Decades of research asserted that the oligodendroglial lineage comprises two cell types:oligodendrocyte precursor cells and oligodendrocytes.However,recent studies employing single-cell RNA sequencing techniques have ...Decades of research asserted that the oligodendroglial lineage comprises two cell types:oligodendrocyte precursor cells and oligodendrocytes.However,recent studies employing single-cell RNA sequencing techniques have uncovered novel cell states,prompting a revision of the existing terminology.Going forward,the oligodendroglial lineage should be delineated into five distinct cell states:oligodendrocyte precursor cells,committed oligodendrocyte precursor cells,newly formed oligodendrocytes,myelin-forming oligodendrocytes,and mature oligodendrocytes.This new classification system enables a deeper understanding of the oligodendroglia in both physiological and pathological contexts.Adopting this uniform terminology will facilitate comparison and integration of data across studies.This,including the consolidation of findings from various demyelinating models,is essential to better understand the pathogenesis of demyelinating diseases.Additionally,comparing injury models across species with varying regenerative capacities can provide insights that may lead to new therapeutic strategies to overcome remyelination failure.Thus,by standardizing terminology and synthesizing data from diverse studies across different animal models,we can enhance our understanding of myelin pathology in central nervous system disorders such as multiple sclerosis,Alzheimer's disease,and amyotrophic lateral sclerosis,all of which involve oligodendroglial and myelin dysfunction.展开更多
Demyelination and remyelination have been major focal points in the study of peripheral nerve regeneration following peripheral nerve injury.Notably,the gene regulatory network of regenerated myelin differs from that ...Demyelination and remyelination have been major focal points in the study of peripheral nerve regeneration following peripheral nerve injury.Notably,the gene regulatory network of regenerated myelin differs from that of native myelin.Silencing of enhancer of zeste homolog 2(EZH2)hinders the differentiation,maturation,and myelination of Schwann cells in vitro.To further determine the role of EZH2 in myelination and recovery post-peripheral nerve injury,conditional knockout mice lacking Ezh2 in Schwann cells(Ezh2^(fl/fl);Dhh-Cre and Ezh2^(fl/fl);Mpz-Cre)were generated.Our results show that a significant proportion of axons in the sciatic nerve of Ezh2-depleted mice remain unmyelinated.This highlights the crucial role of Ezh2 in initiating Schwann cell myelination.Furthermore,we observed that 21 days after inducing a sciatic nerve crush injury in these mice,most axons had remyelinated at the injury site in the control nerve,while Ezh2^(fl/fl);Mpz-Cre mice had significantly fewer remyelinated axons compared with their wild-type littermates.This suggests that the absence of Ezh2 in Schwann cells impairs myelin formation and remyelination.In conclusion,EZH2 has emerged as a pivotal regulatory factor in the process of demyelination and myelin regeneration following peripheral nerve injury.Modulating EZH2 activity during these processes may offer a promising therapeutic target for the treatment of peripheral nerve injuries.展开更多
Traumatic spinal cord injury often leads to the disintegration of nerve cells and axons,resulting in a substantial accumulation of myelin debris that can persist for years.The abnormal buildup of myelin debris at site...Traumatic spinal cord injury often leads to the disintegration of nerve cells and axons,resulting in a substantial accumulation of myelin debris that can persist for years.The abnormal buildup of myelin debris at sites of injury greatly impedes nerve regeneration,making the clearance of debris within these microenvironments crucial for effective post-spinal cord injury repair.In this review,we comprehensively outline the mechanisms that promote the clearance of myelin debris and myelin metabolism and summarize their roles in spinal cord injury.First,we describe the composition and characteristics of myelin debris and explain its effects on the injury site.Next,we introduce the phagocytic cells involved in myelin debris clearance,including professional phagocytes(macrophages and microglia)and non-professional phagocytes(astrocytes and microvascular endothelial cells),as well as other cells that are also proposed to participate in phagocytosis.Finally,we focus on the pathways and associated targets that enhance myelin debris clearance by phagocytes and promote lipid metabolism following spinal cord injury.Our analysis indicates that myelin debris phagocytosis is not limited to monocyte-derived macrophages,but also involves microglia,astrocytes,and microvascular endothelial cells.By modulating the expression of genes related to phagocytosis and lipid metabolism,it is possible to modulate lipid metabolism disorders and influence inflammatory phenotypes,ultimately affecting the recovery of motor function following spinal cord injury.Additionally,therapies such as targeted mitochondrial transplantation in phagocytic cells,exosome therapy,and repeated trans-spinal magnetic stimulation can effectively enhance the removal of myelin debris,presenting promising potential for future applications.展开更多
Myelination,the continuous ensheathment of neuronal axons,is a lifelong process in the nervous system that is essential for the precise,temporospatial conduction of action potentials between neurons.Myelin also provid...Myelination,the continuous ensheathment of neuronal axons,is a lifelong process in the nervous system that is essential for the precise,temporospatial conduction of action potentials between neurons.Myelin also provides intercellular metabolic support to axons.Even minor disruptions in the integrity of myelin can impair neural performance and increase susceptibility to neurological diseases.In fact,myelin degeneration is a well-known neuropathological condition that is associated with normal aging and several neurodegenerative diseases,including multiple sclerosis and Alzheimer’s disease.In the central nervous system,compact myelin sheaths are formed by fully mature oligodendrocytes.However,the entire oligodendrocyte lineage is susceptible to changes in the biological microenvironment and other risk factors that arise as the brain ages.In addition to their well-known role in action potential propagation,oligodendrocytes also provide intercellular metabolic support to axons by transferring energy metabolites and delivering exosomes.Therefore,myelin degeneration in the aging central nervous system is a significant contributor to the development of neurodegenerative diseases.Interventions that mitigate age-related myelin degeneration can improve neurological function in aging individuals.In this review,we investigate the changes in myelin that are associated with aging and their underlying mechanisms.We also discuss recent advances in understanding how myelin degeneration in the aging brain contributes to neurodegenerative diseases and explore the factors that can prevent,slow down,or even reverse age-related myelin degeneration.Future research will enhance our understanding of how reducing age-related myelin degeneration can be used as a therapeutic target for delaying or preventing neurodegenerative diseases.展开更多
