title: Astrocytes and neuroinflammation in Alzheimer's disease.
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.
authors.affiliation: *Department of Neuroscience, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, U.K.
authors.forename: Emma C
authors.initials: EC
authors.lastname: Phillips
authors.affiliation: *Department of Neuroscience, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, U.K.
authors.forename: Cara L
authors.initials: CL
authors.lastname: Croft
authors.affiliation: *Department of Neuroscience, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, U.K.
authors.forename: Ksenia
authors.initials: K
authors.lastname: Kurbatskaya
authors.affiliation: †Eli Lilly and Company, Erl Wood Manor, Windlesham, Surrey GU20 6PH, U.K.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: O'Neill
authors.affiliation: †Eli Lilly and Company, Erl Wood Manor, Windlesham, Surrey GU20 6PH, U.K.
authors.forename: Michael L
authors.initials: ML
authors.lastname: Hutton
authors.affiliation: *Department of Neuroscience, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, U.K.
authors.forename: Diane P
authors.initials: DP
authors.lastname: Hanger
authors.affiliation: ‡Department of Neuroscience, Sheffield Institute for Translational Neuroscience, University of Sheffield, Sheffield S10 2HQ, U.K.
authors.forename: Claire J
authors.initials: CJ
authors.lastname: Garwood
authors.affiliation: *Department of Neuroscience, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, U.K.
authors.forename: Wendy
authors.initials: W
authors.lastname: Noble
mesh_terms: D000544:Alzheimer Disease / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D001253:Astrocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D002450:Cell Communication; D006801:Humans; D009474:Neurons / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D015398:Signal Transduction