دورية أكاديمية
أعرض في EDS

The Novel Omega-6 Fatty Acid Docosapentaenoic Acid Positively Modulates Brain Innate Immune Response for Resolving Neuroinflammation at Early and Late Stages of Humanized APOE-Based Alzheimer's Disease Models.

التفاصيل البيبلوغرافية
العنوان: The Novel Omega-6 Fatty Acid Docosapentaenoic Acid Positively Modulates Brain Innate Immune Response for Resolving Neuroinflammation at Early and Late Stages of Humanized APOE-Based Alzheimer's Disease Models.
المؤلفون: Ma QL; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States., Zhu C; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States.; Department of Neurology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China., Morselli M; Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, United States.; Institute for Genomics and Proteomics, University of California, Los Angeles, Los Angeles, CA, United States.; Institute for Quantitative and Computational Biology, University of California, Los Angeles, Los Angeles, CA, United States., Su T; Institute for Quantitative and Computational Biology, University of California, Los Angeles, Los Angeles, CA, United States.; Department of Biological Chemistry, University of California, Los Angeles, Los Angeles, CA, United States., Pelligrini M; Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, United States.; Institute for Genomics and Proteomics, University of California, Los Angeles, Los Angeles, CA, United States.; Institute for Quantitative and Computational Biology, University of California, Los Angeles, Los Angeles, CA, United States.; Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA, United States., Lu Z; Department of Neurology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China., Jones M; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States., Denver P; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States., Castro D; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States., Gu X; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States., Relampagos F; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States., Caoili K; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States., Teter B; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States., Frautschy SA; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States.; Department of Medicine, University of California, Los Angeles, Los Angeles, CA, United States., Cole GM; Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States.; Geriatric Research and Clinical Center, Greater Los Angeles Veterans Affairs Healthcare System, West Los Angeles VA Medical Center, Los Angeles, CA, United States.; Department of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
المصدر: Frontiers in immunology [Front Immunol] 2020 Oct 16; Vol. 11, pp. 558036. Date of Electronic Publication: 2020 Oct 16 (Print Publication: 2020).
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Lausanne : Frontiers Research Foundation]
مواضيع طبية MeSH: Immunity, Innate*, Alzheimer Disease/*etiology , Alzheimer Disease/*metabolism , Brain/*immunology , Brain/*metabolism , Fatty Acids, Omega-6/*metabolism , Fatty Acids, Unsaturated/*metabolism, Alzheimer Disease/pathology ; Animals ; Apolipoproteins E/genetics ; Apolipoproteins E/metabolism ; Cytokines/metabolism ; Disease Models, Animal ; Disease Susceptibility ; Immunohistochemistry ; Inflammation Mediators/metabolism ; Mice ; Mice, Transgenic ; Microglia/immunology ; Microglia/metabolism ; Neurodegenerative Diseases
مستخلص: Neuroinflammation plays a crucial role in the development and progression of Alzheimer's disease (AD), in which activated microglia are found to be associated with neurodegeneration. However, there is limited evidence showing how neuroinflammation and activated microglia are directly linked to neurodegeneration in vivo . Besides, there are currently no effective anti-inflammatory drugs for AD. In this study, we report on an effective anti-inflammatory lipid, linoleic acid (LA) metabolite docosapentaenoic acid (DPAn-6) treatment of aged humanized EFAD mice with advanced AD pathology. We also report the associations of neuroinflammatory and/or activated microglial markers with neurodegeneration in vivo . First, we found that dietary LA reduced proinflammatory cytokines of IL1-β, IL-6, as well as mRNA expression of COX2 toward resolving neuroinflammation with an increase of IL-10 in adult AD models E3FAD and E4FAD mice. Brain fatty acid assays showed a five to six-fold increase in DPAn-6 by dietary LA, especially more in E4FAD mice, when compared to standard diet. Thus, we tested DPAn-6 in aged E4FAD mice. After DPAn-6 was administered to the E4FAD mice by oral gavage for three weeks, we found that DPAn-6 reduced microgliosis and mRNA expressions of inflammatory, microglial, and caspase markers. Further, DPAn-6 increased mRNA expressions of ADCYAP1, VGF, and neuronal pentraxin 2 in parallel, all of which were inversely correlated with inflammatory and microglial markers. Finally, both LA and DPAn-6 directly reduced mRNA expression of COX2 in amyloid-beta42 oligomer-challenged BV2 microglial cells. Together, these data indicated that DPAn-6 modulated neuroinflammatory responses toward resolution and improvement of neurodegeneration in the late stages of AD models.
(Copyright © 2020 Ma, Zhu, Morselli, Su, Pelligrini, Lu, Jones, Denver, Castro, Gu, Relampagos, Caoili, Teter, Frautschy and Cole.)
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معلومات مُعتمدة: I01 BX000542 United States BX BLRD VA; R21 AG050269 United States AG NIA NIH HHS; R21 AG069100 United States AG NIA NIH HHS
فهرسة مساهمة: Keywords: APOE; Alzheimer's disease; EFAD; docosapentaenoic acid; fatty acid; linoleic acid; neuroinflammation
المشرفين على المادة: 0 (Apolipoproteins E)
0 (Cytokines)
0 (Fatty Acids, Omega-6)
0 (Fatty Acids, Unsaturated)
0 (Inflammation Mediators)
NS3OZT14QT (docosapentaenoic acid)
تواريخ الأحداث: Date Created: 20201112 Date Completed: 20210514 Latest Revision: 20210514
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC7596305
DOI: 10.3389/fimmu.2020.558036
PMID: 33178186
قاعدة البيانات: MEDLINE
الوصف
تدمد:1664-3224
DOI:10.3389/fimmu.2020.558036