In light of these findings and in agreement with previous data on the neuroprotective action of MIF in models of cerebral ischemia/reperfusion associated with reduced caspase-3 activation [69], the authors suggest that at the late stage of AD, a large portion of the extracellular MIF is sequestered by Aβ plaque, which impedes its cerebral biological functioning and is followed by an unsuccessfully compensatory attempt [69]. Here, MIF is linked to Alzheimer disease.