Oligodendrocyte lineage cells, including oligodendrocyte precursor cells (OPCs) and oligodendrocytes (OLs), are essential in establishing and maintaining brain circuits. Autophagy is a conserved process that keeps the...Oligodendrocyte lineage cells, including oligodendrocyte precursor cells (OPCs) and oligodendrocytes (OLs), are essential in establishing and maintaining brain circuits. Autophagy is a conserved process that keeps the quality of organelles and proteostasis. The role of autophagy in oligodendrocyte lineage cells remains unclear. The present study shows that autophagy is required to maintain the number of OPCs/OLs and myelin integrity during brain aging. Inactivation of autophagy in oligodendrocyte lineage cells increases the number of OPCs/OLs in the developing brain while exaggerating the loss of OPCs/OLs with brain aging. Inactivation of autophagy in oligodendrocyte lineage cells impairs the turnover of myelin basic protein (MBP). It causes MBP to accumulate in the cytoplasm as multimeric aggregates and fails to be incorporated into integral myelin, which is associated with attenuated endocytic recycling. Inactivation of autophagy in oligodendrocyte lineage cells impairs myelin integrity and causes demyelination. Thus, this study shows autophagy is required to maintain myelin quality during aging by controlling the turnover of myelin components.展开更多
Myelin formation is considered the last true“invention”in the evolution of vertebrate nervous system cell structure.The rapid jumping pulse propagation achieved by myelin enables the high conduction speed that is th...Myelin formation is considered the last true“invention”in the evolution of vertebrate nervous system cell structure.The rapid jumping pulse propagation achieved by myelin enables the high conduction speed that is the basis of human movement,sensation,and cognitive function.As a key structure in the brain,white matter is the gathering place of myelin.However,with age,white matter-associated functions become abnormal and a large number of myelin sheaths undergo degenerative changes,causing serious neurological and cognitive disorders.Despite the extensive time and effort invested in exploring myelination and its functions,numerous unresolved issues and challenges persist.In-depth exploration of the functional role of myelin may bring new inspiration for the treatment of central nervous system(CNS)diseases and even mental illnesses.In this study,we conducted a comprehensive examination of the structure and key molecules of the myelin in the CNS,delving into its formation process.Specifically,we propose a new hypothesis regarding the source of power for myelin expansion in which membrane compaction may serve as a driving force for myelin extension.The implications of this hypothesis could provide valuable insights into the pathophysiology of diseases involving myelin malfunction and open new avenues for therapeutic intervention in myelin-related disorders.展开更多
Myelin is an essential structure that facilitates rapid saltatory conduction in the nervous system.Discrepancies in myelin microstructure are a hallmark of numerous neurological disorders,rendering the assessment of m...Myelin is an essential structure that facilitates rapid saltatory conduction in the nervous system.Discrepancies in myelin microstructure are a hallmark of numerous neurological disorders,rendering the assessment of myelin integrity and content an indispensable tool in clinical diagnostics and neuroscience research.Extensive research has been dedicated to scrutinizing its biochemical makeup and morphology under normal,pathological,and experimental conditions over the years.In this review,we present an updated summary of the myelin sheath's structure,composition,and developmental trajectory.We systematically enumerate and contrast eight prevalent myelin staining techniques across dimensions of sensitivity,specificity,and resolution,delving into their underlying staining principles.With an initial application of myelin histology on the mouse demyelination model,our review accentuates the accurate delineation of myelination and the microstructural analysis of the myelin sheath.Such insights are anticipated to significantly contribute to the evaluation and understanding of white matter pathologies.展开更多
Differentiation of oligodendrocyte progenitor cells into mature myelin-forming oligodendrocytes contributes to remyelination.Failure of remyelination due to oligodendrocyte progenitor cell death can result in severe n...Differentiation of oligodendrocyte progenitor cells into mature myelin-forming oligodendrocytes contributes to remyelination.Failure of remyelination due to oligodendrocyte progenitor cell death can result in severe nerve damage.Ferroptosis is an iron-dependent form of regulated cell death caused by membrane rupture induced by lipid peroxidation,and plays an important role in the pathological process of ischemic stroke.However,there are few studies on oligodendrocyte progenitor cell ferroptosis.We analyzed transcriptome sequencing data from GEO databases and identified a role of ferroptosis in oligodendrocyte progenitor cell death and myelin injury after cerebral ischemia.Bioinformatics analysis suggested that perilipin-2(PLIN2)was involved in oligodendrocyte progenitor cell ferroptosis.PLIN2 is a lipid storage protein and a marker of hypoxia-sensitive lipid droplet accumulation.For further investigation,we established a mouse model of cerebral ischemia/reperfusion.We found significant myelin damage after cerebral ischemia,as well as oligodendrocyte progenitor cell death and increased lipid peroxidation levels around the infarct area.The ferroptosis inhibitor,ferrostatin-1,rescued oligodendrocyte progenitor cell death and subsequent myelin injury.We also found increased PLIN2 levels in the peri-infarct area that co-localized with oligodendrocyte progenitor cells.Plin2 knockdown rescued demyelination and improved neurological deficits.Our findings suggest that targeting PLIN2 to regulate oligodendrocyte progenitor cell ferroptosis may be a potential therapeutic strategy for rescuing myelin damage after cerebral ischemia.展开更多
The myelin sheath is a lipoprotein-rich,multilayered structure capable of increasing conduction velocity in central and peripheral myelinated nerve fibers.Due to the complex structure and composition of myelin,various...The myelin sheath is a lipoprotein-rich,multilayered structure capable of increasing conduction velocity in central and peripheral myelinated nerve fibers.Due to the complex structure and composition of myelin,various histological techniques have been developed over the centuries to evaluate myelin under normal,pathological or experimental conditions.Today,methods to assess myelin integrity or content are key tools in both clinical diagnosis and neuroscience research.In this review,we provide an updated summary of the composition and structure of the myelin sheath and discuss some histological procedures,from tissue fixation and processing techniques to the most used and practical myelin histological staining methods.Considering the lipoprotein nature of myelin,the main features and technical details of the different available methods that can be used to evaluate the lipid or protein components of myelin are described,as well as the precise ultrastructural techniques.展开更多
