Main Article Content
Ischemic brain damage is associated with the deposition of folding proteins, such as all fragments of the amyloid protein precursor and tau protein, in the intra- and extracellular spaces of neurons. In this chapter, we summarize the protein changes associated with Alzheimer’s disease and their gene expression (amyloid protein precursor and tau protein) after cerebral ischemia and their role in the ischemic etiology of Alzheimer’s disease. Recent advances in understanding the ischemic etiology of Alzheimer’s disease have revealed dysregulation of amyloid protein precursors, β-secretase, presenilin 1 and 2, autophagy, mitophagy, apoptosis, and tau protein genes after ischemic brain injury. However, reduced expression of mRNA of the α-secretase in cerebral ischemia causes neurons to be less resistant to injury. In this chapter, we present the latest evidence that Alzheimer’s disease-related proteins and their genes play a key role in brain damage with ischemia-reperfusion and that ischemic episode is an essential and leading provider of Alzheimer’s disease development. Understanding the underlying processes of linking Alzheimer’s disease-related proteins and their genes in brain ischemia injury with the risk of developing Alzheimer’s disease will provide the most significant goals for therapeutic development to date.
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
Copyright of individual chapters belongs to the respective authors. The authors grant unrestricted publishing and distribution rights to the publisher. The electronic versions of the chapters are published under Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Users are allowed to share and adapt the chapters for any non-commercial purposes as long as the authors and the publisher are explicitly identified and properly acknowledged as the original source. The books in their entirety are subject to copyright by the publisher. The reproduction, modification, republication and display of the books in their entirety, in any form, by anyone, for commercial purposes are strictly prohibited without the written consent of the publisher.