Soluble amyloid triggers a myeloid differentiation factor 88 and interferon regulatory factor 7 dependent neuronal type-1 interferon response in vitro
Myles Robert Minter, Bevan Scott Main, Kate Maree Brody, Moses Zhang, Juliet Marie Taylor, Peter John Crack
JOURNAL OF NEUROINFLAMMATION | BIOMED CENTRAL LTD | Published : 2015
BACKGROUND: Neuro-inflammation has long been implicated as a contributor to the progression of Alzheimer's disease in both humans and animal models. Type-1 interferons (IFNs) are pleiotropic cytokines critical in mediating the innate immune pro-inflammatory response. The production of type-1 IFNs following pathogen detection is, in part, through the activation of the toll-like receptors (TLRs) and subsequent signalling through myeloid differentiation factor-88 (Myd88) and interferon regulatory factors (IRFs). We have previously identified that neuronal type-1 IFN signalling, through the type-1 interferon alpha receptor-1 (IFNAR1), is detrimental in models of AD. Using an in vitro approach, t..View full abstract
This study was supported by grants from the National Health and Medical Research Council (NHMRC) of Australia to PJC and JMT. PJC is an Australian Research Council (ARC) Future Fellow. MRM holds an Alzheimer's Australia Dementia Research Fund (AADRF) postgraduate scholarship.