Myelin is the protective sheath surrounding nerve fibers, and its damage(demyelination) occurs in many central nervous system(CNS) diseases, including multiple sclerosis(MS), traumatic injury, neurodegenerative diseas...Myelin is the protective sheath surrounding nerve fibers, and its damage(demyelination) occurs in many central nervous system(CNS) diseases, including multiple sclerosis(MS), traumatic injury, neurodegenerative diseases such as Alzheimer's disease, and mental disorders such as schizophrenia(Barateiro et al., 2016). Repair of damaged myelin sheaths(remyelination) often fails in MS, leading to neuronal loss and irreversible functional deficits.展开更多
Multiple sclerosis(MS)is the most common chronic disease of the central nervous system(CNS)in young adults and represents the first cause of severe handicap,originally non-traumatic(Oh et al.,2018).MS is chara cterize...Multiple sclerosis(MS)is the most common chronic disease of the central nervous system(CNS)in young adults and represents the first cause of severe handicap,originally non-traumatic(Oh et al.,2018).MS is chara cterized by the infiltration of auto reactive lymphocytes specific to myelin through the blood-brain barrier,which results in the appearance of inflammatory demyelinating lesions caused by the death of the central nervous system myelinating cells,oligodendrocytes(Oh et al.,2018).There is a prevalence sexual with a ratio of three times more affected women than men.展开更多
The rapidly aging population directly contributes to the increasing cases of neurological disorders.Due to the chronic progressive nature of neurodegeneration,numerous neurological conditions are considered“multifact...The rapidly aging population directly contributes to the increasing cases of neurological disorders.Due to the chronic progressive nature of neurodegeneration,numerous neurological conditions are considered“multifactorial”with systemic metabolic alterations.Even so,treatments for neurological disorders have remained unchanged for the past decades.Recently,metabolic drugs such as metformin and glucagon-like peptide 1 agonists have demonstrated promising health outcomes for neurodegeneration.展开更多
Chronic cerebral hypoperfusion can lead to neuronal necrosis,trigger inflammatory responses,promote white matter damage,and ultimately result in cognitive impairment.Consequently,chronic cerebral hypoperfusion is an i...Chronic cerebral hypoperfusion can lead to neuronal necrosis,trigger inflammatory responses,promote white matter damage,and ultimately result in cognitive impairment.Consequently,chronic cerebral hypoperfusion is an important factor influencing the onset and progression of vascular dementia.The myelin sheath is a critical component of white matter,and damage and repair of the white matter are closely linked to myelin sheath integrity.This article reviews the role of microglia in vascular dementia,focusing on their effects on myelin sheaths and the potential therapeutic implications.The findings suggest that ischemia and hypoxia cause disruption of the blood-brain barrier and activate microglia,which may worsen blood-brain barrier damage through the release of matrix-degrading enzymes.Microglia-mediated metabolic reprogramming is recognized as an important driver of inflammation.Damage to the blood-brain barrier and subsequent inflammation can lead to myelin injury and accelerate the progression of vascular dementia.Early activation of microglia is a protective response that contributes to the maintenance of blood-brain barrier integrity through sensing,debris-clearing,and defensive mechanisms.However,prolonged activation can trigger a shift in microglia toward the pro-inflammatory M1 phenotype,resulting in myelin damage and cognitive impairment.Triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells 1 have been identified as potential biomarkers for vascular dementia,as both are closely linked to cognitive decline.Although effective clinical treatments for myelin damage in the central nervous system are currently lacking,researchers are actively working to develop targeted therapies.Several drugs,including nimodipine,dopaminergic agents,simvastatin,biotin,and quetiapine,have been evaluated for clinical use in treating microglial and myelin damage.Future research will face challenges in developing targeted therapeutic strategies for vascular dementia,requiring further investigation into the timing,duration,and specific mechanisms of microglial activation,as well as the exploration of new drug combinations and additional therapeutic targets.展开更多
BACKGROUND Diabetes is associated with increased cognitive decline and dementia due to the loss of myelinated nerve fiber function,which is linked to oligodendrocyte dysfunction.The voltage-gated proton channel 1(Hv1)...BACKGROUND Diabetes is associated with increased cognitive decline and dementia due to the loss of myelinated nerve fiber function,which is linked to oligodendrocyte dysfunction.The voltage-gated proton channel 1(Hv1)is important for the cellular proton extrusion machinery.However,its role in regulating diabetesinduced cognitive dysfunction is unclear.AIM To investigate the role of Hv1 in cognitive impairment induced by diabetes and its potential mechanisms,focusing on neuroinflammation,oligodendrocyte apoptosis,and axonal demyelination.METHODS A diabetes model was established by administering a high-fat diet and streptozotocin injections in mice.Hv1 knockout(KO)and wild-type mice were used to evaluate cognitive function via behavioral tests and neuroinflammation using immunofluorescence.Oligodendrocyte apoptosis was assessed with the terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling assay, and axonal demyelination wasanalyzed using electron microscopy.RESULTSHv1 expression was significantly increased in the corpus callosum of diabetic mice. Hv1 KO alleviated cognitiveimpairment, reduced oligodendrocyte apoptosis, and decreased the expression of inflammatory factors, includinginterleukin-1 and tumor necrosis factor-α, in diabetic mice. Electron microscopy revealed a reduction in myelinthickness and an increased g-ratio in diabetic mice, which were reversed by Hv1 KO.CONCLUSIONHv1 plays a role in diabetes-induced cognitive dysfunction by modulating neuroinflammation and myelinintegrity. Hv1 KO demonstrates therapeutic potential in mitigating diabetes-related cognitive decline andassociated complications.展开更多
Dear Editor,Myelin oligodendrocyte glycoprotein(MOG)is a minor component of myelin,expressed on the external surface of oligodendrocytes in the central nervous system(CNS)[1].Anti-MOG antibodies(MOG-ab)have been impli...Dear Editor,Myelin oligodendrocyte glycoprotein(MOG)is a minor component of myelin,expressed on the external surface of oligodendrocytes in the central nervous system(CNS)[1].Anti-MOG antibodies(MOG-ab)have been implicated in the demyelinating process and are considered unique biomarkers for a group of heterogeneous autoimmune inflammatory CNS diseases known as MOG-associated disorder(MOGAD)[1].MOGAD can present with a range of clinical manifestations,including optic neuritis,transverse myelitis,acute disseminating encephalomyelitis,and brainstem or cerebral encephalitis[1].Optic neuritis is the most common clinical feature of MOGAD in adults,typically manifesting as steroid-sensitive,recurrent,bilateral optic neuritis with optic disc swelling[1].展开更多
