Cellular and molecular interactions involved in neuroinflammation. Potential targets for improved patient outcome.
The most common form of stroke is actue ischemic stroke (aproximately 85% of cases), which is caused by either an atherothrombosis in a major cervical or intracranial artery or an embolism that travels from the heart. The resulting occlusion causes a sudden deficiency of oxygen and glucose in the brain region normally serviced by the blocked artery. Stroke suffers experience a range of neurological deficits including partial paralysis, impaired memory, loss of speech, and/or decreased cognition.
This eBook is an overview of the cellular and molecular interactions involved in neuroinflammation following acute ischemic stroke:
Overview of preclinical models and their utility
Current therapies and therapeutic windows
Cell types involved in post-stroke inflammation
The complex interplay between resident and invading cells and their bioactive effector signaling molecules that initially damage and later protect and repair brain tissue offers many opportunities for pharmacological intervention.
Excerpt from the eBook:
"Over 1,000 other potential stroke therapeutics have been tested in animals and approximately one tenth of these have made it to clinical trials. However, the majority of these efforts have already failed. It is likely that the most effective way to improve outcomes is rapid reperfusion of the ischemic area using thrombolytic means in combination with neuroprotective strategies to salvage cells within the penumbra and prevent them from becoming part of the ischemic core. To this end, researchers have been increasingly focused on post-stroke neuroinflammation and the role it plays in neurotoxicity and neuroprotection."