دورية أكاديمية
أعرض في EDS

Systemic administration of Abeta mAb reduces retinal deposition of Abeta and activated complement C3 in age-related macular degeneration mouse model.

التفاصيل البيبلوغرافية
العنوان: Systemic administration of Abeta mAb reduces retinal deposition of Abeta and activated complement C3 in age-related macular degeneration mouse model.
المؤلفون: Catchpole I; Topical BioPharm Discovery Research and Development Unit, King of Prussia, Philadelphia, Pennsylvania, United States of America. ian.r.catchpole@gsk.com, Germaschewski V, Hoh Kam J, Lundh von Leithner P, Ford S, Gough G, Adamson P, Overend P, Hilpert J, López FJ, Ng YS, Coffey P, Jeffery G
المصدر: PloS one [PLoS One] 2013 Jun 14; Vol. 8 (6), pp. e65518. Date of Electronic Publication: 2013 Jun 14 (Print Publication: 2013).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: Electronic-Print Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Amyloid beta-Peptides/*metabolism , Antibodies, Monoclonal, Murine-Derived/*administration & dosage , Complement C3/*metabolism , Macular Degeneration/*drug therapy , Peptide Fragments/*metabolism , Retina/*metabolism, Amyloid beta-Peptides/immunology ; Animals ; Disease Models, Animal ; Humans ; Hybridomas ; Macular Degeneration/immunology ; Macular Degeneration/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Peptide Fragments/immunology ; Retina/pathology
مستخلص: Age-related macular degeneration (AMD) is a leading cause of legal blindness in the Western world. There are effective treatments for the vascular complications of neo-vascular AMD, but no effective therapies are available for the dry/atrophic form of the disease. A previously described transgenic CFH-gene deficient mouse model, (cfh-/-), shows hallmarks of early AMD. The ocular phenotype has been further analysed to demonstrate amyloid beta (Aβ) rich basement membrane deposits associated with activated complement C3. Cfh-/- mice were treated systemically in both prophylactic and therapeutic regimes with an anti-Aβ monoclonal antibody (mAb), 6F6, to determine the effect on the cfh-/- retinal phenotype. Prophylactic treatment with 6F6 demonstrated a dose dependent reduction in the accumulation of both Aβ and activated C3 deposition. A similar reduction in the retinal endpoints could be seen after therapeutic treatment. Serum Aβ levels after systemic administration of 6F6 show accumulation of Aβ in the periphery suggestive of a peripheral sink mechanism. In summary, anti-Aβ mAb treatment can partially prevent or reverse ocular phenotypes of the cfh-/- mouse. The data support this therapeutic approach in humans potentially modulating two key elements in the pathogenesis of AMD - Aβ and activated, complement C3.
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المشرفين على المادة: 0 (Amyloid beta-Peptides)
0 (Antibodies, Monoclonal, Murine-Derived)
0 (Complement C3)
0 (Peptide Fragments)
0 (amyloid beta-protein (1-42))
تواريخ الأحداث: Date Created: 20130627 Date Completed: 20140130 Latest Revision: 20211021
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC3682980
DOI: 10.1371/journal.pone.0065518
PMID: 23799019
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0065518