Shengyang Beina, Guangdan Yu, Nan-Xin Huang, Lan Xiao
{"title":"Impairment of Oligodendroglial Lineage Cells: An Important Player in the Pathogenesis of Psychiatric Disorders.","authors":"Shengyang Beina, Guangdan Yu, Nan-Xin Huang, Lan Xiao","doi":"10.1007/978-3-031-87919-7_15","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_15","url":null,"abstract":"<p><p>Major psychiatric disorders like schizophrenia, depression and anxiety disorders, etc have serious impact on patients' health, but the pathogenesis remains unknown. With an extensive study on glial cells, their functions in psychiatric disorders have attracted much attention in recent years. Oligodendrocyte lineage cells (OLGs), as major myelination cells in the CNS, not only exhibit dynamic changes compatible with alterations in neurologic function but also regulate synaptic development and brain function from multiple aspects by interacting with neurons, astrocytes, and microglia. Concurrently, a growing number of studies have found extensive myelin loss and abnormal alterations of OLGs in the brains of patients with different types of psychiatric disorders. Moreover, impaired development and/or dysfunction of OLGs can lead to neuropsychiatric symptoms such as anxiety, depression, and social disorders by disrupting synaptic transmission or the glial network in animal models. Thus, targeting OLGs may represent a promising strategy for the treatment of psychiatric disorders.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"433-456"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"An Overview of Oligodendrocyte Metabolism.","authors":"Qi Han, Jin Cheng","doi":"10.1007/978-3-031-87919-7_7","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_7","url":null,"abstract":"<p><p>Oligodendrocytes (OLs) exhibit complex metabolic interactions essential for neuronal function and CNS health. This chapter analyzes the metabolism of OLs, particularly glucose, lipid, and amino acid metabolism, and their impact on myelin synthesis, maintenance, and CNS resilience. OLs utilize glucose for energy through glycolysis and the pentose phosphate pathway, supporting ATP production and antioxidative defenses. Lipid synthesis, including cholesterol and sphingolipid production, is critical for maintaining myelin integrity and rapid signal conduction. Furthermore, amino acid pathways, such as those involving glutamine and serine, modulate OL differentiation and remyelination. OLs also provide metabolic support to neurons through lactate shuttling and their interactions with astrocytes in the Panglial network, ensuring sustained energy flow. Dysregulation of OL metabolic functions underlies demyelinating diseases, such as multiple sclerosis, neurodegenerative disorders, and neuropsychiatric conditions, highlighting the therapeutic potential of targeting OL metabolism to enhance remyelination and neuroprotection.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"155-179"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eneritz López-Muguruza, Carla Peiró-Moreno, Asier Ruiz, Carlos Matute
{"title":"Oligodendrocyte and Myelin Pathophysiology in Multiple Sclerosis.","authors":"Eneritz López-Muguruza, Carla Peiró-Moreno, Asier Ruiz, Carlos Matute","doi":"10.1007/978-3-031-87919-7_12","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_12","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is a chronic autoimmune and progressive neurodegenerative disease of the central nervous system (CNS) that has a highly variable clinical manifestation and course. MS targets primarily myelin and oligodendroglia; however, all glial cells and neurons become involved early in the pathology. Thus, inflammation, which is widely thought to be initiated peripherally, expands through the CNS, with astrocytes and microglia entering an activated state not only around and within lesions but also widespread. This chapter will emphasize the pathophysiological changes in oligodendrocytes and myelin as a consequence of the inflammatory cascade driving the disease onset and progression. Learning about the mechanisms of oligodendrocyte and myelin damage beyond the immune attack will be instrumental in protecting these two CNS compartments from damage. In turn, knowledge about the axon-myelin unit will help in devising therapies to prevent axonal degeneration, a key clinical hallmark of MS, as it strongly correlates with the progression of CNS atrophy and symptoms. Finally, exploiting paradigms of oligodendrocyte repopulation and remyelination will definitively contribute to devising treatments for tissue repair and halting MS course. This chapter aims at summarizing the state of the art in all these experimental developments including the available clinical therapies and the current clinical trials.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"317-361"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jianqin Niu, Alexei Verkhratsky, Arthur Butt, Chenju Yi
