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Astrocytes and neuroinflammation in Alzheimer's disease

Research output: Contribution to journalArticle

Emma C. Phillips, Cara L. Croft, Ksenia Kurbatskaya, Michael J. O'Neill, Michael L. Hutton, Diane P. Hanger, Claire J. Garwood, Wendy Noble

Original languageEnglish
Pages (from-to)1321-1325
Number of pages5
JournalBiochemical Society Transactions
Volume42
Issue number5
DOIs
Published1 Oct 2014

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  • Phillips_BiochemSocTrans

    Phillips_BiochemSocTrans.docx, 36.2 KB, application/vnd.openxmlformats-officedocument.wordprocessingml.document

    Uploaded date:04 Dec 2015

    Version:Accepted author manuscript

    The version made available will be the author’s pre-publication version, i.e. the peer-reviewed, Accepted Manuscript (AM)*.

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Abstract

Increased production of amyloid β-peptide (Aβ) and altered processing of tau in Alzheimer's disease (AD) are associated with synaptic dysfunction, neuronal death and cognitive and behavioural deficits. Neuroinflammation is also a prominent feature of AD brain and considerable evidence indicates that inflammatory events play a significant role in modulating the progression of AD. The role of microglia in AD inflammation has long been acknowledged. Substantial evidence now demonstrates that astrocyte-mediated inflammatory responses also influence pathology development, synapse health and neurodegeneration in AD. Several anti-inflammatory therapies targeting astrocytes show significant benefit in models of disease, particularly with respect to tau-associated neurodegeneration. However, the effectiveness of these approaches is complex, since modulating inflammatory pathways often has opposing effects on the development of tau and amyloid pathology, and is dependent on the precise phenotype and activities of astrocytes in different cellular environments. An increased understanding of interactions between astrocytes and neurons under different conditions is required for the development of safe and effective astrocyte-based therapies for AD and related neurodegenerative diseases.

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