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Abrogation of type-I interferon signalling alters the microglial response to Aβ1-42.

Abstract：

:Neuroinflammation and accompanying microglial dysfunction are now appreciated to be involved in Alzheimer's disease (AD) pathogenesis. Critical to the process of neuroinflammation are the type-I interferon (IFN) family of cytokines. Efforts to phenotypically characterize microglia within AD identify distinct populations associated with type-I IFN signalling, yet how this affects underlying microglial function is yet to be fully elucidated. Here we demonstrate that Aβ1-42 exposure increases bioactive levels of type-I IFN produced by primary microglia alongside increased expression of type-I IFN related genes. Primary microglia isolated from brains of APPswePS1ΔE9 mice with ablated type-I IFN signalling show an increased phagocytic ability to uptake FITC-Aβ1-42. Correlative assessment of plaque sizes in aged APPswePS1ΔE9 mice with abrogated type-I IFN signalling show unchanged deposition levels. Microglia from these mice did however show alterations in morphology. This data further highlights the role of type-I IFN signalling within microglia and identifies a role in phagocytosis. As such, targeting both microglial and global type-I IFN signalling presents as a novel therapeutic strategy for AD management.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Moore Z,Mobilio F,Walker FR,Taylor JM,Crack PJ

doi

10.1038/s41598-020-59917-0

subject

Has Abstract

pub_date

2020-02-21 00:00:00

pages

3153

issue

1

issn

2045-2322

pii

10.1038/s41598-020-59917-0

journal_volume

10

pub_type

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