Stroke is the leading cause of disability worldwide. Ageing is not only an independent risk for stroke, but it also complicates stroke recovery. After the acute phase of stroke, “spontaneous neural repair" commences, which is the basis for the recovery of neurological function after stroke. There exists a relatively “sensitive period” for this spontaneous process, which is characterized by heightened neural plasticity. During this period, a series of changes occurred, including genes, molecules, cells, cell-to-cell communications and cortical remapping, etc., thus realizing the reconstruction of brain tissue and neurophysiological functions, and finally promoting the recovery of neural function. This period also provides a much wider time window than the acute period of revascularization therapy. However, the ability of “spontaneous neural repair” to restore the damaged brain is limited and even worse, this ability may also be limited by ageing. This leaves us with an important question, that is, how to make use of this sensitive period to break the limit and promote the recovery of the brain after stroke. The intrinsic mechanism of “spontaneous neural repair”, the reasons for the high sensitivity during this critical period and ageing-induced repair inhibition are of great value. As the current treatments aimed at promoting neurological recovery during this period have not shown sufficient effects, we need to refocus on this period and deeply analyze the unraveled cellular and molecular targets responsible for “spontaneous neural repair”, which requires an integrated understanding of various cells including neural stem cells (NSCs), neurons, astrocytes, microglia, oligodendrocytes, endothelial cells, pericytes, etc., to carry out morphological and functional remodeling. In the repair of brain tissue injury, changes similar to the brain development process occur, such as axon regeneration, neurogenesis, angiogenesis, blood-brain barrier repair, synaptogenesis and remodeling, myelin formation and so on. Ageing may intervene with these processes. Recent advances in the role of neurons, microglia, reactive astrocytes, T regulatory cells (Treg) and oligodendrocytes have further emphasized the significance of neural repair after stroke.
In order to unravel more feasible and potential translational targets, we organize this special topic to inspire more excellent work on the exploration of key molecule responsible for the “spontaneous neural repair”, specifically during the high sensitivity period and ageing-induced loss of neural repair. We hope that this will encourage an in-depth discussion of post-stroke neural repair, and those with potential translational significance will be greatly valued.
We cordially welcome submissions of Original Research and Review Articles on the following themes:
• Molecular mechanisms of high sensitivity in the critical period of stroke recovery
• Ageing-Induced loss of abilities of neural repair after ischemic stroke
• Strategies targeting for promoting recovery and neural repair after ischemic stroke
Stroke is the leading cause of disability worldwide. Ageing is not only an independent risk for stroke, but it also complicates stroke recovery. After the acute phase of stroke, “spontaneous neural repair" commences, which is the basis for the recovery of neurological function after stroke. There exists a relatively “sensitive period” for this spontaneous process, which is characterized by heightened neural plasticity. During this period, a series of changes occurred, including genes, molecules, cells, cell-to-cell communications and cortical remapping, etc., thus realizing the reconstruction of brain tissue and neurophysiological functions, and finally promoting the recovery of neural function. This period also provides a much wider time window than the acute period of revascularization therapy. However, the ability of “spontaneous neural repair” to restore the damaged brain is limited and even worse, this ability may also be limited by ageing. This leaves us with an important question, that is, how to make use of this sensitive period to break the limit and promote the recovery of the brain after stroke. The intrinsic mechanism of “spontaneous neural repair”, the reasons for the high sensitivity during this critical period and ageing-induced repair inhibition are of great value. As the current treatments aimed at promoting neurological recovery during this period have not shown sufficient effects, we need to refocus on this period and deeply analyze the unraveled cellular and molecular targets responsible for “spontaneous neural repair”, which requires an integrated understanding of various cells including neural stem cells (NSCs), neurons, astrocytes, microglia, oligodendrocytes, endothelial cells, pericytes, etc., to carry out morphological and functional remodeling. In the repair of brain tissue injury, changes similar to the brain development process occur, such as axon regeneration, neurogenesis, angiogenesis, blood-brain barrier repair, synaptogenesis and remodeling, myelin formation and so on. Ageing may intervene with these processes. Recent advances in the role of neurons, microglia, reactive astrocytes, T regulatory cells (Treg) and oligodendrocytes have further emphasized the significance of neural repair after stroke.
In order to unravel more feasible and potential translational targets, we organize this special topic to inspire more excellent work on the exploration of key molecule responsible for the “spontaneous neural repair”, specifically during the high sensitivity period and ageing-induced loss of neural repair. We hope that this will encourage an in-depth discussion of post-stroke neural repair, and those with potential translational significance will be greatly valued.
We cordially welcome submissions of Original Research and Review Articles on the following themes:
• Molecular mechanisms of high sensitivity in the critical period of stroke recovery
• Ageing-Induced loss of abilities of neural repair after ischemic stroke
• Strategies targeting for promoting recovery and neural repair after ischemic stroke