Background:Glucocorticoids are used as anti-inflammatory drugs for the treatment of various diseases,however,their side effects on normal brain tissue remain underinvestigated.Objectives:The study aimed to investigate...Background:Glucocorticoids are used as anti-inflammatory drugs for the treatment of various diseases,however,their side effects on normal brain tissue remain underinvestigated.Objectives:The study aimed to investigate dexamethasone(DXM)effects on cell composition and myelin content in the mouse brain tissue.Methods:C57Bl/6 male mice(n 60)received single and ten multiple intraperitoneal DXM injections(2.5 mg/kg),and the studied=parameters were analysed at 1,3,7,10 days after a single DXM injection and 15,30,60,and 90 days after the multiple injections.Oligodendrocytes,microglia,and astrocytes were assayed by immunohistochemistry with specific antibodies(Olig2,CD68,and GFAP,respectively)in the corpus callosum of the normal brain tissue.The myelin content was estimated by staining with LuxolFastBlue.The presence of GFAP isoforms was determined by western blotting.Results:DXM administration did not affect oligodendrocytes in the mouse brain but temporarily significantly decreased myelin content(1.2-fold,p 0.0058;1.4-fold,p 0.0001)at 3–15 days time points.At the same time,DXM significantly=<decreased the number of microglial cells(1.5–3.5-fold,p 0.0001)and significantly increased astrocytes(1.8-fold,p<<0.0001).Prolonged administration of DXM resulted in the decrease of the main GFAPα-isoform(50 kDa)and the appearance of shorter GFAP isoforms(30 kDa,42 kDa,44 kDa)similar to that in some neurodegenerative animal models.Conclusion:DXM can modify the cell composition of the normal mouse brain tissue by decreasing microglial cells and increasing astrocytes.Long-term use of DXM results in the inhibition of myelin formation and the appearance of truncated GFAP isoforms,suggesting its ability to induce neurodegeneration-like changes in the normal mouse brain.展开更多
Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables th...Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables this dynamic is the white matter(WM),known to be affected in neurodevelopmental disorders(NDDs)(Rokach et al.,2024).WM formation is mediated by myelination,a multifactorial process driven by neuro-glia interactions dependent on proper neuronal functionality(Simons and Trajkovic,2006).Another key aspect of neurodevelopmental abnormalities involves neuronal dynamics and function,with recent advances significantly enhancing our understanding of both neuronal and glial mitochondrial function(Devine and Kittler,2018;Rojas-Charry et al.,2021).Energy homeostasis in neurons,attributed largely to mitochondrial function,is critical for proper functionality and interactions with oligodendrocytes(OLs),the cells forming myelin in the brain’s WM.We herein discuss the interplay between these processes and speculate on potential dysfunction in NDDs.展开更多
This paper provides an overview of autoimmune disorders of the central nervous system,specifically those caused by demyelination.We explore new research regarding potential therapeutic interventions,particularly those...This paper provides an overview of autoimmune disorders of the central nervous system,specifically those caused by demyelination.We explore new research regarding potential therapeutic interventions,particularly those aimed at inducing remyelination.Remyelination is a detailed process,involving many cell types–oligodendrocyte precursor cells(OPCs),astrocytes,and microglia–and both the innate and adaptive immune systems.Our discussion of this process includes the differentiation potential of neural stem cells,the function of adult OPCs,and the impact of molecular mediators on myelin repair.Emerging therapies are also explored,with mechanisms of action including the induction of OPC differentiation,the transplantation of mesenchymal stem cells,and the use of molecular mediators.Further,we discuss current medical advancements in relation to many myelin-related disorders,including multiple sclerosis,optic neuritis,neuromyelitis optica spectrum disorder,myelin oligodendrocyte glycoprotein antibodyassociated disease,transverse myelitis,and acute disseminated encephalomyelitis.Beyond these emerging systemic therapies,we also introduce the dimethyl fumarate/silk fibroin nerve conduit and its potential role in the treatment of peripheral nerve injuries.Despite these aforementioned scientific advancements,this paper maintains the need for ongoing research to deepen our understanding of demyelinating diseases and advance therapeutic strategies that enhance affected patients’quality of life.展开更多
Astrocytes are indispensable for central nervous system development and homeostasis.In response to injury and disease,astrocytes are integral to the immunological-and the,albeit limited,repair response.In this review,...Astrocytes are indispensable for central nervous system development and homeostasis.In response to injury and disease,astrocytes are integral to the immunological-and the,albeit limited,repair response.In this review,we will examine some of the functions reactive astrocytes play in the context of multiple sclerosis and related animal models.We will consider the heterogeneity or plasticity of astrocytes and the mechanisms by which they promote or mitigate demyelination.Finally,we will discuss a set of biomedical strategies that can stimulate astrocytes in their promyelinating response.展开更多
BACKGROUND Cases of myelin oligodendrocyte glycoprotein(MOG)antibody-related disease have a history of coronavirus disease 2019 infection or its vaccination before disease onset.Severe acute respiratory syndrome virus...BACKGROUND Cases of myelin oligodendrocyte glycoprotein(MOG)antibody-related disease have a history of coronavirus disease 2019 infection or its vaccination before disease onset.Severe acute respiratory syndrome virus 2(SARS-CoV-2)infection has been considered to be a trigger of central nervous system autoimmune diseases.CASE SUMMARY Here we report a 20-year male with MOG-associated transverse myelitis after a SARS-CoV-2 infection.The patient received a near-complete recovery after standard immunological treatments.CONCLUSION Attention should be paid to the evaluation of typical or atypical neurological symptoms that may be triggered by SARS-CoV-2 infection.展开更多
基金supported by KU Leuven Internal Funding(C3/21/012)the Research Foundation Flanders(FWO G092222N)(to LM)。
文摘Decades of research asserted that the oligodendroglial lineage comprises two cell types:oligodendrocyte precursor cells and oligodendrocytes.However,recent studies employing single-cell RNA sequencing techniques have uncovered novel cell states,prompting a revision of the existing terminology.Going forward,the oligodendroglial lineage should be delineated into five distinct cell states:oligodendrocyte precursor cells,committed oligodendrocyte precursor cells,newly formed oligodendrocytes,myelin-forming oligodendrocytes,and mature oligodendrocytes.This new classification system enables a deeper understanding of the oligodendroglia in both physiological and pathological contexts.Adopting this uniform terminology will facilitate comparison and integration of data across studies.This,including the consolidation of findings from various demyelinating models,is essential to better understand the pathogenesis of demyelinating diseases.Additionally,comparing injury models across species with varying regenerative capacities can provide insights that may lead to new therapeutic strategies to overcome remyelination failure.Thus,by standardizing terminology and synthesizing data from diverse studies across different animal models,we can enhance our understanding of myelin pathology in central nervous system disorders such as multiple sclerosis,Alzheimer's disease,and amyotrophic lateral sclerosis,all of which involve oligodendroglial and myelin dysfunction.
