Ischemic stroke is a leading cause of death and cognitive impairment worldwide. However, the mechanisms of progressive cognitive decline following brain ischemia are not yet certain. Ongoing interest in cerebrovascular diseases research has provided data showing that Alzheimers proteins and other factors may be involved in the pathogenesis of gradual ischemic brain injury. Thus, both focal and global brain ischemia in rodents produces a stereotyped pattern of selective neuronal degeneration, which is just the same as in Alzheimers type dementia. Data from animal models and clinical studies of ischemic stroke have demonstrated an increase in expression and processing of amyloid precursor protein (APP) to a neurotoxic form of oligomeric β-amyloid peptide (Aβ) and hyperphosphorylation of tau protein. The authors of this review are using advances in methods and technologies to study cerebrovascular diseases and this review examines the hypothesis that pathological mechanisms common to both brain ischemia and Alzheimers dementia are contributing to cognitive impairment and brain ischemia-related dementia.
Keywords: Cerebrovascular diseases, stroke, dementia, cognition, Aβ, progenitor cells, chemoattractant, pericyte migration, endostatin/collagen, hindlimbs, inter-endothelial, mitogenic activity, gene occludin, complementary agents, cord blood cells