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Medicinal Potential of Fenugreek in Neuropathy and Neuroinflammation Associated Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Aman Upaganlawar, Chandrashekhar Upasani, Mayur B. Kale
Oligodendrocyte progenitor cells (OPC) differentiate into mature oligodendrocytes with remyelination. The impairment of this process is suggested to be a major reason for remyelination failure and disease such as multiple sclerosis (Kuhn et al. 2019). Diosgenin from fenugreek was reported to promote OPC differentiation without affecting migration, viability, and proliferation of rat primary oligodendrocyte progenitor cell culture in vitro (Xiao et al. 2012). In the same study, diosgenin was reported to significantly accelerate remyelination of cuprizone-induced demyelination in mice as shown by the increase in the number of mature oligodendrocytes in the corpus callosum without affecting the number of OPCs (Xiao et al. 2012). Subsequently, diosgenin was reported to alleviate experimental autoimmune encephalomyelitis (EAE) progression with reduced central nervous system inflammation and demyelination in a dose-dependent manner (Liu et al. 2017). In myelin oligodendrocyte glycoprotein EAE, diosgenin treatment significantly inhibited the activation of microglia and macrophages, suppressed CD4(+) T-cell proliferation, and hindered Th1/Th17 cell differentiation (Liu et al. 2017).
Demyelinating Neuropathy
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
One of the rare features of demyelination is abnormal myelin periodicity. The normal periodicity in fixed nerve tissue is 18 nm. Increased periodicity (>20 nm) has been observed in many demyelinating diseases of peripheral nerves (Figure 27.2). In uncompacted myelin (UCM), there is a space between two dense lines in which the inner and outer layers of Schwann cell cytoplasm are uncompacted. This results from disruption of remyelination. The most common demyelinating diseases associated with UCM are POEM syndrome, CIDP, and toxic myopathy.
Inflammatory Disorders of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
One suggestion is that exposure to an unidentified nonself antigen “mimics” constitutive peptides of myelin and evokes an antigen-specific, T-cell–mediated immune response. Lymphocytes, macrophages, and humoral factors enter the CNS, and the blood–brain barrier breaks down. B lymphocytes produce oligoclonal IgG in the CSF. Sensitized T cells produce cytokines, which may also damage oligodendrocytes and myelin. Nerve conduction is blocked in demyelinated axons and can be restored by remyelination. In contrast, axonal and neuronal loss lead to a permanent loss of neurologic function, as the CNS axonal regenerative capacity is severely limited.
New targets and therapeutics for neuroprotection, remyelination and repair in multiple sclerosis
Published in Expert Opinion on Investigational Drugs, 2020
Pablo Villoslada, Lawrence Steinman
At present, neuroprotection is being pursued by targeting the pathways used by neurotrophic factors, and by using ion channel modulators or compounds that trigger the antioxidant response [9]. Remyelination is an area in which new drugs have targeted mediators of myelination [10], whereas regeneration lies significantly behind and still awaits the promise of stem cells. Although no drug with such activity has been approved to date, the advances in understanding the underlying biology, the appearance of new theraputics targeting relevant pathological processes, the availability of more informative biomarkers and imaging end-points, and valuable experience in the design of clinical trials for progressive MS, all suggest that we will eventually begin to see new neuroprotective or remyelinating therapies with proven efficacy soon. In this review we will not address secondary neuroprotection by immunomodulatory drugs or the search for new immunomodulatory drugs that focus on compartmentalized inflammation for progressive MS, both of which have recently been reviewed extensively elsewhere [2,4,5].
Clinical implications of myelin regeneration in the central nervous system
Published in Expert Review of Neurotherapeutics, 2018
Christopher E McMurran, Srikirti Kodali, Adam Young, Robin JM Franklin
Remyelination involves the reinstatement of myelin around intact axons that have lost their sheaths by primary demyelination [29]. In the CNS, this process is performed by newly generated oligodendrocytes that derive from a pool of oligodendrocyte progenitor cells (OPCs) following a demyelinating insult. OPCs are present throughout both gray and white matter in the CNS and exhibit features typical of adult stem cells such as self-renewal and multi-potency. In response to demyelination, OPCs proliferate and migrate to the lesion site [36,37] where they differentiate to mature oligodendrocytes, extending processes to remyelinate denuded axons [38]. Consequently, saltatory conduction and function are restored [39,40] and axons are protected from degeneration [41]. The regenerated sheaths never attain the full thickness of those in unlesioned white matter, with expected implications for axonal velocity, though whether this limits the function of neuronal circuits is still unclear. Myelin sheaths generated in adulthood outside an injury context have a similar morphology to remyelination [42], and this could depend in part on the dynamics of the axon being (re)myelinated [35].
The role of feedback in the robotic-assisted upper limb rehabilitation in people with multiple sclerosis: a systematic review
Published in Expert Review of Medical Devices, 2023
Marialuisa Gandolfi, Stefano Mazzoleni, Giovanni Morone, Marco Iosa, Filippo Galletti, Nicola Smania
Functional recovery in MS is achieved and sustained by repair of damage through remyelination, with the resolution of inflammation and functional reorganization. Remyelination is essential for restoring axonal function after acute inflammatory demyelination [7]. Functional reorganization relies on molecular and cellular mechanisms to induce changes in systems-level functional responses involved in perception, action, and cognition [2]. Evidence for the reorganization of brain function after brain lesions comes from early studies on focal ischemic brain damage, where multiple mechanisms of brain plasticity at the molecular, synaptic, and cellular level support post-injury brain plasticity [8–10]. In brief, functional recovery after stroke involves perilesional remapping of cortical representations, functional reorganization in undamaged regions of the affected hemisphere, and activation of cortical areas in the unaffected hemisphere [8]. In the last decades, new insight into the functional reorganization processes in MS has improved our understanding of brain recovery in PwMS, generating novel hypotheses for potential intervention strategies [2]. Evidence supports a similar adaptive role for functional reorganization in PwMS, showing that neuroplasticity is preserved despite widespread pathology across all patient ages and stages of the disease [2,11,12]. However, as the disease advances toward secondary progression, patterns of functional reorganization show an increasingly bilateral distribution involving higher-control sensorimotor areas that are generally recruited for novel or complex tasks in healthy individuals [12].