Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death

摘要

Cells (WT: wild type, MyD88 : MyD88 knockout, TLR4 : TLR4 knock out and TLR2 : TLR2 knockout) were stimulated with Aβ Fibrils (0.1–400 nM) and Aβ oligomers together with monomer (total monomer concentration 0.02–80 μM) for 24 h. The levels of the pro-inflammatory mediators TNF-α and IL-1β were measured. TNF-α production remained unchanged at all concentrations with the addition of Fibrils (  = 5, ±sem). TNF-α production significantly increases with increasing oligomer concentrations in all except the TLR4 knockout cells (  = 5, ±sem). IL-1β levels production significantly increases with increasing oligomer concentrations in all except the TLR4 knockout cells (  = 5, mean ± sem).