Arachidonic or Docosahexaenoic Acid Diet Prevents Memory Impairment in Tg2576 Mice

DOI Web Site PubMed 被引用文献3件 参考文献79件
  • Takashi Hosono
    Department of Chemistry and Life Science, Nihon University Graduate School of Bioresource Sciences, Fujisawa, Japan
  • Akihiro Mouri
    Division of Clinical Sciences and Neuropsychopharmacology, Faculty of Pharmacy, Meijo University, Nagoya, Japan
  • Kazuchika Nishitsuji
    Department of Alzheimer’s Disease, National Center for Geriatrics and Gerontology, Obu, Japan
  • Cha-Gyun Jung
    Department of Alzheimer’s Disease, National Center for Geriatrics and Gerontology, Obu, Japan
  • Masanori Kontani
    Institute for Health Care Science, Suntory Wellness Ltd., Osaka, Japan
  • Hisanori Tokuda
    Institute for Health Care Science, Suntory Wellness Ltd., Osaka, Japan
  • Hiroshi Kawashima
    Institute for Health Care Science, Suntory Wellness Ltd., Osaka, Japan
  • Hiroshi Shibata
    Institute for Health Care Science, Suntory Wellness Ltd., Osaka, Japan
  • Toshiharu Suzuki
    Laboratory of Neuroscience, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan
  • Toshitaka Nabehsima
    NPO Japanese Drug Organization of Appropriate Use and Research, Nagoya, Japan
  • Makoto Michikawa
    Department of Alzheimer’s Disease, National Center for Geriatrics and Gerontology, Obu, Japan

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説明

It is believed that the amyloid β-protein (Aβ) plays a causative role in the development of Alzheimer's disease (AD). The amyloid-β protein precursor (AβPP), a substrate of Aβ, and β-secretase and γ-secretase complex proteins, which process AβPP to generate Aβ, are all membrane proteins. Thus, it is reasonable to assume that alterations in brain lipid metabolism modulate AβPP and/or Aβ metabolism. However, the role of cellular polyunsaturated fatty acids in AβPP processing has not been completely understood yet. We report here that 4 months of treatment of Tg2576 mice with an arachidonic acid (ARA)- or a docosahexaenoic acid (DHA)-containing (ARA+ or DHA+) diet prevented memory impairment at 13 months of age. Although, AβPP processing to generate soluble AβPP and induce Aβ synthesis was enhanced, Aβ(1- 42)/Aβ(1- 40) ratio decreased in 14-month-old Tg2576 mice fed with the ARA+ or DHA+ diet. The ARA+ or DHA+ diet did not alter the AβPP levels and the expression levels of Aβ-degrading enzymes. In cortical primary neuron cultures, ARA or DHA treatment also increased soluble AβPP and Aβ(1- 40) levels, and decreased Aβ(1- 42)/Aβ(1- 40) ratio, which are similar to what were observed in Tg2576 mice fed with ARA+ or DHA+ diet. These findings suggest that not only the DHA+ diet, but also the ARA+ diet could prevent cognitive dysfunction in Tg2576 mice through the alteration of AβPP processing.

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