Abstract
Only very little is know about the neurovascular niche after cardioembolic stroke. Three processes implicated in neurorepair: angiogenesis, neurogenesis and synaptic plasticity, would be naturally produced in adult brains, but also could be stimulated through endogen neurorepair phenomena. Angiogenesis stimulation generates new vessels with the aim to increase collateral circulation. Neurogenesis is controlled by intrinsic genetic mechanisms and growth factors but also ambiental factors are important. The leading process of the migrating neural progenitor cells (NPCs) is closely associated with blood vessels, suggesting that this interaction provides directional guidance to the NPCs. These findings suggest that blood vessels play an important role as a scaffold for NPCs migration toward the damaged brain region. DNA microarray technology and blood genomic profiling in human stroke provided tools to investigate the expression of thousands of genes. Critical comparison of gene expression profiles after stroke in humans with those in animal models should lead to a better understanding of the pathophysiology of brain ischaemia. Probably the most important part of early recovery after stroke is limited capacity of penumbra/infarct neurones to recover. It became more clear in the last years, that penumbra is not just passively dying over time but it is also actively recovering. This initial plasticity in majority contributes towards later neurogenesis, angiogenesis and final recovery. Penumbra is a principal target in acute phase of stroke. Thus, the origin of newly formed vessels and the pathogenic role of neovascularization and neurogenesis are important unresolved issues in our understanding of the mechanisms after stroke. Biomaterials for promoting brain protection, repair and regeneration are new hot target. Recently developed biomaterials can enable and increase the target delivery of drugs or therapeutic proteins to the brain, allow cell or tissue transplants to be effectively delivered to the brain and help to rebuild damaged circuits. These new approaches are gaining clear importance because nanotechnology allows better control over material-cell interactions that induce specific developmental processes and cellular responses including differentiation, migration and outgrowth.
Highlights
Atrial fibrillation is the most common cardiac arrhythmias, and a major cause of morbidity and mortality due to cardioembolic stroke
There are three mechanisms related with brain plasticity[2, 3]: 1) Brain circuits regulation with the activation of parallel pathways for restore impaired functions; 2) Unmasking of silent functional pathways
Analysis of ischemic brain tissue with techniques which are capable of Current Cardiology Reviews, 2010, Vol 6, No 3 239 studying multiple transcripts simultaneously can identify gene expression changes previously not known to be implicated in ischemic pathophysiology, and evaluation of their physiological significance
Summary
Atrial fibrillation is the most common cardiac arrhythmias, and a major cause of morbidity and mortality due to cardioembolic stroke. The left atrial appendage is the major site of thrombus formation in non-valvular atrial fibrillation. Thrombus formation is multifactorial, and much more than blood flow irregularities are implicated. The three processes implicated in neurorepair (angiogenesis, neurogenesis and synaptic plasticity) would be naturally produced in adult brains and after different pathological situations, and could be stimulated through endogen neurorepair phenomena with different pharmacological treatments, always having in mind that the therapeutical window for neurorepair drugs is more wide than for neuroprotective drugs, being able to treat almost all the stroke patients [4]. Key Mechanisms in Stroke Neurorepair generates new vessels with the aim to increase collateral circulation. Angiogenesis is directly related with neurogenesis since blood supply is necessary for new neuronal survival and development [2, 3]. Studying mechanisms regulating above processes will help to design future strategies in neurorepair
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