Pub Date : 2023-05-22DOI: 10.1212/nxi.0000000000200136
Josep O. Dalmau
The success of Neurology® Neuroimmunology & Neuroinflammation derives from the publication of excellent manuscripts which requires the time and effort of our reviewers. Their thoughtful comments on clinical trials, experimental research, and novel methodologies or techniques are critical to that success. We appreciate their dedication to the journal and their commitment to excellence.
{"title":"Acknowledgment to Reviewers","authors":"Josep O. Dalmau","doi":"10.1212/nxi.0000000000200136","DOIUrl":"https://doi.org/10.1212/nxi.0000000000200136","url":null,"abstract":"The success of Neurology® Neuroimmunology & Neuroinflammation derives from the publication of excellent manuscripts which requires the time and effort of our reviewers. Their thoughtful comments on clinical trials, experimental research, and novel methodologies or techniques are critical to that success. We appreciate their dedication to the journal and their commitment to excellence.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135380589","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}
Pub Date : 2021-07-13DOI: 10.20517/2347-8659.2021.05
Tiffany C. Miller, S. Morgera, S. Saddow, A. Takshi, M. Mullarkey, Matthew Palm
{"title":"Neurological connections and endogenous biochemistry - potentially useful in electronic-nose diagnostics for coronavirus diseases","authors":"Tiffany C. Miller, S. Morgera, S. Saddow, A. Takshi, M. Mullarkey, Matthew Palm","doi":"10.20517/2347-8659.2021.05","DOIUrl":"https://doi.org/10.20517/2347-8659.2021.05","url":null,"abstract":"","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43611992","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}
Pub Date : 2021-03-18DOI: 10.20517/2347-8659.2021.01
Rosella Mechelli, C. Romano, R. Reniè, Grazia Manfrè, M. C. Buscarinu, S. Romano, A. Marrone, R. Bigi, Gianmarco Bellucci, C. Ballerini, Benedetta Angeloni, Virginia Rinaldi, M. Salvetti, G. Ristori
Rosella Mechelli, Carmela Romano, Roberta Reniè, Grazia Manfrè, Maria Chiara Buscarinu, Silvia Romano, Antonio Marrone, Rachele Bigi, Gianmarco Bellucci, Chiara Ballerini, Benedetta Angeloni, Virginia Rinaldi, Marco Salvetti, Giovanni Ristori Department of Human science and promotion of quality of life, San Raffaele Roma Open University, Rome 00166, Italy. IRCCS San Raffaele Pisana, Rome 00166, Italy. Centre for Experimental Neurological Therapies (CENTERS), Department of Neurosciences, Mental Health and Sensory Organs, Sapienza University of Rome, Rome 00189, Italy. IRCCS Istituto Neurologico Mediterraneo (INM) Neuromed, Pozzilli 86077, Italy. Neuroimmunology Unit, IRCCS Fondazione Santa Lucia, Rome, 00179, Italy.
{"title":"Viruses and neuroinflammation in multiple sclerosis","authors":"Rosella Mechelli, C. Romano, R. Reniè, Grazia Manfrè, M. C. Buscarinu, S. Romano, A. Marrone, R. Bigi, Gianmarco Bellucci, C. Ballerini, Benedetta Angeloni, Virginia Rinaldi, M. Salvetti, G. Ristori","doi":"10.20517/2347-8659.2021.01","DOIUrl":"https://doi.org/10.20517/2347-8659.2021.01","url":null,"abstract":"Rosella Mechelli, Carmela Romano, Roberta Reniè, Grazia Manfrè, Maria Chiara Buscarinu, Silvia Romano, Antonio Marrone, Rachele Bigi, Gianmarco Bellucci, Chiara Ballerini, Benedetta Angeloni, Virginia Rinaldi, Marco Salvetti, Giovanni Ristori Department of Human science and promotion of quality of life, San Raffaele Roma Open University, Rome 00166, Italy. IRCCS San Raffaele Pisana, Rome 00166, Italy. Centre for Experimental Neurological Therapies (CENTERS), Department of Neurosciences, Mental Health and Sensory Organs, Sapienza University of Rome, Rome 00189, Italy. IRCCS Istituto Neurologico Mediterraneo (INM) Neuromed, Pozzilli 86077, Italy. Neuroimmunology Unit, IRCCS Fondazione Santa Lucia, Rome, 00179, Italy.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43098692","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}
Pub Date : 2021-02-09DOI: 10.20517/2347-8659.2020.63
Rehab A. Ismaeil, C. K. Hui, K. Affandi, Batoul Alallam, Wael M. Y. Mohamed, M. Noor
