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Neuroscience Bulletin ; (6): 912-920, 2018.
Article in English | WPRIM | ID: wpr-775500

ABSTRACT

Astrocytes are closely associated with Alzheimer's disease (AD). However, their precise roles in AD pathogenesis remain controversial. One of the reasons behind the different results reported by different groups might be that astrocytes were targeted at different stages of disease progression. In this study, by crossing hAPP (human amyloid precursor protein)-J20 mice with a line of GFAP-TK mice, we found that astrocytes were activated specifically at an early stage of AD before the occurrence of amyloid plaques, while microglia were not affected by this crossing. Activation of astrocytes at the age of 3-5 months did not affect the proteolytic processing of hAPP and amyloid plaque loads in the brains of hAPP-J20 mice. Our data suggest that early activation of astrocytes does not affect the deposition of amyloid β in an animal model of AD.


Subject(s)
Animals , Humans , Mice , Aldehyde Dehydrogenase , Metabolism , Alzheimer Disease , Genetics , Metabolism , Pathology , Amyloid beta-Peptides , Metabolism , Amyloid beta-Protein Precursor , Genetics , Metabolism , Astrocytes , Metabolism , Brain , Pathology , Calcium-Binding Proteins , Metabolism , Cell Proliferation , Disease Models, Animal , Gene Expression Regulation , Genetics , Glial Fibrillary Acidic Protein , Glutamine , Metabolism , Green Fluorescent Proteins , Genetics , Metabolism , Ki-67 Antigen , Metabolism , Mice, Transgenic , Microfilament Proteins , Metabolism , Mutation , Genetics , Nerve Tissue Proteins , Metabolism
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