Multiple sclerosis (MS) is a chronic inflammatory, demyelinating disease of the central nervous system (CNS). Although MS affects mostly the CNS myelinating cells, oligodendrocytes (OLs), other features of neurodegeneration (neuronal atrophy, neuronal death and axonal transection) already occur at early stages of the disease. To compensate the damage and recover the clinical symptoms, the endogenous multipotent neural stem cells (NSCs) are able to self-renew, migrate and differentiate into neurons or glial cells. Although NSCs are profuse at developmental stages, they become more restricted in numbers and locations in the adult CNS. In view of their differentiation plasticity and renewal ability, the presence of these endogenous NSCs of the adult CNS (aNSC) is crucial for CNS repair in MS and many other neurodegenerative disorders. However, despite aNSC relevant contribution to brain homeostasis and its exciting therapeutic potential, their activation and potentiation of this process in pathophysiological conditions remain largely underestimated.
In the adult brain, NSC generation arise at two restricted and specialized niches: the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the hippocampus, and the spinal cord ependyma. In physiological conditions, aNSCs from the SVZ divide and generate proliferating progenitors, which later give rise to neuroblasts and oligodendrocyte progenitor cells (OPCs), which in pathophysiological conditions, contribute to the repair process . However, their efficiency in repairing damages remains limited to nearby lesions. Despite the recent advances in understanding the signals that stimulate the activity of aNSCs, currently there is no effective treatment to restore the lack of myelin and regeneration, and therefore to ameliorate the clinical course of patients affected by neurodegenerative/ demyelinating disorders. Better knowledge of the signals that activate and promote the activity of endogenous aNSC might be beneficial for the repair of lesions in a broad spectrum of neurodegenerative diseases associated with myelin loss such as MS.
To provide a more comprehensive overview of the role of CNS endogenous aNSC in MS and other neurodegenerative diseases, we invite any type of contribution (original research manuscripts, reviews, perspectives), about related research topics including but not limited to the following: (1) Cellular and molecular mechanisms of aNSCs-inflammatory factors crosstalk in the pathology of MS and other neurodegenerative disorders. (2) Transcriptional and proteasomal profile of aNSCs during the pathogenesis of MS and other neurodegenerative diseases. (3) Novel therapeutic treatment targeting aNSCs and potentiated them in MS and other neurodegenerative disorders (4) Contributions from all research areas, including disease modelling, human neuropathology, biochemical, molecular, genomics, proteomics or therapeutic interventions are welcome. We hope that interested investigators will share their valuable research on this research topic to exploit the potential of ESCs regulation in the future therapy of neurodegenerative diseases.
Multiple sclerosis (MS) is a chronic inflammatory, demyelinating disease of the central nervous system (CNS). Although MS affects mostly the CNS myelinating cells, oligodendrocytes (OLs), other features of neurodegeneration (neuronal atrophy, neuronal death and axonal transection) already occur at early stages of the disease. To compensate the damage and recover the clinical symptoms, the endogenous multipotent neural stem cells (NSCs) are able to self-renew, migrate and differentiate into neurons or glial cells. Although NSCs are profuse at developmental stages, they become more restricted in numbers and locations in the adult CNS. In view of their differentiation plasticity and renewal ability, the presence of these endogenous NSCs of the adult CNS (aNSC) is crucial for CNS repair in MS and many other neurodegenerative disorders. However, despite aNSC relevant contribution to brain homeostasis and its exciting therapeutic potential, their activation and potentiation of this process in pathophysiological conditions remain largely underestimated.
In the adult brain, NSC generation arise at two restricted and specialized niches: the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the hippocampus, and the spinal cord ependyma. In physiological conditions, aNSCs from the SVZ divide and generate proliferating progenitors, which later give rise to neuroblasts and oligodendrocyte progenitor cells (OPCs), which in pathophysiological conditions, contribute to the repair process . However, their efficiency in repairing damages remains limited to nearby lesions. Despite the recent advances in understanding the signals that stimulate the activity of aNSCs, currently there is no effective treatment to restore the lack of myelin and regeneration, and therefore to ameliorate the clinical course of patients affected by neurodegenerative/ demyelinating disorders. Better knowledge of the signals that activate and promote the activity of endogenous aNSC might be beneficial for the repair of lesions in a broad spectrum of neurodegenerative diseases associated with myelin loss such as MS.
To provide a more comprehensive overview of the role of CNS endogenous aNSC in MS and other neurodegenerative diseases, we invite any type of contribution (original research manuscripts, reviews, perspectives), about related research topics including but not limited to the following: (1) Cellular and molecular mechanisms of aNSCs-inflammatory factors crosstalk in the pathology of MS and other neurodegenerative disorders. (2) Transcriptional and proteasomal profile of aNSCs during the pathogenesis of MS and other neurodegenerative diseases. (3) Novel therapeutic treatment targeting aNSCs and potentiated them in MS and other neurodegenerative disorders (4) Contributions from all research areas, including disease modelling, human neuropathology, biochemical, molecular, genomics, proteomics or therapeutic interventions are welcome. We hope that interested investigators will share their valuable research on this research topic to exploit the potential of ESCs regulation in the future therapy of neurodegenerative diseases.
