The pathogenesis of VaD is complex and is the result of a variety of cardiovascular or genetic risk factors associated with Apolipoprotein E (APOE), angiotensin I converting enzyme (ACE), paraoxonase 1 (PON1), or presenilin 1 (PSEN1) genes, or due to stroke (O’Brien and Thomas, 2015). This evidence concerns the gene APOE and stroke disorder.