Furthermore, in a cystathionine-β-synthase heterozygote mouse model (Cbs+/−, a genetic model of hyperhomocysteinemia), hyperhomocysteinemia has been reported to cause a considerable reduction in VE-cadherin in the cerebrovasculature, as well as increased BBB permeability and cerebrovascular deposition of Aβ and fibrinogen (Muradashvili et al., 2014). The gene discussed is CDH5; the disease is hyperhomocysteinemia.