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.