基金financially supported by the National Natural Science Foundation of China,Nos.82172104(to CX),81873767(to HZ)a grant from Jiangsu Provincial Research Hospital,Nos.YJXYY202204(to HZ),YJXYY202204-ZD04(to HZ)+5 种基金a grant from Jiangsu Provincial Key Medical CenterJiangsu Provincial Medical Innovation Center,No.CXZX202212Jiangsu Provincial Medical Key Discipline,No.ZDXK202240the Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD)Technology Project of Nantong,No.MS22022008(to HZ)Postgraduate Research&Practice Innovation Program of Jiangsu Province,No.SJCX21_1457(to WW)。
文摘Demyelination and remyelination have been major focal points in the study of peripheral nerve regeneration following peripheral nerve injury.Notably,the gene regulatory network of regenerated myelin differs from that of native myelin.Silencing of enhancer of zeste homolog 2(EZH2)hinders the differentiation,maturation,and myelination of Schwann cells in vitro.To further determine the role of EZH2 in myelination and recovery post-peripheral nerve injury,conditional knockout mice lacking Ezh2 in Schwann cells(Ezh2^(fl/fl);Dhh-Cre and Ezh2^(fl/fl);Mpz-Cre)were generated.Our results show that a significant proportion of axons in the sciatic nerve of Ezh2-depleted mice remain unmyelinated.This highlights the crucial role of Ezh2 in initiating Schwann cell myelination.Furthermore,we observed that 21 days after inducing a sciatic nerve crush injury in these mice,most axons had remyelinated at the injury site in the control nerve,while Ezh2^(fl/fl);Mpz-Cre mice had significantly fewer remyelinated axons compared with their wild-type littermates.This suggests that the absence of Ezh2 in Schwann cells impairs myelin formation and remyelination.In conclusion,EZH2 has emerged as a pivotal regulatory factor in the process of demyelination and myelin regeneration following peripheral nerve injury.Modulating EZH2 activity during these processes may offer a promising therapeutic target for the treatment of peripheral nerve injuries.
基金supported by the National Natural Science Foundation of China,Nos.82271411(to RG),51803072(to WL)the International Cooperative Project of Talent Cultivation“Xinghai Project”at the China-Japan Union Hospital of Jilin University,No.XHLH202404(to WL)+1 种基金the Science and Technology Development Plan of Jilin Province,No.YDZJ202201ZYTS038(to WL)Jilin Provincial Finance Program,No.2022SCZ10(to WL)。
文摘Traumatic spinal cord injury often leads to the disintegration of nerve cells and axons,resulting in a substantial accumulation of myelin debris that can persist for years.The abnormal buildup of myelin debris at sites of injury greatly impedes nerve regeneration,making the clearance of debris within these microenvironments crucial for effective post-spinal cord injury repair.In this review,we comprehensively outline the mechanisms that promote the clearance of myelin debris and myelin metabolism and summarize their roles in spinal cord injury.First,we describe the composition and characteristics of myelin debris and explain its effects on the injury site.Next,we introduce the phagocytic cells involved in myelin debris clearance,including professional phagocytes(macrophages and microglia)and non-professional phagocytes(astrocytes and microvascular endothelial cells),as well as other cells that are also proposed to participate in phagocytosis.Finally,we focus on the pathways and associated targets that enhance myelin debris clearance by phagocytes and promote lipid metabolism following spinal cord injury.Our analysis indicates that myelin debris phagocytosis is not limited to monocyte-derived macrophages,but also involves microglia,astrocytes,and microvascular endothelial cells.By modulating the expression of genes related to phagocytosis and lipid metabolism,it is possible to modulate lipid metabolism disorders and influence inflammatory phenotypes,ultimately affecting the recovery of motor function following spinal cord injury.Additionally,therapies such as targeted mitochondrial transplantation in phagocytic cells,exosome therapy,and repeated trans-spinal magnetic stimulation can effectively enhance the removal of myelin debris,presenting promising potential for future applications.
基金supported by grants from Guangdong Basic and Applied Basic Research Foundation,No.2021A1515110801(to SW)the National Natural Science Foundation of China,No.82301511(to SW)+1 种基金“Double First-Class”Construction Project of NPU,Nos.0515023GH0202320(to JC),0515023SH0201320(to JC)973 Program,No.2011CB504100(to JC).
文摘Myelination,the continuous ensheathment of neuronal axons,is a lifelong process in the nervous system that is essential for the precise,temporospatial conduction of action potentials between neurons.Myelin also provides intercellular metabolic support to axons.Even minor disruptions in the integrity of myelin can impair neural performance and increase susceptibility to neurological diseases.In fact,myelin degeneration is a well-known neuropathological condition that is associated with normal aging and several neurodegenerative diseases,including multiple sclerosis and Alzheimer’s disease.In the central nervous system,compact myelin sheaths are formed by fully mature oligodendrocytes.However,the entire oligodendrocyte lineage is susceptible to changes in the biological microenvironment and other risk factors that arise as the brain ages.In addition to their well-known role in action potential propagation,oligodendrocytes also provide intercellular metabolic support to axons by transferring energy metabolites and delivering exosomes.Therefore,myelin degeneration in the aging central nervous system is a significant contributor to the development of neurodegenerative diseases.Interventions that mitigate age-related myelin degeneration can improve neurological function in aging individuals.In this review,we investigate the changes in myelin that are associated with aging and their underlying mechanisms.We also discuss recent advances in understanding how myelin degeneration in the aging brain contributes to neurodegenerative diseases and explore the factors that can prevent,slow down,or even reverse age-related myelin degeneration.Future research will enhance our understanding of how reducing age-related myelin degeneration can be used as a therapeutic target for delaying or preventing neurodegenerative diseases.
