TLR2 and Stroke: Our previous reports have demonstrated that overexpression of TDP-43 in transgenic mice increases expression of inflammatory markers and TLR2 in glial cells [17, 24]; thus, we hypothesized that increase in TDP-43 levels and the formation of ubiquitin/TDP-43-positive inclusions observed predominately in 12-month-old mice would favor shift of microglial profiles toward pro-inflammatory phenotype resulting in an increase of the TLR2 response after stroke.