Other studies of animal models have demonstrated that the expression levels of netrin-1 and its receptors (DCC and neogenin) are upregulated after brain ischemia [24, 25], and that intracerebral injection of netrin-1 reduces the number of dying neurons and protects the infarct tissue from p53-mediated apoptosis after stroke [22]. This evidence concerns the gene NTN1 and brain ischemia.