Clearance of Amyloid-β Protein Deposits in Transgenic Mice following Focal Cerebral Ischemia
| Autor: | Judianne Davis, Feng Xu, W E Van Nostrand, Mary Lou Previti |
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| Rok vydání: | 2012 |
| Předmět: |
Paper
Genetically modified mouse Pathology medicine.medical_specialty Time Factors Amyloid β Transgene Ischemia Enzyme-Linked Immunosorbent Assay Mice Transgenic Functional Laterality Brain Ischemia Brain ischemia Amyloid beta-Protein Precursor Mice medicine Animals Humans Protein precursor Amyloid beta-Peptides Microglia business.industry Macrophages medicine.disease Disease Models Animal medicine.anatomical_structure Neurology Mutation Neurology (clinical) business Infiltration (medical) |
| Zdroj: | Neurodegenerative Diseases. 10:108-111 |
| ISSN: | 1660-2862 1660-2854 |
| Popis: | Background/Aims: There is increased amyloid-β protein precursor (AβPP) expression and amyloid-β protein (Aβ) production in the brain shortly following cerebral ischemic stroke in rodent models. It has been postulated that this may seed amyloid deposition in the brain. On the other hand, it remains unclear how cerebral ischemia affects preexisting Aβ deposits in the brain. Here we determine the consequences of focal ischemic stroke on existing Aβ pathology in Tg-SwDI transgenic mice. Methods: At 12 months of age, Tg-SwDI mice were subjected to photo-induced focal cerebral ischemia in one hemisphere. One, 7, or 21 days after lesioning, the amount of deposited Aβ in the ischemic and control hemispheres was measured using ELISA. Image analysis was used to visualize deposited Aβ and the presence of microglia/macrophages. Results: After 7 days, and further after 21 days, there was a dramatic reduction in the amount of deposited Aβ and increased presence of microglia/macrophages in the ischemic hemisphere of the mice. Conclusions: Focal cerebral ischemia leads to clearance of deposited Aβ in Tg-SwDI mice starting at 7 days with almost complete removal in the ischemic area by 21 days. The delayed clearance of Aβ following focal cerebral ischemia may involve the infiltration of activated neuroinflammatory cells. |
| Databáze: | OpenAIRE |
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