Damages to the nervous system caused by traumas or the pathogenesis of neurodegenerative diseases often lead to permanent loss of axonal connection and functional impairments. The central nervous system (CNS) neurons are susceptible to neuronal cell death, and the survived neurons failed to regenerate beyond the lesion due to limited intrinsic growth capacity. Growth-inhibitory substrates around the CNS lesion are also a major obstacle for successful axon regeneration. Prolonged glial activation often resulted in secondary damages to neuronal tissues. Unlike CNS neurons, peripheral neurons are capable of axon regeneration. However, some patients with proximal peripheral nerve injuries or peripheral neuropathy still exhibited persistent functional deficits largely due to incomplete nerve repair or regeneration failure. There are only limited treatment options for nerve repair, in which most of them remained largely ineffective. Therefore, there is an urgent need to develop novel therapies for patients to promote nerve repair and functional restoration.
Identifying molecular targets that facilitate axon regeneration is fundamental to developing highly effective therapies for nerve repairs and functional restoration. Apart from the detrimental effects, some recent studies pinpointed that activated glial cells contributed to the clearance of growth-inhibitory myelin debris and production of neurotrophic factors, highlighting the importance of controlled glial activation after CNS traumas. Moreover, manipulations of the intrinsic regenerative ability of adult neurons demonstrated a promising approach to promote nerve repair and functional restoration. For instance, overexpression of a regeneration-associated gene promoted the growth capability of injured neurons and improved functional restoration after severe peripheral nerve injuries and various types of peripheral neuropathies. Removal of intrinsic growth barriers from adult CNS neurons enabled long-distance axon regeneration which reinnervated their original visual targets in the brain after injuries. The availability of new bioinformatic tools offers an opportunity to facilitate the discovery of universal molecular targets (protein-coding genes, long non-coding RNAs, epigenetic modifiers, etc.) which enabled drug screening programs to manipulate these newly identified targets for functional restoration. Therefore, the goals of this Research Topic are to gather our current understandings of the molecular mechanisms underlying regeneration failure after nerve damages and to develop novel therapeutic approaches to restore neurological functions.
We strongly encourage investigators to contribute Original Research or Review articles focusing on, but not limited to, the following:
• Functional characterization of new molecular targets (protein-coding genes, long non-coding RNAs, epigenetic modifiers, etc.) or bioactive compounds that modulate the immune response, or promote axon regeneration and functional restoration after neurotrauma and neurodegenerative diseases
• Understanding the mechanisms and signaling pathways underlying neuroinflammation, neuronal cell death, regeneration failure or/and functional restoration in various forms of neurotrauma and neurodegenerative diseases
•Development of novel therapeutic approaches which targeted to modulate neuroinflammation and promote axon regeneration for functional restoration
• Investigation of new and innovative therapeutic interventions that aim to target functional deficits or promote neurorestoration following neurotrauma
Damages to the nervous system caused by traumas or the pathogenesis of neurodegenerative diseases often lead to permanent loss of axonal connection and functional impairments. The central nervous system (CNS) neurons are susceptible to neuronal cell death, and the survived neurons failed to regenerate beyond the lesion due to limited intrinsic growth capacity. Growth-inhibitory substrates around the CNS lesion are also a major obstacle for successful axon regeneration. Prolonged glial activation often resulted in secondary damages to neuronal tissues. Unlike CNS neurons, peripheral neurons are capable of axon regeneration. However, some patients with proximal peripheral nerve injuries or peripheral neuropathy still exhibited persistent functional deficits largely due to incomplete nerve repair or regeneration failure. There are only limited treatment options for nerve repair, in which most of them remained largely ineffective. Therefore, there is an urgent need to develop novel therapies for patients to promote nerve repair and functional restoration.
Identifying molecular targets that facilitate axon regeneration is fundamental to developing highly effective therapies for nerve repairs and functional restoration. Apart from the detrimental effects, some recent studies pinpointed that activated glial cells contributed to the clearance of growth-inhibitory myelin debris and production of neurotrophic factors, highlighting the importance of controlled glial activation after CNS traumas. Moreover, manipulations of the intrinsic regenerative ability of adult neurons demonstrated a promising approach to promote nerve repair and functional restoration. For instance, overexpression of a regeneration-associated gene promoted the growth capability of injured neurons and improved functional restoration after severe peripheral nerve injuries and various types of peripheral neuropathies. Removal of intrinsic growth barriers from adult CNS neurons enabled long-distance axon regeneration which reinnervated their original visual targets in the brain after injuries. The availability of new bioinformatic tools offers an opportunity to facilitate the discovery of universal molecular targets (protein-coding genes, long non-coding RNAs, epigenetic modifiers, etc.) which enabled drug screening programs to manipulate these newly identified targets for functional restoration. Therefore, the goals of this Research Topic are to gather our current understandings of the molecular mechanisms underlying regeneration failure after nerve damages and to develop novel therapeutic approaches to restore neurological functions.
We strongly encourage investigators to contribute Original Research or Review articles focusing on, but not limited to, the following:
• Functional characterization of new molecular targets (protein-coding genes, long non-coding RNAs, epigenetic modifiers, etc.) or bioactive compounds that modulate the immune response, or promote axon regeneration and functional restoration after neurotrauma and neurodegenerative diseases
• Understanding the mechanisms and signaling pathways underlying neuroinflammation, neuronal cell death, regeneration failure or/and functional restoration in various forms of neurotrauma and neurodegenerative diseases
•Development of novel therapeutic approaches which targeted to modulate neuroinflammation and promote axon regeneration for functional restoration
• Investigation of new and innovative therapeutic interventions that aim to target functional deficits or promote neurorestoration following neurotrauma
