Abstract
Recent years have seen remarkable progress in research into free radicals oxidative stress, particularly in the context of post-ischemic recirculation brain injury. Oxidative stress in post-ischemic tissues violates the integrity of the genome, causing DNA damage, death of neuronal, glial and vascular cells, and impaired neurological outcome after brain ischemia. Indeed, it is now known that DNA damage and repair play a key role in post-stroke white and gray matter remodeling, and restoring the integrity of the blood-brain barrier. This review will present one of the newly characterized mechanisms that emerged with genomic and proteomic development that led to brain ischemia to a new level of post-ischemic neuropathological mechanisms, such as the presence of amyloid plaques and the development of neurofibrillary tangles, which further exacerbate oxidative stress. Finally, we hypothesize that modified amyloid and the tau protein, along with the oxidative stress generated, are new key elements in the vicious circle important in the development of post-ischemic neurodegeneration in a type of Alzheimer’s disease proteinopathy.
Highlights
The human brain accounts for only 2% of the total body weight, uses about 20% of the oxygen supplied to the whole body [1,2] and produces more free radicals than other organs of the body [2,3]
The following is the amyloidogenic processing of the postischemic amyloid protein precursor that is associated with the production and deposition of amyloid in the brain following ischemia [67,68,69]
The imbalance between pro-oxidative and antioxidant cellular molecules leads to a vicious cycle where free radical oxidative stress causes oxidation of DNA, lipids and proteins in neurons and their death after ischemia
Summary
The human brain accounts for only 2% of the total body weight, uses about 20% of the oxygen supplied to the whole body [1,2] and produces more free radicals than other organs of the body [2,3]. Elastin-derived polypeptides have been reported to induce overproduction of β-amyloid peptides in a model of Alzheimer’s disease [20,21,22] Among these various neuropathological phenomena, free radical changes in brain tissue play an important role in the process of ischemic brain damage during recovery of blood flow at the primary ischemic focus. Oxidative stress is a common and key factor in post-ischemic brain injury during recirculation It consists of an increased generation of reactive oxygen species and reactive nitrogen species that damage various components of the cell such as DNA, lipids and proteins [29]. In this review we will discuss the hypothesis that modified amyloid with tau protein hyperphosphorylation and oxidative stress are new key elements in the vicious cycle important in post-ischemic neurodegeneration with Alzheimer’s disease-type proteinopathy. We will focus on the role of two main factors, such as amyloid and tau protein, which trigger oxidative stress in post-ischemic reperfusion injury in the vicious cycle
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