among the AD patients may also inhibit the glial activation resulting in the improvement of cognition.
缩醛磷脂（Pls）是一种特殊的磷脂，据报道，在阿尔茨海默病（AD）患者的脑和血样中其含量会降低，这表明口服缩醛磷脂有可能预防疾病进展。有趣的是，临床研究表明，轻度AD患者每日口服缩醛磷脂可改善认知能力。然而，口服缩醛磷脂是否能抑制大脑中类似AD的变化，例如神经胶质细胞激活和β淀粉样蛋白（Aβ）的积累，目前尚不清楚。为了阐明口服缩醛磷脂的有益作用，我们使用了慢性脂多糖（LPS）注射模型小鼠，该模型中神经胶质细胞激活和Aβ积累已有充分报道。在本研究中，我们发现，以0.1μg/ml和10μg/ml的剂量饮用缩醛磷脂3个月可减轻小鼠大脑中的神经胶质细胞激活和β淀粉样蛋白（Aβ）的积累。有趣的是，LPS注射降低了对照小鼠的海马依赖性记忆，但饮用缩醛磷脂的小鼠组在记忆测试中表现更好，这表明口服缩醛磷脂可以抑制LPS介导的与大脑中神经胶质细胞激活减少和Aβ积累相关的记忆丧失。因此，我们认为AD患者口服缩醛磷脂也可能抑制神经胶质细胞激活，从而改善认知能力。
