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Regulation of Glial Function by Insulin Peptides
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Ana M. Fernandez, Laura Martinez-Rachadell, Patricia Miranda-Azpiazu, Ignacio Torres Aleman
Oligodendrocytes were also first described by del Rio-Hortega (81), and are the myelinating cells of the CNS, while Schwann cells are their counter-part in the peripheral nervous system. Both are from neuroepithelial lineage. Oligodendrocyte precursors (usually refer as NG-2 glia) remain in high numbers in the adult brain and constitute a renewal pool for these glial cells, generated all along ontogeny. Accordingly, this source of precursor cells is important for endogenous re-myelination (82) and is modulated by ILPs (83, 84). Myelinated axons are a key component of the mammalian brain, providing fast conductance capacities to neurons and forming the white matter of the brain. Other roles of oligodendroglia in the adult CNS that are increasingly emerging (85), may also be regulated by ILPs, but more work is needed.
Role of Oxidative Stress in Neurodegeneration
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Neelam Yadav, Pradeep K. Shukla
The pathological signature of MS is perivenular inflammatory lesions, leading to demyelinating plaques (Karussis 2014). The inflammatory infiltrates contain T‐lymphocytes, dominated by MHC class I restricted CD8+ T‐cells, B‐cells, and plasma cells (Lassmann 2013). Oligodendrocyte damage and demyelination occur as a result of inflammation. Axons are relatively preserved in the early stages of the disease; however, as disease progresses, irreversible axonal damage develops (Trapp et al. 1998). Excess reactive oxygen species (ROS), lead to oxidative stress which have been implicated as the mediators of demyelination and axonal damage in MS (Ohl, Tenbrock, and Kipp 2016). Cells are capable of counteracting excess ROS and protecting against oxidative damage. Oxidative stress response is mainly controlled by transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2). It protects cells against oxidative stress through its capability of regulating basal and inducible expression of various antioxidant proteins and enzymes. Nrf2 plays an important role in glutathione (GSH) synthesis, as well as regulating thioredoxin (Trx) enzyme system and detoxifying enzymes such as heme oxygenase(s) (HO) or NAD(P) H: quinone oxidoreductase 1 (Ohl, Tenbrock, and Kipp 2016; Kensler, Wakabayashi, and Biswal 2007).
Propagation of the Action Potential
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The solution, in the form of myelinated axons, is ingeniously simple and highly effective. The axon is surrounded by a myelin sheath consisting of up to 200 layers or so of passive cell membrane interrupted at regular intervals in what are referred to as the nodes of Ranvier (Figure 4.7). The region between adjacent nodes is the internode, whose length is roughly 100–150 times the axon diameter and ranges in length between about 200 µm and 2.5 mm, depending on axon diameter. The sheath is wrapped around the axon during embryonic development by specialized satellite cells of the nervous system – the glial cells (Section 1.2.3). In the central nervous system, the glial cells that form the myelin sheath are referred to as oligodendrocytes, with each oligodendrocyte forming one internode of myelin for up to about 50 adjacent axons. In the peripheral nervous system, a glial cell referred to as a Schwann cell forms one internode of only a single axon.
Nanoparticles-based anti-aging treatment of Alzheimer’s disease
Published in Drug Delivery, 2022
Jian-Jian Chu, Wen-Bo Ji, Jian-Hua Zhuang, Bao-Feng Gong, Xiao-Han Chen, Wen-Bin Cheng, Wen-Danqi Liang, Gen-Ru Li, Jie Gao, You Yin
In the CNS, myelin is an extension of oligodendrocytes concentrically wrapped around nerve axons (Kuhn et al., 2019). Functionally, myelin facilitates rapid transmission of axonal potentials and provides metabolic support to wrapped nerve axons. They are highly vulnerable to oxidative stress (Giacci et al., 2018). White matter changes in AD are thought to reflect both demyelination and axonal damage (Prins & Scheltens, 2015), while SA-β-Gal upregulation of oligodendrocyte in human cerebral tissue of white matter lesion (WML) may be evidence of oligodendrocyte senescence in AD (Al-Mashhadi et al., 2015). In the brains of human patients with AD and APP/PS1 mice model, OPCs with high expression of senescent phenotypes (p21, p16, and SA-β-Gal) were correlated with amyloid plaques, whereas in age-matched subjects without dementia, these senescent phenotypes were not obvious (Zhang et al., 2019). OPCs are very important for myelin regeneration following injury (Kuhn et al., 2019). Young mice had highly active myelination, while in aged mice, it was greatly inhibited, which coincides with spatial memory deficits (Wang et al., 2020). The impaired function of senescent OPCs may play a crucial role in disease progression, and reduced self-healing capacity could be due to the aging process and pathological factors such as Aβ deposition or NFT (Cai & Xiao, 2016; Zhang et al., 2019).
Histopathological effects of topical coenzyme q 10 + Vit E TPGS in experimental ischemic optic neuropathy
Published in Ultrastructural Pathology, 2022
Oğuzhan Oruz, Kemal Yar, Dilek Şaker, Arbil Açıkalın, Yusuf Kenan Dağlıoğlu, Sait Polat
In the electron microscopic examination of optic nerve bundles of this group, in which coenzyme Q10 + vit E TPGS was applied after ischemia, slight degenerative changes were observed in the myelin sheath in some myelinated nerve fibers. It was observed that oligodendrocytes surrounded the myelinated axons. Despite the increase in heterochromatin in the nucleus in some regions and focal degenerative changes in the cytoplasmic organelles in oligodendrocytes, it was generally observed that these cells preserved their normal fine structures. However, in some areas, clustering of heterochromatin in the nucleus of astrocytes and a slight increase in lysosomes and filamentous structures in the cytoplasm were also observed (Figure 4a,b). No side effects were observed in the treatment group.
Hyperammonemia in the setting of Roux-en-Y gastric bypass presenting with osmotic demyelination syndrome
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Carly Rosenberg, Michael Rhodes
The correlation between cerebral edema and hyperammonemia has been fairly well established; however, no significant correlation has yet been made between osmotic demyelination syndrome and hyperammonemia. There have been but a minor number of case reports associating such, mostly in the pediatric population. Most often, osmotic demyelination is associated with rapid correction of hyponatremia. Hyponatremia in itself can cause cerebral edema, but with rapid correction, this causes extracellular tonicity, which leads to osmotic fluid shifts that deplete cells essentially causing dehydration [10]. Oligodendrocytes, the primary cell in the myelination of the nervous system, are susceptible to this type of damage, and this consequently leads to destruction of myelin [10]. In this patient, her sodium level was normal throughout admission; however, ultimately ended up with osmotic demyelination.