A stroke can occur when blood flow to a specific area of the brain is interrupted. There has been extensive research in both animal models and humans that has characterized the pathophysiology of the first few weeks following stroke. However, there has been far less research into the chronic stage of infarction. This is an important area for research because more than 10 million individuals worldwide suffer a stroke each year. Approximately one-third of these survivors develop dementia in the first year after their stroke. The cause behind this dementia is currently unclear, and there are no neuro-protective drugs that can improve recovery and provide cognitive protection in the chronic time period. Therefore, the chronic stage of stroke recovery is a promising target for future therapeutics for stroke-related dementia and, as will be shown later in the paper, Alzheimer’s disease as there are likely to be neurodegenerative processes that proceed for months following stroke. The goal of this thesis is to provide a review of what is currently known about the pathophysiology of chronic stroke infarcts (an area of brain tissue that has necrotized due to a blockage in an artery in the brain causing a lack of oxygen), explain why so little is known, and how we can learn more, and provide potential mechanistic links between the response to dead brain tissue and the development of dementia.
|Commitee:||Elliott, David, Lybarger, Lonnie|
|School:||The University of Arizona|
|Department:||Cellular and Molecular Medicine|
|School Location:||United States -- Arizona|
|Source:||MAI 57/05M(E), Masters Abstracts International|
|Subjects:||Medicine, Health sciences, Immunology|
|Keywords:||Alzheimer's disease, Chronic, Ide, Insulin degrading enzyme, Liquefactive necrosis, Stroke|
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