About this Research Topic
In the past several years, multiple sclerosis (MS) research has achieved significant progress in identifying novel disease mechanisms, diagnostic markers and therapeutic targets. This has facilitated more accurate and early diagnosis, monitoring the disease course and effective clinical management, thus preventing or delaying disease progression. The concept of NEDA-3 (no evidence of disease activity: no relapses, no disability, no MRI activity) seems nowadays realistic for a significant proportion of the patients on immune therapies. Further definitions of the NEDA (from NEDA-4 which also considers the brain volume loss up to NEDA-6 which also takes into account cognitive changes) are being developed to optimize MS research. “Hit hard and early” or “hit smart and early” are common concepts which are often discussed as early treatment strategies.
Although the efficacy of currently available disease modifying therapies is indisputable, their
effectiveness on both neurodegeneration and neural repair is far from satisfactory. While MS symptoms can be treated, there are minimal treatment strategies to revert neurological disability or to effectively prevent gradual accumulation of disabilities. In this context, one of the main unmet needs is a better understanding of both the mechanisms driving progressive tissue loss, and the neuroplastic processes that attempt to compensate for the functional and structural tissue damage. Several studies have explored the pathways that regulate recovery from relapses and the processes that might be responsible for reverting disability progression. Investigating pharmacological and non-pharmacological interventions that facilitate remyelination and brain reorganization has resulted in several promising approaches.
While neuroplasticity can be described as a general term addressing the ability of the nervous system to adapt and modify both its structure and function in response to stimuli and experience, in this
topic we would like to focus on the neuroplasticity of the central nervous system (CNS) in patients with MS and animal models of MS. We are particularly interested which molecular mechanisms determine clinical improvement after CNS demyelination; how the potential of the respective neuroplasticity processes can be measured – in both clinical and imaging/laboratory terms; which molecules or processes might serve as protective factors against demyelination or facilitate more efficient recovery; and last but not least whether immune therapies differ in their remyelination potential and how it can be maximized. We welcome various approaches and different types of articles – both original and reviews – which would broaden our understanding of this important process in MS. Channeling these efforts and their findings into a research topic would give a global
overview of the different methods, approaches and fields which are active in the study of neuroplasticity in MS.
Although the efficacy of currently available disease modifying therapies is indisputable, their
effectiveness on both neurodegeneration and neural repair is far from satisfactory. While MS symptoms can be treated, there are minimal treatment strategies to revert neurological disability or to effectively prevent gradual accumulation of disabilities. In this context, one of the main unmet needs is a better understanding of both the mechanisms driving progressive tissue loss, and the neuroplastic processes that attempt to compensate for the functional and structural tissue damage. Several studies have explored the pathways that regulate recovery from relapses and the processes that might be responsible for reverting disability progression. Investigating pharmacological and non-pharmacological interventions that facilitate remyelination and brain reorganization has resulted in several promising approaches.
While neuroplasticity can be described as a general term addressing the ability of the nervous system to adapt and modify both its structure and function in response to stimuli and experience, in this
topic we would like to focus on the neuroplasticity of the central nervous system (CNS) in patients with MS and animal models of MS. We are particularly interested which molecular mechanisms determine clinical improvement after CNS demyelination; how the potential of the respective neuroplasticity processes can be measured – in both clinical and imaging/laboratory terms; which molecules or processes might serve as protective factors against demyelination or facilitate more efficient recovery; and last but not least whether immune therapies differ in their remyelination potential and how it can be maximized. We welcome various approaches and different types of articles – both original and reviews – which would broaden our understanding of this important process in MS. Channeling these efforts and their findings into a research topic would give a global
overview of the different methods, approaches and fields which are active in the study of neuroplasticity in MS.
Keywords: Multiple Sclerosis, Neuroplasticity, Neuroprotection, Neuroregeneration, Remyelination, BDNF, Clemastine, Disability Improvement, Reorganization, Neural Repair
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