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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).
Issues in aging following traumatic brain injury
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Grace S. Griesbach, Mark J. Ashley, Alan Weintraub
Age-related change in remyelination may contribute to the pathogenesis of certain degenerative conditions or to an overall diminution of neurologic function with aging. Remyelination in the brain changes with advancing age, becoming less efficient. Oligodendrocyte progenitor cells are recruited at a decreased rate as age advances as does the rate at which oligodendrocytes differentiate into remyelinating ones.77 In some individuals, a coincidental decrease in growth hormone production, key to oligodendrocyte genesis and function, may contribute to compounding decrements in remyelination. Remyelination is dependent upon cholesterol availability within the CNS and is also impacted by decrements in neuroendocrine function. Oligodendrocyte loss arising from the original injury will predispose the brain to decreased remyelination capacity. The majority of remyelination is due to oligodendrocyte function although some contribution is made by Schwann cells in the lesion area when astrocytes are absent and in the vicinity of blood vessels.77 Myelin repair in the CNS requires as much as half the brain energy expenditure. Impairments of energy transduction within the CNS after injury may impact energy availability for myelin repair. Myelin provides for axonal protection; thus, axonal vulnerability is higher when myelin integrity is compromised.
Are electrophysiological and oligodendrocyte alterations an element in the development of multiple sclerosis at the same time as or before the immune response?
Published in International Journal of Neuroscience, 2021
Genaro Gabriel Ortiz, Mario A. Mireles-Ramírez, Fermín P. Pacheco-Moisés, Luis J. Ramírez-Jirano, Oscar K. Bitzer-Quintero, Daniela L. C. Delgado-Lara, L. Javier Flores-Alvarado, Miriam A. Mora-Navarro, Miguel Huerta, Blanca M. G. Torres-Mendoza
Oligodendrocyte heterogeneity could limit efficient remyelination in MS and previous studies in animal models of demyelinating diseases suggested that the formation of new oligodendrocytes from adult oligodendrocyte progenitor cells is an essential event in myelin repair [51]. Thus, it is interesting to study if the formation of new olygondrocytes participates in an efficient remyelination process in multiple sclerosis. Recent experiments in which 14C concentration in genomic DNA is quantified by accelerator mass spectrometry in oligodendrocytes from MS patients indicated that there was no formation of new oligodendrocytes in the shadow plaques (they are believed to have been produced remyelination lesions). This finding suggests that mature oligodendrocytes may remyelinate axons and the generation of oligodendrocytes is minimal if it exists in these plaques. Therefore, early treatments in patients with multiple sclerosis can help preserve oligodendrocytes and this raises the question of how the process is blocked.
Delayed effects of a single-dose whole-brain radiation therapy on glucose metabolism and myelin density: a longitudinal PET study
Published in International Journal of Radiation Biology, 2020
Andrea Parente, Elisa Scandiuzzi Maciel, Rudi A. J. O. Dierckx, Johannes A. Langendijk, Erik F. J. de Vries, Janine Doorduin
In our study, the control group showed lower 11C-MeDAS uptake at days 60 and 90 than at baseline, suggesting a decrease in myelin density between baseline and days 60–90. We observed a similar pattern in myelin density changes in irradiated rats as in controls, although there appeared to be a non-significant tendency toward an increase in myelin density 3 months after radiation therapy, as compared to day 60. In line with our data, previous studies suggested that demyelination after 25-Gy WBRT in rodents is a process that mainly occurs in the acute phase (Burns et al. 2016), with myelin density recovering to normal levels after around 3–6 months (Panagiotakos et al. 2007; Fu et al. 2017). This recovery is hypothesized to occur mainly due to the capacity of oligodendrocyte progenitor cells to migrate to the sites of myelin damage and remyelinate the injured white matter tracts.
The ceramide-S1P pathway as a druggable target to alleviate peripheral neuropathic pain
Published in Expert Opinion on Therapeutic Targets, 2020
Michiel Langeslag, Michaela Kress
Oligodendrocytes play a crucial role in CNS development and myelination. Oligodendrocytes are also important during CNS repair after neuronal injury, particularly in neuronal remyelination. This occurs through proliferation, migration, and differentiation of oligodendrocyte progenitor cells (OPC). Oligodendrocytes express S1P1 [135,136], S1P2 [136] and S1P5 [137,138]. Oligodendrocytes lacking S1P1 show a marginal decrease of myelination-related proteins and form a slightly thinner myelination of neurons. Mice with S1P1-ablated oligodendrocytes are more susceptible to demyelinating agents indicating that S1P1 might be involved in myelination [139,140]. The reduction in myelination in S1P1 conditional knock-out oligodendrocytes is associated with a decreased activation of ERKs and PAKs and increased expression of tropomodulin1 [141]. Migration of OPC is inhibited by activating S1P5 and subsequently the G12/13-RhoA signaling pathway, rather than acting via Gi [136]. Mice where S1P5 is conditionally knocked out in oligodendrocytes do not develop an obvious myelination deficit. It rather appears that S1P5 is critically important for the survival of mature oligodendrocytes [137]. The S1P2 is known to inhibit the migration of various cells [26,97], however, in OPCs, a clear role for S1P2 still needs to be determined [136].