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1. The Increased Densities, But Different Distributions, of Both C3 and S100A10 Immunopositive Astrocyte-Like Cells in Alzheimer’s Disease Brains Suggest Possible Roles for Both A1 and A2 Astrocytes in the Disease Pathogenesis

Author

Andrew King, Boglarka Szekely, Eda Calapkulu, Hanan Ali, Francesca Rios, Shalmai Jones, and Claire Troakes

Subjects
Alzheimer’s, dementia, immunohistochemistry, A1, A2, astrocytes, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

There is increasing evidence of astrocyte dysfunction in the pathogenesis of Alzheimer’s disease (AD). Animal studies supported by human post-mortem work have demonstrated two main astrocyte types: the C3 immunopositive neurotoxic A1 astrocytes and the S100A10 immunopositive neuroprotective A2 astrocytes. A1 astrocytes predominate in AD, but the number of cases has been relatively small. We examined post-mortem brains from a larger cohort of AD cases and controls employing C3 and S100 immunohistochemistry to identify the astrocytic subtypes. There were a number of C3 immunopositive astrocyte-like cells (ASLCs) in the control cases, especially in the lower cerebral cortex and white matter. In AD this cell density appeared to be increased in the upper cerebral cortex but was similar to controls in other regions. The S100A10 showed minimal immunopositivity in the control cases in the cortex and white matter, but there was increased ASLC density in upper/lower cortex and white matter in AD compared to controls. In AD and control cases the numbers of C3 immunopositive ASLCs were greater than those for S100A10 ASLCs in all areas studied. It would appear that the relationship between A1 and A2 astrocytes and their possible role in the pathogenesis of AD is complex and requires more research.

Published
2020
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2. The Increased Densities, But Different Distributions, of Both C3 and S100A10 Immunopositive Astrocyte-Like Cells in Alzheimer’s Disease Brains Suggest Possible Roles for Both A1 and A2 Astrocytes in the Disease Pathogenesis

Author

Hanan Ali, Andy King, Shalmai Jones, Claire Troakes, Boglarka Szekely, Francesca Rios, and Eda Calapkulu

Subjects
Pathology, medicine.medical_specialty, Neuroprotection, Article, lcsh:RC321-571, White matter, Pathogenesis, 03 medical and health sciences, 0302 clinical medicine, Cortex (anatomy), medicine, C3, A1, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, A2, 030304 developmental biology, 0303 health sciences, biology, General Neuroscience, Neurodegeneration, neurodegeneration, astrocytes, S100A10, glial, medicine.disease, medicine.anatomical_structure, Cerebral cortex, immunohistochemistry, biology.protein, Alzheimer’s, 030217 neurology & neurosurgery, dementia, Astrocyte
Abstract

There is increasing evidence of astrocyte dysfunction in the pathogenesis of Alzheimer&rsquo, s disease (AD). Animal studies supported by human post-mortem work have demonstrated two main astrocyte types: the C3 immunopositive neurotoxic A1 astrocytes and the S100A10 immunopositive neuroprotective A2 astrocytes. A1 astrocytes predominate in AD, but the number of cases has been relatively small. We examined post-mortem brains from a larger cohort of AD cases and controls employing C3 and S100 immunohistochemistry to identify the astrocytic subtypes. There were a number of C3 immunopositive astrocyte-like cells (ASLCs) in the control cases, especially in the lower cerebral cortex and white matter. In AD this cell density appeared to be increased in the upper cerebral cortex but was similar to controls in other regions. The S100A10 showed minimal immunopositivity in the control cases in the cortex and white matter, but there was increased ASLC density in upper/lower cortex and white matter in AD compared to controls. In AD and control cases the numbers of C3 immunopositive ASLCs were greater than those for S100A10 ASLCs in all areas studied. It would appear that the relationship between A1 and A2 astrocytes and their possible role in the pathogenesis of AD is complex and requires more research.

Published
2020

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