Author:
Fujita Yu,Kano Kuniyuki,Kishino Shigenobu,Nagao Toshihiro,Shen Xuefeng,Sato Chiharu,Hatakeyama Hatsune,Ota Yume,Niibori Sho,Nomura Ayako,Kikuchi Kota,Yasuno Wataru,Takatori Sho,Kikuchi Kazunori,Sano Yoshitake,Tomita Taisuke,Suzuki Toshiharu,Aoki Junken,Zou Kun,Natori Shunji,Komano Hiroto
Abstract
AbstractConjugated linoleic acid (CLA) is an isomer of linoleic acid (LA). The predominant dietary CLA is cis-9, trans-11-CLA (c-9, t-11-CLA), which constitutes up to ~ 90% of total CLA and is thought to be responsible for the positive health benefits associated with CLA. However, the effects of c-9, t-11-CLA on Alzheimer’s disease (AD) remain to be elucidated. In this study, we investigated the effect of dietary intake of c-9, t-11-CLA on the pathogenesis of an AD mouse model. We found that c-9, t-11-CLA diet-fed AD model mice significantly exhibited (1) a decrease in amyloid-β protein (Aβ) levels in the hippocampus, (2) an increase in the number of microglia, and (3) an increase in the number of astrocytes expressing the anti-inflammatory cytokines, interleukin-10 and 19 (IL-10, IL-19), with no change in the total number of astrocytes. In addition, liquid chromatography–tandem mass spectrometry (LC–MS/MS) and gas chromatographic analysis revealed that the levels of lysophosphatidylcholine (LPC) containing c-9, t-11-CLA (CLA-LPC) and free c-9, t-11-CLA were significantly increased in the brain of c-9, t-11-CLA diet-fed mice. Thus, dietary c-9, t-11-CLA entered the brain and appeared to exhibit beneficial effects on AD, including a decrease in Aβ levels and suppression of inflammation.
Publisher
Springer Science and Business Media LLC
Cited by
13 articles.
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