基金supported by the STI2030-Major Projects(2021ZD0204001)the National Natural Science Foundation of China(92049120,81870897,81271424,81671111,and 62475179)+8 种基金the Sino German Cooperation and Exchange Project(M-0679)the Guangdong Key Project in the Development of New Tools for the Diagnosis and Treatment of Autism(2018B030335001)the Natural Science Foundation of Jiangsu Province(BK20181436)the Priority Academic Program Development of Jiangsu Higher Education Institutions,the Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases(BM2013003)Suzhou International Joint Laboratory for Diagnosis and Treatment of Brain Diseases,Suzhou Science and Technology Plan Medical and Health Care Science and Technology Innovation Applied Basic Research(SKY2022161)the Research Project of Neurological Diseases in the Second Affiliated Hospital of Soochow University Research Center(ND2023A01)Boxi clinical research project of The First Affiliated Hospital of Soochow University(BXQN202204)Suzhou Science&Technology Projects for People's Livelihood(SKY2021065)Wuxi Municipal Health Commission(M202204).
文摘Oligodendrocyte lineage cells, including oligodendrocyte precursor cells (OPCs) and oligodendrocytes (OLs), are essential in establishing and maintaining brain circuits. Autophagy is a conserved process that keeps the quality of organelles and proteostasis. The role of autophagy in oligodendrocyte lineage cells remains unclear. The present study shows that autophagy is required to maintain the number of OPCs/OLs and myelin integrity during brain aging. Inactivation of autophagy in oligodendrocyte lineage cells increases the number of OPCs/OLs in the developing brain while exaggerating the loss of OPCs/OLs with brain aging. Inactivation of autophagy in oligodendrocyte lineage cells impairs the turnover of myelin basic protein (MBP). It causes MBP to accumulate in the cytoplasm as multimeric aggregates and fails to be incorporated into integral myelin, which is associated with attenuated endocytic recycling. Inactivation of autophagy in oligodendrocyte lineage cells impairs myelin integrity and causes demyelination. Thus, this study shows autophagy is required to maintain myelin quality during aging by controlling the turnover of myelin components.
基金supported by the National Natural Science Foundation of China(No.U21A20400)the Natural Science Foundation of Beijing(No.8217153264)the Key Project of Beijing University of Chinese Medicine(No.2022-JYB-JBZR-004),China.
文摘Myelin formation is considered the last true“invention”in the evolution of vertebrate nervous system cell structure.The rapid jumping pulse propagation achieved by myelin enables the high conduction speed that is the basis of human movement,sensation,and cognitive function.As a key structure in the brain,white matter is the gathering place of myelin.However,with age,white matter-associated functions become abnormal and a large number of myelin sheaths undergo degenerative changes,causing serious neurological and cognitive disorders.Despite the extensive time and effort invested in exploring myelination and its functions,numerous unresolved issues and challenges persist.In-depth exploration of the functional role of myelin may bring new inspiration for the treatment of central nervous system(CNS)diseases and even mental illnesses.In this study,we conducted a comprehensive examination of the structure and key molecules of the myelin in the CNS,delving into its formation process.Specifically,we propose a new hypothesis regarding the source of power for myelin expansion in which membrane compaction may serve as a driving force for myelin extension.The implications of this hypothesis could provide valuable insights into the pathophysiology of diseases involving myelin malfunction and open new avenues for therapeutic intervention in myelin-related disorders.
文摘Myelin is an essential structure that facilitates rapid saltatory conduction in the nervous system.Discrepancies in myelin microstructure are a hallmark of numerous neurological disorders,rendering the assessment of myelin integrity and content an indispensable tool in clinical diagnostics and neuroscience research.Extensive research has been dedicated to scrutinizing its biochemical makeup and morphology under normal,pathological,and experimental conditions over the years.In this review,we present an updated summary of the myelin sheath's structure,composition,and developmental trajectory.We systematically enumerate and contrast eight prevalent myelin staining techniques across dimensions of sensitivity,specificity,and resolution,delving into their underlying staining principles.With an initial application of myelin histology on the mouse demyelination model,our review accentuates the accurate delineation of myelination and the microstructural analysis of the myelin sheath.Such insights are anticipated to significantly contribute to the evaluation and understanding of white matter pathologies.
基金supported by the National Natural Science Foundation of China,Nos.82071307(to HL),82271362(to HL),82171294(to JW),82371303(to JW),and 82301460(to PX)the Natural Science Foundation of Jiangsu Province,No.BK20211552(to HL)+1 种基金Suzhou Medical Technology Innovation Project-Clinical Frontier,No.SKY2022002(to ZY)the Science and Education Foundation for Health of Suzhou for Youth,No.KJXW2023001(to XL)。
文摘Differentiation of oligodendrocyte progenitor cells into mature myelin-forming oligodendrocytes contributes to remyelination.Failure of remyelination due to oligodendrocyte progenitor cell death can result in severe nerve damage.Ferroptosis is an iron-dependent form of regulated cell death caused by membrane rupture induced by lipid peroxidation,and plays an important role in the pathological process of ischemic stroke.However,there are few studies on oligodendrocyte progenitor cell ferroptosis.We analyzed transcriptome sequencing data from GEO databases and identified a role of ferroptosis in oligodendrocyte progenitor cell death and myelin injury after cerebral ischemia.Bioinformatics analysis suggested that perilipin-2(PLIN2)was involved in oligodendrocyte progenitor cell ferroptosis.PLIN2 is a lipid storage protein and a marker of hypoxia-sensitive lipid droplet accumulation.For further investigation,we established a mouse model of cerebral ischemia/reperfusion.We found significant myelin damage after cerebral ischemia,as well as oligodendrocyte progenitor cell death and increased lipid peroxidation levels around the infarct area.The ferroptosis inhibitor,ferrostatin-1,rescued oligodendrocyte progenitor cell death and subsequent myelin injury.We also found increased PLIN2 levels in the peri-infarct area that co-localized with oligodendrocyte progenitor cells.Plin2 knockdown rescued demyelination and improved neurological deficits.Our findings suggest that targeting PLIN2 to regulate oligodendrocyte progenitor cell ferroptosis may be a potential therapeutic strategy for rescuing myelin damage after cerebral ischemia.
