Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). It affects 2.5 million people worldwide and is a leading cause of non-traumatic disability in young people. Two of every three MS patients are female with an average disease onset age around 30-years-old. Twenty years after their onset, 60% of patients will be unable to walk, representing a burden for families, patients, society and healthcare systems. Most people with MS have a relapsing-remitting disease course. They experience periods of new relapses that develop over days or weeks. These relapses are followed by quiet periods of disease remission. About 60-70 percent of people with relapsing-remitting MS eventually develop a steady progression of symptoms, with or without periods of remission, known as secondary-progressive MS. Some people with MS experience a primary-progressive form where the disease progresses without any remission or relapse phase. However new subtypes of MS are now being recognized.
In terms of disease mechanisms, it is known that the patients’ immune system starts to attack its own CNS. Once the peripheral immune cells get to the CNS, they attack a neuronal structure called myelin. This attack is further potentiated by local glial cells that reside in CNS tissues. This demyelination leads ultimately to neurodegeneration and neuronal death, resulting in permanent loss of neurological functions including walking, bladder control, and cognition. There is no cure for MS and available treatments only slow down the initial phases of the disease. This is partially due to the fact that later-disease mechanisms are poorly understood and do not directly correlate with the activity of immune system cells (the targets of available treatments). Rather, some evidence suggests that disease progression is better correlated with the maintenance of a low-grade persistent inflammation inside the CNS, driven by local glial cells (astrocytes and microglia). In addition, being a demyelinating disease, the role of oligodendrocytes is of utmost relevance for the disease mechanism. In addition to the possible role of some mature oligodendrocytes in remyelination, both mature and oligodendrocytes precursor cells were recently shown to be active immunomodulators in MS.
To move forward, an understanding of novel basic cellular disease mechanisms is needed in order to pave the way for the discovery of new diagnostic and prognostic disease biomarkers and of new possible treatments. In this Research Topic we aim to bring together all this knowledge through the publication of Original Research, Review and Opinion articles and Methods covering recent advances in our understanding of the MS pathology focused on aspects of (i) immune system (innate, humoral and adaptive) and of (ii) CNS cells.
Specifically, we aim to receive contributions that will bring new data in the following topics:
- Role of specific immune mediators in MS;
- Clarification of the role of monocytes/macrophages, NK cells and dendritic cells in MS;
- New insights regarding the role of B and T cells in MS;
- Role of microglia, astrocytes, and oligodendrocytes in MS;
- Novel pathways/mediators involved in brain inflammation and neurodegeneration with a potential role in MS
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). It affects 2.5 million people worldwide and is a leading cause of non-traumatic disability in young people. Two of every three MS patients are female with an average disease onset age around 30-years-old. Twenty years after their onset, 60% of patients will be unable to walk, representing a burden for families, patients, society and healthcare systems. Most people with MS have a relapsing-remitting disease course. They experience periods of new relapses that develop over days or weeks. These relapses are followed by quiet periods of disease remission. About 60-70 percent of people with relapsing-remitting MS eventually develop a steady progression of symptoms, with or without periods of remission, known as secondary-progressive MS. Some people with MS experience a primary-progressive form where the disease progresses without any remission or relapse phase. However new subtypes of MS are now being recognized.
In terms of disease mechanisms, it is known that the patients’ immune system starts to attack its own CNS. Once the peripheral immune cells get to the CNS, they attack a neuronal structure called myelin. This attack is further potentiated by local glial cells that reside in CNS tissues. This demyelination leads ultimately to neurodegeneration and neuronal death, resulting in permanent loss of neurological functions including walking, bladder control, and cognition. There is no cure for MS and available treatments only slow down the initial phases of the disease. This is partially due to the fact that later-disease mechanisms are poorly understood and do not directly correlate with the activity of immune system cells (the targets of available treatments). Rather, some evidence suggests that disease progression is better correlated with the maintenance of a low-grade persistent inflammation inside the CNS, driven by local glial cells (astrocytes and microglia). In addition, being a demyelinating disease, the role of oligodendrocytes is of utmost relevance for the disease mechanism. In addition to the possible role of some mature oligodendrocytes in remyelination, both mature and oligodendrocytes precursor cells were recently shown to be active immunomodulators in MS.
To move forward, an understanding of novel basic cellular disease mechanisms is needed in order to pave the way for the discovery of new diagnostic and prognostic disease biomarkers and of new possible treatments. In this Research Topic we aim to bring together all this knowledge through the publication of Original Research, Review and Opinion articles and Methods covering recent advances in our understanding of the MS pathology focused on aspects of (i) immune system (innate, humoral and adaptive) and of (ii) CNS cells.
Specifically, we aim to receive contributions that will bring new data in the following topics:
- Role of specific immune mediators in MS;
- Clarification of the role of monocytes/macrophages, NK cells and dendritic cells in MS;
- New insights regarding the role of B and T cells in MS;
- Role of microglia, astrocytes, and oligodendrocytes in MS;
- Novel pathways/mediators involved in brain inflammation and neurodegeneration with a potential role in MS
