Journal article

Deletion of the type-1 interferon receptor in APP(SWE)/PS1(Delta E9) mice preserves cognitive function and alters glial phenotype

Myles R Minter, Zachery Moore, Moses Zhang, Kate M Brody, Nigel C Jones, Sandy R Shultz, Juliet M Taylor, Peter J Crack



A neuro-inflammatory response is evident in Alzheimer's disease (AD), yet the precise mechanisms by which neuro-inflammation influences the progression of Alzheimer's disease (AD) remain poorly understood. Type-1 interferons (IFNs) are master regulators of innate immunity and have been implicated in multiple CNS disorders, however their role in AD progression has not yet been fully investigated. Hence, we generated APPSWE/PS1ΔE9 mice lacking the type-1 IFN alpha receptor-1 (IFNAR1, APPSWE/PS1ΔE9 x IFNAR1(-/-)) aged to 9 months to investigate the role of type-1 IFN signaling in a well-validated model of AD. APPSWE/PS1ΔE9 x IFNAR1(-/-) mice displayed a modest reduction in Aβ monomer levels, de..

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Funding Acknowledgements

This study was supported by grants from the National Health and Medical Research Council (NHMRC) of Australia to P.J.C and J.M.T. P.J.C is an Australian Research Council (ARC) Future Fellow. M.R.M holds an Alzheimer's Australia Dementia Research Fund (AADRF) postgraduate scholarship.