In this paper we review the hard-earned data, which present ischemic induction of amyloid precursor protein, presenilins, apolipoproteins and secretases genes, playing key roles in β-amyloid peptide generation. Presented data are strongly supporting a hypothesis that brain ischemia may be involved in the aetiology of sporadic Alzheimer's disease. Potential contribution and impact of ischemically activated genes on the development of sporadic Alzheimer's disease remain to be established at both genetic and functional levels. The identification of the genes involved in sporadic Alzheimer's disease induced by ischemia will enable to further define the events leading to Alzheimer's disease-related abnormalities. Additionally, knowledge gained from the reviewed studies should facilitate the elaboration of effective treatment and/or prevention of sporadic Alzheimer's disease.