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.
journal_name
Biochem Soc Transjournal_title
Biochemical Society transactionsauthors
Phillips EC,Croft CL,Kurbatskaya K,O'Neill MJ,Hutton ML,Hanger DP,Garwood CJ,Noble Wdoi
10.1042/BST20140155subject
Has Abstractpub_date
2014-10-01 00:00:00pages
1321-5issue
5eissn
0300-5127issn
1470-8752pii
BST20140155journal_volume
42pub_type
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