基金supported by the Spanish“Plan Nacional de Investigación Científica,Desarrollo e Innovación Tecnológica,Ministerio de Economía y Competitividad(Instituto de Salud CarlosⅢ)”,Grant FIS PI20-0318 co-financed by“Fondo Europeo de Desarrollo Regional ERDF-FEDER European Union”Grant P18-RT-5059“Plan Andaluz de Investigación,Desarrollo e Innovación(PAIDI 2020),Consejería de Transformación Económica,Industria,Conocimiento y Universidades,Junta de Andalucía,Espana”(all to VC)Grant PPJIA202219“Ayudas del plan propio UGR 2022,Plan propio de investigación y transferencia,Universidad de Granada,Espana”(to JCA andóDGG)。
文摘The myelin sheath is a lipoprotein-rich,multilayered structure capable of increasing conduction velocity in central and peripheral myelinated nerve fibers.Due to the complex structure and composition of myelin,various histological techniques have been developed over the centuries to evaluate myelin under normal,pathological or experimental conditions.Today,methods to assess myelin integrity or content are key tools in both clinical diagnosis and neuroscience research.In this review,we provide an updated summary of the composition and structure of the myelin sheath and discuss some histological procedures,from tissue fixation and processing techniques to the most used and practical myelin histological staining methods.Considering the lipoprotein nature of myelin,the main features and technical details of the different available methods that can be used to evaluate the lipid or protein components of myelin are described,as well as the precise ultrastructural techniques.
基金supported by a grant from Aston University,Birmingham,UK (to DM)。
文摘Myelin is the protective sheath surrounding nerve fibers, and its damage(demyelination) occurs in many central nervous system(CNS) diseases, including multiple sclerosis(MS), traumatic injury, neurodegenerative diseases such as Alzheimer's disease, and mental disorders such as schizophrenia(Barateiro et al., 2016). Repair of damaged myelin sheaths(remyelination) often fails in MS, leading to neuronal loss and irreversible functional deficits.
基金supported by a grant from the French Multiple Sclerosis Society(ARSEP,Grant Number:R20163LL)(to AMG)。
文摘Multiple sclerosis(MS)is the most common chronic disease of the central nervous system(CNS)in young adults and represents the first cause of severe handicap,originally non-traumatic(Oh et al.,2018).MS is chara cterized by the infiltration of auto reactive lymphocytes specific to myelin through the blood-brain barrier,which results in the appearance of inflammatory demyelinating lesions caused by the death of the central nervous system myelinating cells,oligodendrocytes(Oh et al.,2018).There is a prevalence sexual with a ratio of three times more affected women than men.
文摘The rapidly aging population directly contributes to the increasing cases of neurological disorders.Due to the chronic progressive nature of neurodegeneration,numerous neurological conditions are considered“multifactorial”with systemic metabolic alterations.Even so,treatments for neurological disorders have remained unchanged for the past decades.Recently,metabolic drugs such as metformin and glucagon-like peptide 1 agonists have demonstrated promising health outcomes for neurodegeneration.
基金supported by the Natural Science Foundation of Beijing,No.7232279(to XW)the National Natural Science Foundation of China,No.U21A20400(to QW)Key Project of Beijing University of Chinese Medicine,Nos.2022-JYB-JBZR-004(to XW),2024-JYB-JBZD-043(to CL).
文摘Chronic cerebral hypoperfusion can lead to neuronal necrosis,trigger inflammatory responses,promote white matter damage,and ultimately result in cognitive impairment.Consequently,chronic cerebral hypoperfusion is an important factor influencing the onset and progression of vascular dementia.The myelin sheath is a critical component of white matter,and damage and repair of the white matter are closely linked to myelin sheath integrity.This article reviews the role of microglia in vascular dementia,focusing on their effects on myelin sheaths and the potential therapeutic implications.The findings suggest that ischemia and hypoxia cause disruption of the blood-brain barrier and activate microglia,which may worsen blood-brain barrier damage through the release of matrix-degrading enzymes.Microglia-mediated metabolic reprogramming is recognized as an important driver of inflammation.Damage to the blood-brain barrier and subsequent inflammation can lead to myelin injury and accelerate the progression of vascular dementia.Early activation of microglia is a protective response that contributes to the maintenance of blood-brain barrier integrity through sensing,debris-clearing,and defensive mechanisms.However,prolonged activation can trigger a shift in microglia toward the pro-inflammatory M1 phenotype,resulting in myelin damage and cognitive impairment.Triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells 1 have been identified as potential biomarkers for vascular dementia,as both are closely linked to cognitive decline.Although effective clinical treatments for myelin damage in the central nervous system are currently lacking,researchers are actively working to develop targeted therapies.Several drugs,including nimodipine,dopaminergic agents,simvastatin,biotin,and quetiapine,have been evaluated for clinical use in treating microglial and myelin damage.Future research will face challenges in developing targeted therapeutic strategies for vascular dementia,requiring further investigation into the timing,duration,and specific mechanisms of microglial activation,as well as the exploration of new drug combinations and additional therapeutic targets.
基金Supported by the National Natural Science Foundation of China,No.82300894.
文摘BACKGROUND Diabetes is associated with increased cognitive decline and dementia due to the loss of myelinated nerve fiber function,which is linked to oligodendrocyte dysfunction.The voltage-gated proton channel 1(Hv1)is important for the cellular proton extrusion machinery.However,its role in regulating diabetesinduced cognitive dysfunction is unclear.AIM To investigate the role of Hv1 in cognitive impairment induced by diabetes and its potential mechanisms,focusing on neuroinflammation,oligodendrocyte apoptosis,and axonal demyelination.METHODS A diabetes model was established by administering a high-fat diet and streptozotocin injections in mice.Hv1 knockout(KO)and wild-type mice were used to evaluate cognitive function via behavioral tests and neuroinflammation using immunofluorescence.Oligodendrocyte apoptosis was assessed with the terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling assay, and axonal demyelination wasanalyzed using electron microscopy.RESULTSHv1 expression was significantly increased in the corpus callosum of diabetic mice. Hv1 KO alleviated cognitiveimpairment, reduced oligodendrocyte apoptosis, and decreased the expression of inflammatory factors, includinginterleukin-1 and tumor necrosis factor-α, in diabetic mice. Electron microscopy revealed a reduction in myelinthickness and an increased g-ratio in diabetic mice, which were reversed by Hv1 KO.CONCLUSIONHv1 plays a role in diabetes-induced cognitive dysfunction by modulating neuroinflammation and myelinintegrity. Hv1 KO demonstrates therapeutic potential in mitigating diabetes-related cognitive decline andassociated complications.
