For example, a seven-day administration of Wnt-3a increased BDNF expression, proliferation, and migration of neuroblasts from the subventricular zone after ischemia modeling [32], while the inhibitor of the Wnt/β-catenin pathway suppressed the expression of Wnt3a, nuclear β-catenin, BDNF, and MBP, and worsened the neurological status of animals after stroke [33]. Here, WNT3A is linked to ischemia.