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Microarray analysis of the astrocyte transcriptome in the aging brain: relationship to Alzheimer's pathology and APOE genotype

星形胶质细胞 生物 阿尔茨海默病 神经纤维缠结 神经退行性变 病理 胶质纤维酸性蛋白 激光捕获显微切割 神经科学 老年斑 基因表达 医学 遗传学 免疫学 中枢神经系统 疾病 基因 免疫组织化学
作者
Julie A. Simpson,Paul G. Ince,Christopher Shaw,Paul T. Heath,Rohini Raman,Claire J. Garwood,Catherine Gelsthorpe,Lynne F. Baxter,Gillian Forster,Fiona E. Matthews,Carol Brayne,Stephen B. Wharton
出处
期刊:Neurobiology of Aging [Elsevier]
卷期号:32 (10): 1795-1807 被引量:152
标识
DOI:10.1016/j.neurobiolaging.2011.04.013
摘要

Astrocytes contribute to a variety of functions in the brain, including homeostasis, synapse formation, plasticity, and metabolism. Astrocyte dysfunction may disrupt their normal role, including neuronal support, thereby contributing to neurodegenerative pathologies, including Alzheimer's disease (AD). To understand the role of astrocytes in the pathogenesis of age-related disorders, we isolated astrocytes by laser capture microdissection, using glial fibrillary acidic protein (GFAP) as a marker, and characterized the astrocyte transcriptome at different Braak neurofibrillary tangle stages in postmortem temporal cortex samples derived from the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS) cohort, using microarray analysis. The largest number of significant, differentially expressed genes were identified when the expression profile of astrocytes from isocortical stages of neurofibrillary tangle pathology (Braak stages V-VI) were compared with entorhinal stages (Braak stages I-II). Dysregulation of genes associated with the actin cytoskeleton, proliferation, apoptosis, and ubiquitin-mediated proteolysis occurred at low Braak stages, while altered regulation of intracellular signaling pathways, including insulin, phosphatidylinositol 3-kinase (PI3K)/Akt, and mitogen-activated protein kinase (MAPK) pathways were primarily associated with high levels of Alzheimer-type pathology, and occurred at lower Braak stages in individuals with the APOEε4 allele. Our findings implicate astrocyte dysfunction in the pathogenesis of neurodegenerative pathology in the aging brain, and provide a basis for future candidate studies based on specific pathways.

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