Amyloid pathology in the brain after ischemia

Abstract

As the population is aging all over the world, the economic burden of ischemic brain injuries is constantly increasing. Human brain ischemia is one of the leading causes of premature death, significant morbidity and physical and mental disabilities, resulting in a lower quality of life and unusually high costs of health and social care. One of the most difficult problems associated with the pathology of the brain after ischemia is progressive dementia observed in people who survived the stroke. More recently, brain ischemia has been shown to elicit Alzheimer's disease neuropathologic change, possibly facilitating the development of dementia due to the amyloidogenic processing of Alzheimer's disease-related amyloid protein precursor into amyloid. The main purpose of this review is to present the development of Alzheimer's disease neuropathologic change in the brain after human and experimental ischemia, with a particular emphasis on proteins and genes involved in the amyloidogenic processing of the amyloid protein precursor to amyloid.

Keywords: amyloid; amyloid protein precursor; cognitive decline; dementia; gene; ischemic stroke; presenilin 1; presenilin 2; protein; β-secretase; brain ischemia.