4.6 Article

Astroglial Cell Subtypes in the Cerebella of Normal Adults, Elderly Adults, and Patients with Alzheimer's Disease: A Histological and Immunohistochemical Comparison

Journal

GLIA
Volume 63, Issue 2, Pages 287-312

Publisher

WILEY
DOI: 10.1002/glia.22751

Keywords

cerebellar cortex; astroglia; golgi epithelial cell; ageing; Alzheimer's disease

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Objectives and experimental design Cerebella of young adults, elderly adults, and patients with Alzheimer's disease (AD) (with and without cerebellar amyloid deposits) were studied by Golgi staining and glial fibrillary acid protein (GFAP) immunocytochemical methods. Observations Three subtypes of Golgi epithelial cells and nine subtypes of stellate neuroglia (both normal and hypertrophic) were defined by their morphology, their GFAP-reactivity, their specific location in the cortical layers, and their responses in senility and AD. The GFAP immunoreaction was subtype specific. In aged and AD cerebella, different morphological and GFAP-immunoreactive subtype-specific changes were observed: in the white matter, the subtypes were always GFAP-immunopositive, but in the grey matter some astroglial subtypes showed a variable or no increase in GFAP staining. The astrocytes at the limits of the granule cell layer showed more and longer processes. Variations were seen in one or more folia, involving one or more subtypes and affecting different numbers of cells of each subtype. No clear differences were seen in glial reactivity between beta-amyloid positive and -amyloid (A) negative AD cerebella. No important relationships were found between A deposits. In aged and AD cerebella, different subtypes expressed new proteins (APP, calretinin). Conclusions The existence of different glial subtypes in different locations suggests they have different functions. General and local variations in these subtypes suggest that both general and local induction factors must also exist. The responses of glial cells to as-yet undefined stimuli might lead to general or local neuronal changes important in senility and the pathogenic course of AD. GLIA 2015;63:287-312

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