Abeta-induced inflammatory processes in microglia cells of APP23 transgenic mice
Autor: | Matthias Staufenbiel, Bernd Sommer, Karl-Heinz Wiederhold, Chantal Pauli, Lisa Schnell, Mathias Jucker, T. Martina Stalder, Florian Ermini, Klaus D. Bornemann |
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Rok vydání: | 2001 |
Předmět: |
Genetically modified mouse
Male Amyloid Antigens Differentiation Myelomonocytic Inflammation Mice Inbred Strains Mice Transgenic Receptors Fc Pathology and Forensic Medicine Amyloid beta-Protein Precursor Mice Antigen Phagocytosis Antigens CD medicine Amyloid precursor protein Animals Humans Lymphocytes Scavenger receptor Receptor Amyloid beta-Peptides Microglia biology Histocompatibility Antigens Class II Brain Immunohistochemistry Cell biology Mice Inbred C57BL medicine.anatomical_structure Immunology biology.protein Female medicine.symptom Regular Articles |
Zdroj: | The American journal of pathology. 158(1) |
ISSN: | 0002-9440 |
Popis: | A microglial response is part of the inflammatory processes in Alzheimer’s disease (AD). We have used APP23 transgenic mice overexpressing human amyloid precursor protein with the Swedish mutation to characterize this microglia response to amyloid deposits in aged mice. Analyses with MAC-1 and F4/80 antibodies as well as in vivo labeling with bromodeoxyuridine demonstrate that microglia in the plaque vicinity are in an activated state and that proliferation contributes to their accumulation at the plaque periphery. The amyloid-induced microglia activation may be mediated by scavenger receptor A, which is generally elevated, whereas the increased immunostaining of the receptor for advanced glycation end products is more restricted. Although components of the phagocytic machinery such as macrosialin and Fc receptors are increased in activated microglia, efficient clearance of amyloid is missing seemingly because of the lack of amyloid-bound autoantibodies. Similarly, although up-regulation of major histocompatibility complex class II (IA) points toward an intact antigen-presenting function of microglia, lack of T and B lymphocytes does not indicate a cell-mediated immune response in the brains of APP23 mice. The similar characteristics of microglia in the APP23 mice and in AD render the mouse model suitable to study the role of inflammatory processes during AD pathogenesis. |
Databáze: | OpenAIRE |
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