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              <text>&lt;a href="http://doi.org/10.1016/j.bbadis.2017.11.004" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1016/j.bbadis.2017.11.004&lt;/a&gt;</text>
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              <text>432–443</text>
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              <text>1864</text>
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                <text>Epigenetic regulation of astrocyte function in neuroinflammation and neurodegeneration.</text>
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                <text>Biochimica et biophysica acta. Molecular basis of disease</text>
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                <text>*Astrocyte; *DNA methylation; *Epigenesis; *Epigenetic; *Histone; *Neurodegeneration; *Neuroinflammation; Acetylation; Alzheimer Disease/genetics/pathology; Animals; Astrocytes/*cytology/immunology; Cell Differentiation; DNA Methylation; Genetic; Histones/metabolism; Humans; Inflammation/*pathology; Methylation; MicroRNAs/metabolism; Neurodegenerative Diseases/genetics/*pathology; Neuroglia/metabolism; Neurons/immunology; Parkinson Disease/genetics/pathology</text>
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                <text>Neal Matthew; Richardson Jason R</text>
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                <text>Epigenetic mechanisms control various functions throughout the body, from cell fate determination in development to immune responses and inflammation. Neuroinflammation is one of the prime contributors to the initiation and progression of neurodegeneration in a variety of diseases, including Alzheimer's and Parkinson's diseases. Because astrocytes are the largest population of glial cells, they represent an important regulator of CNS function, both in health and disease. Only recently have studies begun to identify the epigenetic mechanisms regulating astrocyte responses in neurodegenerative diseases. These epigenetic mechanisms, along with the epigenetic marks involved in astrocyte development, could elucidate novel pathways to potentially modulate astrocyte-mediated neuroinflammation and neurotoxicity. This review examines the known epigenetic mechanisms involved in regulation of astrocyte function, from development to neurodegeneration, and links these mechanisms to potential astrocyte-specific roles in neurodegenerative disease with a focus on potential opportunities for therapeutic intervention.</text>
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                <text>&lt;a href="http://doi.org/10.1016/j.bbadis.2017.11.004" target="_blank" rel="noreferrer noopener"&gt;10.1016/j.bbadis.2017.11.004&lt;/a&gt;</text>
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