A significantly increased level of Fn1 in young and aged mice after stroke can be either a result of an inflow of the soluble form of Fn1 from plasma or caused by the higher production of Fn1, which can be related with the upregulation of Fn1. In addition, the analysis revealed a rapid increase in Fn1 protein expression on D3 after pMCAo in young adult and aged animals. This evidence concerns the gene FN1 and stroke disorder.