Stroke remains the leading cause of long-term disability worldwide with a widespread dysfunction in sensorimotor function, speaking, cognition, swallowing, etc. Stroke does not only cause neuron loss but also impairs the structural and functional integrity of entire brain networks. Rehabilitative therapies are recognized as the cornerstone of functional recovery in stroke which is focused on neuroplastic regulation to rebuild and normalize the stroke-disrupted neural networks and circuits. Spontaneous neuroplasticity occurs within hours of stroke insult and reaches a plateau by three to four weeks within the global brain in animal studies.
Residential microglia and infiltrated macrophages in the brain serve as the first line of defense after stroke and play diverse roles in the pathophysiological process of stroke. They are highly plastic cells and constantly exhibit different activation profiles based on the response to microenvironmental changes. Microglia and infiltrated macrophages initially activate towards an anti-inflammatory state after stroke, but gradually transform into a detrimental pro-inflammatory state. Microglial reactivity has been found at both proximal and remote brain regions to the primary ischemic injury. Microglial reactivity coincides with neuroplasticity after stroke, providing the fundamental base for the microglia-mediated neuroinflammation involved in the entire neural network rewiring and brain repair. Convincing evidence shows that microglia are emerging as key players in brain plasticity after stroke. Anti-inflammatory microglia have shown beneficial effects in synaptic plasticity, neurogenesis, axonal regeneration, dendritic branching, angiogenesis, vascular repair, and interhemispheric connections following stroke. The fact that microglia modulate global neuroinflammation and impact neuroplasticity after stroke makes this special glial cell population an attractive candidate for targeting stroke recovery. However, many open issues remain to be answered.
In this Research Topic, we would like to invite investigators to contribute original research articles and review articles that covers a topic regarding modulating microglia to enhance neuroplasticity for restoring brain function after stroke. Relevant topics include, but are not limited to, the following:
- Cellular and molecular mechanisms of microglial regulation including microglial reactivity or pyroptosis after stroke.
- Switching microglia by manipulating intracellular specific genes and/or surface receptors to favorable reactivity profile and coordinate them in the chronic phase definitely improve the neuroplastic recovery following stroke.
- Understanding of microglial reactivity with different spatiotemporal manners in distinct animal models and human brains.
- New techniques distinguishing microglia and macrophages. Peripheral monocytes/macrophages infiltrate into the injured brain and exhibit various phenotypes, distinct activation roles.
- The role of crosstalk between microglia and peripheral immune cells in the neuroplastic recovery following stroke.
- The role and mechanisms of microglia-mediated neuroinflammation in synaptic plasticity, neurogenesis, axonal regeneration, and so on.
- Impacts of microglial regulation following a stroke on the rewiring of neural networks and circuits, remyelination, neurogenesis, angiogenesis, dendritic spine generation, synaptic plasticity, axonal regeneration, interhemispheric connections, etc.
- Relationship between stroke recovery induced by rehabilitative interventions such as pharmacological therapy, cell therapy, non-invasive brain stimulation, physical exercise, etc and microglial functions (reactivity, pyroptosis, phagocytosis, etc).
Stroke remains the leading cause of long-term disability worldwide with a widespread dysfunction in sensorimotor function, speaking, cognition, swallowing, etc. Stroke does not only cause neuron loss but also impairs the structural and functional integrity of entire brain networks. Rehabilitative therapies are recognized as the cornerstone of functional recovery in stroke which is focused on neuroplastic regulation to rebuild and normalize the stroke-disrupted neural networks and circuits. Spontaneous neuroplasticity occurs within hours of stroke insult and reaches a plateau by three to four weeks within the global brain in animal studies.
Residential microglia and infiltrated macrophages in the brain serve as the first line of defense after stroke and play diverse roles in the pathophysiological process of stroke. They are highly plastic cells and constantly exhibit different activation profiles based on the response to microenvironmental changes. Microglia and infiltrated macrophages initially activate towards an anti-inflammatory state after stroke, but gradually transform into a detrimental pro-inflammatory state. Microglial reactivity has been found at both proximal and remote brain regions to the primary ischemic injury. Microglial reactivity coincides with neuroplasticity after stroke, providing the fundamental base for the microglia-mediated neuroinflammation involved in the entire neural network rewiring and brain repair. Convincing evidence shows that microglia are emerging as key players in brain plasticity after stroke. Anti-inflammatory microglia have shown beneficial effects in synaptic plasticity, neurogenesis, axonal regeneration, dendritic branching, angiogenesis, vascular repair, and interhemispheric connections following stroke. The fact that microglia modulate global neuroinflammation and impact neuroplasticity after stroke makes this special glial cell population an attractive candidate for targeting stroke recovery. However, many open issues remain to be answered.
In this Research Topic, we would like to invite investigators to contribute original research articles and review articles that covers a topic regarding modulating microglia to enhance neuroplasticity for restoring brain function after stroke. Relevant topics include, but are not limited to, the following:
- Cellular and molecular mechanisms of microglial regulation including microglial reactivity or pyroptosis after stroke.
- Switching microglia by manipulating intracellular specific genes and/or surface receptors to favorable reactivity profile and coordinate them in the chronic phase definitely improve the neuroplastic recovery following stroke.
- Understanding of microglial reactivity with different spatiotemporal manners in distinct animal models and human brains.
- New techniques distinguishing microglia and macrophages. Peripheral monocytes/macrophages infiltrate into the injured brain and exhibit various phenotypes, distinct activation roles.
- The role of crosstalk between microglia and peripheral immune cells in the neuroplastic recovery following stroke.
- The role and mechanisms of microglia-mediated neuroinflammation in synaptic plasticity, neurogenesis, axonal regeneration, and so on.
- Impacts of microglial regulation following a stroke on the rewiring of neural networks and circuits, remyelination, neurogenesis, angiogenesis, dendritic spine generation, synaptic plasticity, axonal regeneration, interhemispheric connections, etc.
- Relationship between stroke recovery induced by rehabilitative interventions such as pharmacological therapy, cell therapy, non-invasive brain stimulation, physical exercise, etc and microglial functions (reactivity, pyroptosis, phagocytosis, etc).
