دورية أكاديمية
Immune Suppression of Glia Maturation Factor Reverses Behavioral Impairment, Attenuates Amyloid Plaque Pathology and Neuroinflammation in an Alzheimer's Disease Mouse Model.
العنوان: | Immune Suppression of Glia Maturation Factor Reverses Behavioral Impairment, Attenuates Amyloid Plaque Pathology and Neuroinflammation in an Alzheimer's Disease Mouse Model. |
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المؤلفون: | Ahmed ME; Department of Neurology and Center for Translational Neuroscience, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA.; Harry S. Truman Memorial Veterans Hospital, Columbia, MO, USA., Selvakumar GP; Department of Neurology and Center for Translational Neuroscience, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA.; Harry S. Truman Memorial Veterans Hospital, Columbia, MO, USA., Thangavel R; Department of Neurology and Center for Translational Neuroscience, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA.; Harry S. Truman Memorial Veterans Hospital, Columbia, MO, USA., Kempuraj D; Department of Neurology and Center for Translational Neuroscience, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA.; Harry S. Truman Memorial Veterans Hospital, Columbia, MO, USA., Raikwar SP; Department of Neurology and Center for Translational Neuroscience, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA.; Harry S. Truman Memorial Veterans Hospital, Columbia, MO, USA., Zaheer S; Department of Neurology and Center for Translational Neuroscience, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA., Iyer S; Department of Neurology and Center for Translational Neuroscience, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA.; Harry S. Truman Memorial Veterans Hospital, Columbia, MO, USA., Zaheer A; Department of Neurology and Center for Translational Neuroscience, School of Medicine, University of Missouri, 1 Hospital Drive, Columbia, MO, USA. zaheera@health.missouri.edu.; Harry S. Truman Memorial Veterans Hospital, Columbia, MO, USA. zaheera@health.missouri.edu. |
المصدر: | Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology [J Neuroimmune Pharmacol] 2021 Jun; Vol. 16 (2), pp. 363-375. Date of Electronic Publication: 2020 Jun 05. |
نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S. |
اللغة: | English |
بيانات الدورية: | Publisher: Springer Science + Business Media Country of Publication: United States NLM ID: 101256586 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1557-1904 (Electronic) Linking ISSN: 15571890 NLM ISO Abbreviation: J Neuroimmune Pharmacol Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: New York, NY : Springer Science + Business Media, c2006- |
مواضيع طبية MeSH: | Alzheimer Disease/*pathology , Brain/*pathology , Glia Maturation Factor/*antagonists & inhibitors , Plaque, Amyloid/*pathology, Animals ; Behavior, Animal ; Disease Models, Animal ; Inflammation/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Degeneration/pathology |
مستخلص: | Alzheimer's disease (AD) is an irreversible progressive neurodegenerative disorder recognized by accumulation of amyloid-plaques (APs) and neurofibrillary tangles (NFTs) and eventually loss of memory. Glia maturation factor (GMF), a neuroinflammatory protein first time isolated and cloned in our laboratory plays an important role in the pathogenesis of AD. However, no studies have been reported on whether anti-GMF antibody administration could downregulate neuroinflammation and attenuate amyloid pathology in AD brain. We investigated the potential effect of single dose of (2 mg/kg b.wt/mouse) intravenously (iv) injected with anti-GMF antibodyon cognitive function, neuroprotection, neuroinflammation and Aβ load in the brain of 9-month-old 5XFAD mice. Following 4 weeks of anti-GMF antibody delivery in mice, we found reduced expression of GMF, astrocytic glial fibrillary acidic protein (GFAP) and microglial ionizing calcium binding adaptor molecule 1 (Iba1) as well as improvement inneuroinflammatory response via inhibition of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) production and amyloid pathology in the cerebral cortex and hippocampal CA1 region of 5XFAD mice. Correspondingly, blockade of GMF function with anti-GMF antibody improved spatial learning, memory, and long-term recognition memory in 5XFAD mice. The present study demonstrates that the immune checkpoint blockade of GMF function with anti-GMF antibody coordinates anti-inflammatory effects to attenuate neurodegeneration in the cortex and hippocampal CA1 region of 5XFAD mouse brain. Further, our data suggest, that pharmacological immune neutralization of GMF is a promising neuroprotective strategy totherapeutically target neuroinflammation and neurodegeneration in AD. Graphical Abstract 5XFAD mice Polyclonal anti-GMF antibody. |
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معلومات مُعتمدة: | R01 AG048205 United States AG NIA NIH HHS; AG048205 United States AG NIA NIH HHS; VA Research Career Scientist Award U.S. Department of Veterans Affairs; AG048205 United States AG NIA NIH HHS |
فهرسة مساهمة: | Keywords: Alzheimer’s disease; Amyloid pathology; Anti-GMF antibody; Cognition; Neuroinflammation |
المشرفين على المادة: | 0 (Glia Maturation Factor) |
تواريخ الأحداث: | Date Created: 20200607 Date Completed: 20211206 Latest Revision: 20211214 |
رمز التحديث: | 20221213 |
مُعرف محوري في PubMed: | PMC8240471 |
DOI: | 10.1007/s11481-020-09929-4 |
PMID: | 32504312 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1557-1904 |
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DOI: | 10.1007/s11481-020-09929-4 |