Aim: Alzheimer’s disease (AD) is marked by insufficient blood supply to the brain, leading to progressive loss of memory and cognitive skills. The continuous reduction of cerebral blood flow resulting from chronic cerebral hypoperfusion leads to the overproduction of reactive oxygen species that triggers inflammation, causing cognitive decline. Till now, there is no cure for AD and the only option is symptomatic treatment. The current study evaluates the effect of edible bird’s nest (EBN) on hippocampal neurons, specifically in the CA1 hippocampal region, by using a rat model of chronic cerebral hypoperfusion-induced neuroinflammation. Methods: Chronic cerebral hypoperfusion (CCH) was induced by permanent bilateral common carotid artery occlusion (2VO) in rats to trigger the neuroinflammatory process. Rats were divided into 4 groups: sham, 2VO, and two 2VO groups treated with two different doses (60 mg/kg, 120 mg/kg) of EBN, which was administered daily by oral gavage. After 8 consecutive weeks, rats were euthanized and the hippocampi were examined histopathologically by counting viable neuronal cells and the levels of F2Isoprostane in hippocampal tissue was
{"title":"Neuroprotective effect of edible bird’s nest in chronic cerebral hypoperfusion induced neurodegeneration in rats","authors":"Rehab A. Ismaeil, C. K. Hui, K. Affandi, Batoul Alallam, Wael M. Y. Mohamed, M. Noor","doi":"10.20517/2347-8659.2020.63","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.63","url":null,"abstract":"Aim: Alzheimer’s disease (AD) is marked by insufficient blood supply to the brain, leading to progressive loss of memory and cognitive skills. The continuous reduction of cerebral blood flow resulting from chronic cerebral hypoperfusion leads to the overproduction of reactive oxygen species that triggers inflammation, causing cognitive decline. Till now, there is no cure for AD and the only option is symptomatic treatment. The current study evaluates the effect of edible bird’s nest (EBN) on hippocampal neurons, specifically in the CA1 hippocampal region, by using a rat model of chronic cerebral hypoperfusion-induced neuroinflammation. Methods: Chronic cerebral hypoperfusion (CCH) was induced by permanent bilateral common carotid artery occlusion (2VO) in rats to trigger the neuroinflammatory process. Rats were divided into 4 groups: sham, 2VO, and two 2VO groups treated with two different doses (60 mg/kg, 120 mg/kg) of EBN, which was administered daily by oral gavage. After 8 consecutive weeks, rats were euthanized and the hippocampi were examined histopathologically by counting viable neuronal cells and the levels of F2Isoprostane in hippocampal tissue was","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48141804","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}
Pub Date : 2021-02-09DOI: 10.20517/2347-8659.2020.60
A. Hodges, T. Piers, David Collier, Oliver Cousins, J. Pocock
Microglia in the brain are exquisitely vigilant to their surroundings. They are dispersed throughout the brain parenchyma where they continually receive and integrate large numbers of incoming signals. They become activated once a tightly controlled signalling threshold is reached. This can lead to a cascade of cellular and molecular changes culminating in the recognition and engulfment of self and non-self structures ranging from macromolecules to whole cells depending on the initiating signal. Once internalised, they digest and where appropriate, present antigens to aid future recognition of pathogens. Their response to pathogenic signals in diseases such as Alzheimer’s disease (AD) has long been recognised, but recent genetic findings have cemented their direct causal contribution to AD and thus the potential to target them or their effector pathways as a possible treatment strategy. Around 25% of the ~84 AD risk genes have enriched or exclusive expression in microglia and/or are linked to immune function*. Ongoing work suggests many of these genes connect within important microglial molecular networks as ligand activators ( IL34 ), immune receptors ( TREM2, MS4A4A, HLA-DQA1 & CD33 ), signalling intermediates ( PLCG2 , PTK2B & INPP5D) or effector mechanisms (ABI3 & EPHA1 ). In some cases, evidence links them to specific core pathogenic immune responses and cell mechanisms such as complement (CR1 & CLU) or cytoskeletal machinery ( ABI3 , EPHA1 and FERMT2 ). However, more work is needed to establish whether these risk variants lead to gain or loss of protein function and to connect them to other genes within effector pathways and downstream cell processes which themselves could be tractable targets for treatment development. Brain tissue analysis and cell models of genetic risk carriers will help enormously to