{"title":"Oligodendroglia in Ageing and Age-Dependent Neurodegenerative Diseases.","authors":"Jianqin Niu, Alexei Verkhratsky, Arthur Butt, Chenju Yi","doi":"10.1007/978-3-031-87919-7_13","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_13","url":null,"abstract":"<p><p>The central nervous system is susceptible to gradual decline with age, affecting all types of glial cells in the process. Compared to other glial cells, the oligodendroglial lineage is highly vulnerable to ageing and undergoes significant characteristic changes that impact upon its structure and impair its physiological functions. Therefore, the ageing and degeneration of oligodendroglia become major risk factors for neurodegenerative diseases. During the age-related disease process, changes in oligodendroglia lead to a decline in their ability to regenerate myelin and respond to the aged microenvironment, which are closely linked to the pathogenesis of neurodegenerative diseases, facilitating the emergence of these diseases in older populations. In this chapter, we introduce the physiological changes of oligodendroglia during ageing and the related mechanisms and then summarise their pathophysiological contributions to age-related cognitive disorders. Finally, we discuss potential therapeutic strategies that target oligodendroglia for future research on neurodegenerative diseases.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"363-405"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Seeing Is Believing: Insights into Myelination and Remyelination in Zebrafish.","authors":"Peng Liu, Qiang Chen, Cheng He","doi":"10.1007/978-3-031-87919-7_4","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_4","url":null,"abstract":"<p><p>Myelin is the lipid-rich insulating layer that wraps axons, providing trophic support and ensuring rapid propagation of the electrical impulses that underlie nervous system function. In the CNS, myelin is produced by mature oligodendrocytes (OLs) that arise from oligodendrocyte precursor cells (OPCs). Myelination is regulated by a variety of molecules, including growth factors, hormones, and extracellular molecules, which activate signaling cascades that drive cellular maturation. Key signaling molecules and downstream pathways that control myelination have been identified in cell culture and rodent models. Although much is known about the development of OL and its progenitor cell in vitro and in vivo, how CNS myelin is dynamically formed through OL processes is still unclear. Zebrafish share significant genetic and physiological similarities with mammals, including humans, making them a relevant model for studying complex biological processes like myelination. Due to its transparent larval development, zebrafish facilitates live imaging studies, enabling dynamic visualizations of cellular and molecular processes in real-time studies. In this chapter, we reviewed the latest insights into OL development and myelin formation, with a particular emphasis on the mechanisms regulating dynamic myelination in zebrafish. We highlight the dynamic extension and retraction of myelin sheath segments and the role of neuronal activity in regulating the developmental myelination in zebrafish. In addition, we also discussed the mechanisms of Ranvier node positioning and axon targeting of myelin sheaths in the spinal cord of zebrafish larvae. Finally, we reviewed the recent progress of zebrafish as a demyelinating disease model for drug discovery of pharmacological compounds favoring myelin regeneration.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"81-95"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Development of Oligodendroglia and Myelin.","authors":"Hao Huang, Xiaofeng Xu, Mengsheng Qiu","doi":"10.1007/978-3-031-87919-7_3","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_3","url":null,"abstract":"<p><p>Myelin sheaths formed by oligodendrocytes (OLs) wrap around neuronal axons and allow for saltatory conduction of nerve impulses, significantly increasing the speed of electrical signal transmission. The development of oligodendrocyte lineage consists of several coordinated steps. Briefly, oligodendrocyte precursor cells (OPCs) are first generated from neural precursor cells of certain neuroepithelial regions, and then they proliferate and migrate to other regions of the central nervous system (CNS), where they differentiate into oligodendrocytes and form myelin sheaths around the axons of neurons. These developmental processes are tightly and precisely regulated during animal development by a cohort of intracellular molecular and extracellular signals.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"61-79"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ai Guo, Yuzhen Wei, Alexei Verkhratsky, Fu-Dong Shi
{"title":"Oligodendroglia in Neuromyelitis Optica Spectrum Disorder.","authors":"Ai Guo, Yuzhen Wei, Alexei Verkhratsky, Fu-Dong Shi","doi":"10.1007/978-3-031-87919-7_16","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_16","url":null,"abstract":"<p><p>Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory autoimmune disease of the central nervous system, in which aquaporin-4 immunoglobulin G (AQP4-IgG) targets the water channel aquaporin-4 (AQP4) localized at astrocytic endfeet, thus triggering inflammatory lesions and tissue damage. The pathological characteristics of NMOSD are early loss of oligodendrocytes, extensive demyelination, and axonal injury. The pathogenesis of oligodendrocyte damage in NMOSD includes complement-dependent bystander effect, antibody-dependent cell-mediated cytotoxicity bystander effect, glutamate toxicity, connexin dysregulation, and blood-brain barrier disruption. Remyelination levels in acute NMOSD lesions are low.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"457-472"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jianqin Niu, Alexei Verkhratsky, Arthur Butt, Chenju Yi
