This might be related to the increased expression of Bax in the hippocampus of vascular dementia rats, the oligomerization in the nuclear membrane of nerve cells that affected the permeability of the nuclear membrane, increased the entry of the cytochrome into the cytoplasm, and activated the cascade of caspase-3, while the polymerization of Bcl-2 and Bax into a dimer, inhibited the production of Bcl-2, and thereby broke the balance between Bcl-2 and Bax, and induced neuronal apoptosis [18]. This evidence concerns the gene CASP3 and vascular dementia.