• Alpha-Linolenic Acid In Neurodegeneration

    From ironjustice@21:1/5 to All on Wed Nov 29 16:52:21 2017
    Alpha-Linolenic Acid from Perilla frutescens var. japonica Oil Protects Aβ-Induced Cognitive Impairment through Regulation of APP Processing and Aβ Degradation
    Ah Young Lee , Myoung Hee Lee, Sanghyun Lee, and Eun Ju Cho
    Department of Food Science and Nutrition and Kimchi Research Institute, Pusan National University, Busan 46241, Republic of Korea
    Department of Southern Area Crop Science, National Institute of Crop Science, Rural Development Administration, Gyeongnam 50424, Republic of Korea
    Department of Integrative Plant Science, Chung-Ang University, Gyeonggi 17546, Republic of Korea
    J. Agric. Food Chem.,
    DOI: 10.1021/acs.jafc.7b03941
    November 2, 2017
    Copyright © 2017 American Chemical Society
    *E-mail for E.J.C.: ejcho at pusan.ac.kr. Tel: +82-51-510-2837. Fax: +82-51-583-3648.

    Alzheimer’s disease (AD) is characterized by progressive cognitive and memory impairment. The major pathological hallmark of AD is the accumulation of amyloid beta (Aβ), which is produced from the amyloid precursor protein (APP) through cleavage of β-
    and γ-secretase. Recently, dietary plant oil containing ω-3 polyunsaturated fatty acid has become an attractive alternative source to fish oil containing eicosapentaenoic acid or docosahexaenoic acid (DHA). We investigated whether ALA isolated from
    perilla oil has direct effects on improvement of cognitive ability and molecular mechanisms in APP processing in comparison with DHA. In the present study, ICR mice were treated orally with ALA or DHA (100 mg/kg/day) for 14 days after i.c.v. injection of
    Aβ25–35. Administration of ALA resulted in a prevention of learning and memory deficit in Aβ25–35-injected mice compared with the control group, as observed in T-maze, novel object recognition, and Morris water maze tests. ALA supplementation also
    markedly ameliorated the Aβ25–35-induced oxidative stress by inhibition of lipid peroxidation and nitric oxide overproduction in the mouse brain, liver, and kidney, almost down to the levels in DHA-administered group. These effects of ALA on
    protective mechanisms were related to the regulation of APP processing via promoting nonamyloidogenic pathway such as up-regulation of soluble APP alpha, C-terminal fragment alpha/beta ratio, and A disintegrin and metalloprotease10 protein expressions.
    Furthermore, ALA inhibited the amyloidogenic pathway through the down-regulation of β-site APP-cleaving enzyme and presenilin2. ALA also enhanced Aβ degradation enzyme, insulin-degrading enzyme. In conclusion, the present study indicated a beneficial
    effect of ALA in improving the cognitive ability against Aβ25–35, and these effects were comparable to those exerted by DHA. Its neuroprotective effects are mediated, in part, by regulation of APP processing and Aβ degradation, and thus, ALA might be
    a potential candidate for prevention or treatment of neurodegenerative diseases such as AD.

    Keywords: alpha-linolenic acid; Alzheimer’s disease; Aβ25−35; cognitive ability; Perilla frutescens

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