Multiple sclerosis (MS) is a chronic, progressive, inflammatory, and neurodegenerative disease with an unknown primary aetiology, which affects an estimated 2.3 to 2.5 million people worldwide. Evidence thus far indicates the disease is the result of a combination of genetic, environmental and lifestyle factors. While the processes that drive the disease progression have been, to some extent, identified and characterized, many unanswered questions remain such as how to promote functional myelin repair? What are the specific neuroprotective and neuroregenerative mechanisms that we can exploit? This Research Topic will focus on the molecular mechanisms and potential drug targets for remyelination and neuroregeneration in MS and other demyelinating and neurodegenerative pathologies.
Recent years have seen the advent of disease-modifying therapies (DMTs), especially for the relapsing-remitting form of MS. There are currently 23 FDA-approved DMTs available on the market. Even though these new DMTs have significantly extended and improved the quality of life of MS patients, they carry serious and possibly lethal side effects. Moreover, the licenced DMTs act mainly on the peripheral immune system, either by reducing neuroinflammatory signalling or by limiting peripheral lymphocyte infiltration into the CNS, while having a very limited secondary effect on neuroregeneration or remyelination. Importantly, the loss of brain matter starts right from the beginning of the disease onset and continues to progress at equal rates and irrespective of MS subtype. Therefore, it is tremendously important to identify druggable targets that can protect from neurodegeneration or stimulate neuroregeneration and/or remyelination.
The aim of this Research Topic is to feature a collection of articles on molecular mechanisms of remyelination and/or neuroregeneration and potential drug targets for new remyelinating and/or neuroregenerative therapies. The topics of interest are (but not limited to):
- Molecular mechanisms of formation of new myelin sheath
- Activation, migration, recruitment, proliferation, differentiation, and viability of oligodendrocyte progenitor cells and/or adult oligodendrocytes
- Protection of the function and/or integrity of neurons/axons
- Protection against the destruction of myelin
- Reduced oxidative stress, apoptosis, and cellular dysfunction in the central nervous system
- Modulation of neurotrophins and growth factors in the central nervous system
- Increased formation of new myelin
- Improved neurological function
- Modulation of inflammatory mediators in the central nervous system
- Microglial and/or astrocyte activation
- Disruption and permeability of the blood-brain barrier
- Blood, cerebrospinal fluid or imaging markers of remyelination and/or regeneration
- Imaging techniques of remyelination and/or regeneration
Multiple sclerosis (MS) is a chronic, progressive, inflammatory, and neurodegenerative disease with an unknown primary aetiology, which affects an estimated 2.3 to 2.5 million people worldwide. Evidence thus far indicates the disease is the result of a combination of genetic, environmental and lifestyle factors. While the processes that drive the disease progression have been, to some extent, identified and characterized, many unanswered questions remain such as how to promote functional myelin repair? What are the specific neuroprotective and neuroregenerative mechanisms that we can exploit? This Research Topic will focus on the molecular mechanisms and potential drug targets for remyelination and neuroregeneration in MS and other demyelinating and neurodegenerative pathologies.
Recent years have seen the advent of disease-modifying therapies (DMTs), especially for the relapsing-remitting form of MS. There are currently 23 FDA-approved DMTs available on the market. Even though these new DMTs have significantly extended and improved the quality of life of MS patients, they carry serious and possibly lethal side effects. Moreover, the licenced DMTs act mainly on the peripheral immune system, either by reducing neuroinflammatory signalling or by limiting peripheral lymphocyte infiltration into the CNS, while having a very limited secondary effect on neuroregeneration or remyelination. Importantly, the loss of brain matter starts right from the beginning of the disease onset and continues to progress at equal rates and irrespective of MS subtype. Therefore, it is tremendously important to identify druggable targets that can protect from neurodegeneration or stimulate neuroregeneration and/or remyelination.
The aim of this Research Topic is to feature a collection of articles on molecular mechanisms of remyelination and/or neuroregeneration and potential drug targets for new remyelinating and/or neuroregenerative therapies. The topics of interest are (but not limited to):
- Molecular mechanisms of formation of new myelin sheath
- Activation, migration, recruitment, proliferation, differentiation, and viability of oligodendrocyte progenitor cells and/or adult oligodendrocytes
- Protection of the function and/or integrity of neurons/axons
- Protection against the destruction of myelin
- Reduced oxidative stress, apoptosis, and cellular dysfunction in the central nervous system
- Modulation of neurotrophins and growth factors in the central nervous system
- Increased formation of new myelin
- Improved neurological function
- Modulation of inflammatory mediators in the central nervous system
- Microglial and/or astrocyte activation
- Disruption and permeability of the blood-brain barrier
- Blood, cerebrospinal fluid or imaging markers of remyelination and/or regeneration
- Imaging techniques of remyelination and/or regeneration