文摘Dear Editor,Myelin oligodendrocyte glycoprotein(MOG)is a minor component of myelin,expressed on the external surface of oligodendrocytes in the central nervous system(CNS)[1].Anti-MOG antibodies(MOG-ab)have been implicated in the demyelinating process and are considered unique biomarkers for a group of heterogeneous autoimmune inflammatory CNS diseases known as MOG-associated disorder(MOGAD)[1].MOGAD can present with a range of clinical manifestations,including optic neuritis,transverse myelitis,acute disseminating encephalomyelitis,and brainstem or cerebral encephalitis[1].Optic neuritis is the most common clinical feature of MOGAD in adults,typically manifesting as steroid-sensitive,recurrent,bilateral optic neuritis with optic disc swelling[1].
基金funded by the budgetary funding to FRC FTM for the project“Post-Genomic High-Tech Research on the Mechanisms of Development of Socially Significant Diseases and Stress-Induced Conditions”(Grant No.125031203556-7).
文摘Background:Glucocorticoids are used as anti-inflammatory drugs for the treatment of various diseases,however,their side effects on normal brain tissue remain underinvestigated.Objectives:The study aimed to investigate dexamethasone(DXM)effects on cell composition and myelin content in the mouse brain tissue.Methods:C57Bl/6 male mice(n 60)received single and ten multiple intraperitoneal DXM injections(2.5 mg/kg),and the studied=parameters were analysed at 1,3,7,10 days after a single DXM injection and 15,30,60,and 90 days after the multiple injections.Oligodendrocytes,microglia,and astrocytes were assayed by immunohistochemistry with specific antibodies(Olig2,CD68,and GFAP,respectively)in the corpus callosum of the normal brain tissue.The myelin content was estimated by staining with LuxolFastBlue.The presence of GFAP isoforms was determined by western blotting.Results:DXM administration did not affect oligodendrocytes in the mouse brain but temporarily significantly decreased myelin content(1.2-fold,p 0.0058;1.4-fold,p 0.0001)at 3–15 days time points.At the same time,DXM significantly=<decreased the number of microglial cells(1.5–3.5-fold,p 0.0001)and significantly increased astrocytes(1.8-fold,p<<0.0001).Prolonged administration of DXM resulted in the decrease of the main GFAPα-isoform(50 kDa)and the appearance of shorter GFAP isoforms(30 kDa,42 kDa,44 kDa)similar to that in some neurodegenerative animal models.Conclusion:DXM can modify the cell composition of the normal mouse brain tissue by decreasing microglial cells and increasing astrocytes.Long-term use of DXM results in the inhibition of myelin formation and the appearance of truncated GFAP isoforms,suggesting its ability to induce neurodegeneration-like changes in the normal mouse brain.
文摘Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables this dynamic is the white matter(WM),known to be affected in neurodevelopmental disorders(NDDs)(Rokach et al.,2024).WM formation is mediated by myelination,a multifactorial process driven by neuro-glia interactions dependent on proper neuronal functionality(Simons and Trajkovic,2006).Another key aspect of neurodevelopmental abnormalities involves neuronal dynamics and function,with recent advances significantly enhancing our understanding of both neuronal and glial mitochondrial function(Devine and Kittler,2018;Rojas-Charry et al.,2021).Energy homeostasis in neurons,attributed largely to mitochondrial function,is critical for proper functionality and interactions with oligodendrocytes(OLs),the cells forming myelin in the brain’s WM.We herein discuss the interplay between these processes and speculate on potential dysfunction in NDDs.
文摘This paper provides an overview of autoimmune disorders of the central nervous system,specifically those caused by demyelination.We explore new research regarding potential therapeutic interventions,particularly those aimed at inducing remyelination.Remyelination is a detailed process,involving many cell types–oligodendrocyte precursor cells(OPCs),astrocytes,and microglia–and both the innate and adaptive immune systems.Our discussion of this process includes the differentiation potential of neural stem cells,the function of adult OPCs,and the impact of molecular mediators on myelin repair.Emerging therapies are also explored,with mechanisms of action including the induction of OPC differentiation,the transplantation of mesenchymal stem cells,and the use of molecular mediators.Further,we discuss current medical advancements in relation to many myelin-related disorders,including multiple sclerosis,optic neuritis,neuromyelitis optica spectrum disorder,myelin oligodendrocyte glycoprotein antibodyassociated disease,transverse myelitis,and acute disseminated encephalomyelitis.Beyond these emerging systemic therapies,we also introduce the dimethyl fumarate/silk fibroin nerve conduit and its potential role in the treatment of peripheral nerve injuries.Despite these aforementioned scientific advancements,this paper maintains the need for ongoing research to deepen our understanding of demyelinating diseases and advance therapeutic strategies that enhance affected patients’quality of life.
基金supported by the Heart and Stroke Foundation and Ontario Institute of Regenerative Medicine (New Ideas Grant)Canada First Research Excellence Fund(Medicine by Design)+2 种基金the National Sciences and Engineering Research Councilthe Jurgen Manchot Foundationthe Christiane and Claudia Hempel Foundation for Clinical Stem Cell Research and the James and Elisabeth Cloppenburg,Peek and Cloppenburg Düsseldorf Stiftung (to PK)
文摘Astrocytes are indispensable for central nervous system development and homeostasis.In response to injury and disease,astrocytes are integral to the immunological-and the,albeit limited,repair response.In this review,we will examine some of the functions reactive astrocytes play in the context of multiple sclerosis and related animal models.We will consider the heterogeneity or plasticity of astrocytes and the mechanisms by which they promote or mitigate demyelination.Finally,we will discuss a set of biomedical strategies that can stimulate astrocytes in their promyelinating response.
基金Supported by the Shenzhen University Teaching Reform Fund,No.JG2023166the Shenzhen Science and Technology Innovation Commission Fund,No.JCYJ2022081802810022the Shenzhen Science and Technology Innovation Commission Basic Research Key Projects Fund,No.JCYJ20210324115800003.
文摘BACKGROUND Cases of myelin oligodendrocyte glycoprotein(MOG)antibody-related disease have a history of coronavirus disease 2019 infection or its vaccination before disease onset.Severe acute respiratory syndrome virus 2(SARS-CoV-2)infection has been considered to be a trigger of central nervous system autoimmune diseases.CASE SUMMARY Here we report a 20-year male with MOG-associated transverse myelitis after a SARS-CoV-2 infection.The patient received a near-complete recovery after standard immunological treatments.CONCLUSION Attention should be paid to the evaluation of typical or atypical neurological symptoms that may be triggered by SARS-CoV-2 infection.
