From Brain Ischemia-Reperfusion Injury to Possible Sporadic Alzheimers Disease

Ryszard      Pluta

doi:10.2174/1567202043361839

Abstract

Understanding of the molecular basis of dementias such as Alzheimers disease has not improved greatly in recent years. In this situation the study of neurobiology of Alzheimers disease, now more than ever, needs an infusion of new concept. Recent evidence suggests that the neuropathological picture of Alzheimers disease comprises more than amyloid accumulation, neurofibrillary tangles and finally brain atrophy. At least one third of Alzheimer type of dementia cases exhibit different cerebrovascular diseases. In addition, micro- and macroinfarctions and ischemic white matter changes are also evident in brains of Alzheimers disease patients. The presence of vascular abnormalities seems usually ignored and regarded by researchers as insignificant or considered incidental in Alzheimers disease etiology. The “ischemia-reperfusion hypothesis” was primarily aimed at stimulating research and redirecting the focus of studies towards ischemic cellular mechanisms of Alzheimers disease. Considerable progress has been made in recent years in understanding the role of ischemia in the aging process and in contributing to the development of Alzheimers disease. To accommodate the recent ischemic progress of study in Alzheimers disease there is a need to synthesize all the divergent pieces of data into a coherent story. In this review, current knowledge on the relation between cerebrovascular disease factors and Alzheimers type dementia will be reviewed. We will summarize the results with a special focus on Alzheimer lesions in experimental brain ischemia.

Keywords: alzheimers disease, brain ischemia, amyloid peptide, apolipoprotein, presenilin, tau, cytokine, alpha-synuclein, secretase, vaccination