{"title":"Oligodendroglia and Myelin: Supporting the Connectome.","authors":"Jianqin Niu, Alexei Verkhratsky, Arthur Butt, Chenju Yi","doi":"10.1007/978-3-031-87919-7_1","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_1","url":null,"abstract":"<p><p>Oligodendroglia are the only cell lineage of the central nervous system (CNS) responsible for producing myelin. They originate from precursor cells known as oligodendrocyte precursor cells (OPCs), which are born around the ventricular zones of the brain and spinal cord and migrate throughout the developing CNS, and many of them ultimately differentiate into mature myelinating oligodendrocytes. Recent research has shown that OPCs and oligodendrocytes possess distinct characteristics when compared either to other types of glial cells in the CNS or to each other. Under different physiological and pathophysiological conditions, the processes of development or regeneration, the features, and, in some cases, even the functions of oligodendroglia can be modified. These changes can contribute to disease progression and affect the functional status of the nervous system. For instance, experience-dependent \"adaptive\" myelination plays a crucial role in the plasticity of neuronal circuits and influences learning processes; additionally, the non-myelinating functions of oligodendroglia expand their pathological potential, allowing them to regulate neuronal development and activity, angiogenesis, astrocyte maturation, and neuroinflammation. This chapter serves as a comprehensive introduction to oligodendroglia by presenting evidence from fundamental studies and fresh insights into their development, physiological and pathophysiological attributes, as well as the newly discovered non-myelinating functions.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"1-37"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alexei Verkhratsky, Jianqin Niu, Chenju Yi, Arthur Butt
{"title":"Neuroglial Pathophysiology of Leukodystrophies.","authors":"Alexei Verkhratsky, Jianqin Niu, Chenju Yi, Arthur Butt","doi":"10.1007/978-3-031-87919-7_10","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_10","url":null,"abstract":"<p><p>Leukodystrophies are a diverse group of inherited diseases characterised by white matter degenerative pathology. Leukodystrophies have a highly heterogeneous genetic background linked mainly to mutations in oligodendrocyte and astrocyte genes and, to lesser extent, microglia. The most prevalent leukodystrophies are caused by mutations in oligodendrocyte genes that encode the essential myelin proteins PLP1 and GalC in Pelizaeus-Merzbacher disease and Krabbe disease, respectively. Astrocyte leukodystrophies are led by Alexander disease, caused by mutations in the astrocyte gene GFAP. Vanishing white matter disease, the most prevalent inherited white matter pathology in children, is associated with astrocyte atrophy and cystic degeneration of the cerebral white matter. The pathogenic mechanisms in leukodystrophies depend on the genetic mutations and hence are extremely varied, but the diseases have in common white matter atrophy caused by the loss of oligodendrocytes and myelin, with or without marked reactive astrogliosis and microglia activation. The development of a range of animal models with the disruption of specific genes causing leukodystrophies and the use of pluripotent stem cells from people with different forms of leukodystrophy is advancing the understanding of the functional and cellular pathophysiology of these rare diseases.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"257-279"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Arthur Butt, Adam Willis, Ian Hunter, Jianqin Niu, Chenju Yi, Alexei Verkhratsky
{"title":"Physiology of Oligodendroglia.","authors":"Arthur Butt, Adam Willis, Ian Hunter, Jianqin Niu, Chenju Yi, Alexei Verkhratsky","doi":"10.1007/978-3-031-87919-7_6","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_6","url":null,"abstract":"<p><p>Oligodendroglia are highly specialised to myelinate axons and ensure rapid electrical conduction of action potentials in the central nervous system (CNS). The oligodendroglial cell lineage comprises mature myelinating oligodendrocytes, together with oligodendrocyte precursor cells (OPCs) and immature premyelinating oligodendrocytes, their numerical density depending on developmental age. In early embryonic and postnatal development, OPCs and immature oligodendrocytes predominate, whereas in the adult CNS, mature myelinating oligodendrocytes comprise over 90% of the lineage, with OPCs making up a small but significant population (3-9%). Adult OPCs provide for myelin repair and plasticity throughout life. Oligodendroglial cells express diverse ion channels and neurotransmitter receptors, together with transporters and gap junctions, which enables these cells to sense and respond to their environment and fulfil their myelinating function as well as providing metabolic and homeostatic support for axons.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"125-153"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}