On the other hand, studies have reported blunted neuroinflammatory responses in older animals, including: reductions in TNF-α, IL-1β, IL-6, CCL2, CCL5, RANTES and TGFβ1 following stroke [65, 87]; curtailed expression of equivalent markers in middle aged and senescent hippocampus following radiation [88]; diminished levels of arginase, IL-1β, and CCL2 expression in spinal cord after injury [89]; and reduced GFAP [16] and CD11b immunoreactivities [14] in senescent and middle-aged spinal cord following CCI. This evidence concerns the gene CCL2 and stroke disorder.