Astrocytes and neuroinflammation in Alzheimer's disease
Astrocytes and neuroinflammation in Alzheimer's disease
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.
1321-1325
Phillips, Emma
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Croft, Cara L.
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Kurbatskaya, Ksenia
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O'Neill, Michael
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Hutton, Michael L.
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Hanger, Diane P.
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Garwood, Claire J.
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Noble, Wendy
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1 October 2014
Phillips, Emma
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Croft, Cara L.
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Kurbatskaya, Ksenia
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O'Neill, Michael
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Hutton, Michael L.
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Hanger, Diane P.
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Garwood, Claire J.
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Noble, Wendy
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Phillips, Emma, Croft, Cara L., Kurbatskaya, Ksenia, O'Neill, Michael, Hutton, Michael L., Hanger, Diane P., Garwood, Claire J. and Noble, Wendy
(2014)
Astrocytes and neuroinflammation in Alzheimer's disease.
Biochemical Society Transactions, 42 (5), .
(doi:10.1042/BST20140155).
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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e-pub ahead of print date: 18 September 2014
Published date: 1 October 2014
Identifiers
Local EPrints ID: 420386
URI: http://eprints.soton.ac.uk/id/eprint/420386
ISSN: 0300-5127
PURE UUID: e7e0d5eb-20de-4186-88e7-513bdd1ef023
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Date deposited: 04 May 2018 16:30
Last modified: 16 Mar 2024 04:29
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Contributors
Author:
Emma Phillips
Author:
Cara L. Croft
Author:
Michael O'Neill
Author:
Michael L. Hutton
Author:
Diane P. Hanger
Author:
Claire J. Garwood
Author:
Wendy Noble
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