Is the ischemic blood–brain barrier insufficiency responsible for full-blown Alzheimer's disease?

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Abstract
The goal of this paper is to provide scientists with a comprehensive review of the state-of-the-art influence the ischemic blood-brain barrier (BBB) has on the final development of Alzheimer's disease and to provide detailed food-for-thought which will hopefully stimulate more researchers in this area of neuroscience. Understanding new and fundamental concepts about the behavior of the BBB during long-term reperfusion after ischemia with a variety of new neuropathogenic factors can hopefully provide some interesting clues related to the pathologic processes issues that have been receiving considerable attention in the human clinic. We present the recent data to understand the role of the BBB in maturation of both diseases and try to differentiate between primary and secondary pathologic mechanisms. In conclusion, the neuropathogenesis of Alzheimer's disease involves an initial ischemic neuronal alterations leading to enhanced neuronal vulnerability to beta-amyloid peptide and the ischemic breakdown of the BBB with leakage of serum borne beta-amyloid peptide into brain parenchyma, activation of beta-amyloid peptide-dependent toxicity culminating in the formation of amyloid plaques and finally end in full-blown Alzheimer's disease. In summary, probably we have combined mechanism(s) of ischemia processes, ischemic and chronic BBB dysfunction and beta-amyloid peptide-dependent injury in pathology of neurodegeneration that is observed in Alzheimer's disease. We speculate that Alzheimer's disease may be caused by silent and sublethal ischemic episodes that attack and slowly steal the minds of its victims. Finally, our review proposes the ischemic BBB-dependent mechanism(s) that probably are responsible for full-blown Alzheimer's disease.

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