{"title":"Pathways linking Alzheimer’s disease risk genes expressed highly in microglia","authors":"A. Hodges, T. Piers, David Collier, Oliver Cousins, J. Pocock","doi":"10.20517/2347-8659.2020.60","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.60","url":null,"abstract":"Microglia in the brain are exquisitely vigilant to their surroundings. They are dispersed throughout the brain parenchyma where they continually receive and integrate large numbers of incoming signals. They become activated once a tightly controlled signalling threshold is reached. This can lead to a cascade of cellular and molecular changes culminating in the recognition and engulfment of self and non-self structures ranging from macromolecules to whole cells depending on the initiating signal. Once internalised, they digest and where appropriate, present antigens to aid future recognition of pathogens. Their response to pathogenic signals in diseases such as Alzheimer’s disease (AD) has long been recognised, but recent genetic findings have cemented their direct causal contribution to AD and thus the potential to target them or their effector pathways as a possible treatment strategy. Around 25% of the ~84 AD risk genes have enriched or exclusive expression in microglia and/or are linked to immune function*. Ongoing work suggests many of these genes connect within important microglial molecular networks as ligand activators ( IL34 ), immune receptors ( TREM2, MS4A4A, HLA-DQA1 & CD33 ), signalling intermediates ( PLCG2 , PTK2B & INPP5D) or effector mechanisms (ABI3 & EPHA1 ). In some cases, evidence links them to specific core pathogenic immune responses and cell mechanisms such as complement (CR1 & CLU) or cytoskeletal machinery ( ABI3 , EPHA1 and FERMT2 ). However, more work is needed to establish whether these risk variants lead to gain or loss of protein function and to connect them to other genes within effector pathways and downstream cell processes which themselves could be tractable targets for treatment development. Brain tissue analysis and cell models of genetic risk carriers will help enormously to","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43943425","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}
Pub Date : 2021-01-25DOI: 10.20517/2347-8659.2020.58
Tori K. Lee, Eva L. Yankee
Parkinson’s disease (PD) is a neurodegenerative illness and has a common onset between the ages of 55 and 65 years. There is progressive development of both motor and non-motor symptoms, greatly affecting one’s overall quality of life. While there is no cure, various treatments have been developed to help manage the symptoms of PD. Management of PD is a growing field and targets new treatment methods, as well as improvements to old ones. Pharmacological, surgical, and therapeutic treatments have allowed physicians to treat not only the main motor symptoms of PD, but target patient-specific problems as they arise. This review discusses both the established and new possibilities for PD treatment that can provide patient-specific care and mitigate side effects for common treatments.
{"title":"A review on Parkinson’s disease treatment","authors":"Tori K. Lee, Eva L. Yankee","doi":"10.20517/2347-8659.2020.58","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.58","url":null,"abstract":"Parkinson’s disease (PD) is a neurodegenerative illness and has a common onset between the ages of 55 and 65 years. There is progressive development of both motor and non-motor symptoms, greatly affecting one’s overall quality of life. While there is no cure, various treatments have been developed to help manage the symptoms of PD. Management of PD is a growing field and targets new treatment methods, as well as improvements to old ones. Pharmacological, surgical, and therapeutic treatments have allowed physicians to treat not only the main motor symptoms of PD, but target patient-specific problems as they arise. This review discusses both the established and new possibilities for PD treatment that can provide patient-specific care and mitigate side effects for common treatments.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45882609","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}
Pub Date : 2021-01-15DOI: 10.20517/2347-8659.2020.57
Chianna Umamahesan, Aisha D. Augustin, B. Hayee, M. Ibrahim, David Taylor, C. Weller, A. Charlett, R. