Publisher's Synopsis
This book presents a summary of Alzheimers disease-related ischemic protein changes and gene expression as risk factors for the late-onset of sporadic Alzheimers disease, and their role in Alzheimers disease ischemic etiology. Ischemic brain changes were noted in the staining of different parts of an amyloid protein precursor, presenilin 1 and 2, tau protein, alfa-synuclein, and apolipoproteins A1, E and J. Current advances in understanding the ischemic etiology of Alzheimers disease has revealed dysregulation of Alzheimers disease-associated genes including presenilin 1 and 2, ß-secretase, amyloid protein precursor, apoptosis, autophagy, mitophagy, and tau proteins. This book presents the relationship between these genes, dysregulated by cerebral ischemia, and the cellular and tissue neuropathology characteristic of Alzheimers disease. This book draws attention to the latest research confirming the theory that Alzheimers disease-related proteins and genes play an important role in ischemic brain damage, and ischemia is an essential and leading supplier for the onset and progression of sporadic Alzheimers disease. The above data comes from the latest research from leading and renowned scientists around the world, who present important information on the understanding of the ischemic etiology of Alzheimers disease. In the future, it is likely that the manipulation of ischemia and ischemia-activated Alzheimers disease-associated genes and their proteins will give new hope for the development of causal therapies urgently needed to prevent or treat neurodegenerative diseases such as Alzheimers disease. An innovative/modern approach to the etiology of Alzheimers disease in the chapter XII Ischemic etiology of Alzheimers disease will give the reader a glimpse of what is on the horizon.
