The way for explanation postischemic dementia processes has been one fraught with a wide range of complications and frequent revisions with a lack of a final clear solution. Data from animal models of brain ischemia and human ischemic brains studies have demonstrated an overexpression of amyloid precursor protein and increase production of a β-amyloid peptide. Restoration brain activity following ischemic brain episode is delayed and not always complete due to an alteration related with increase in the level of the β-amyloid peptide. In this paper, we will propose our idea about production of the β-amyloid peptide from the amyloid precursor protein in ischemic brain lesions, and how this protein presents etiological and therapeutic targets that are now under consideration. Maturation of the ischemic brain tissue pathology may be caused not only by a neurodegeneration of selectively vulnerable neuronal cells destroyed following ischemia but also by acute and chronic pathology of resistant parts of the brain and chronic changes in the blood-brain barrier. We propose that in dementia following ischemia an initial ischemic episode precedes the brain tissue deposition of β-amyloid peptide, which in turn amplifies the vascular dysfunction after first episode of ischemia triggering next focal ischemic episodes as vicious cycle preceding final ischemic degenerative changes and may gradually over a lifetime, progress to brain atrophy and finally to postischemic dementia with Alzheimer's phenotype.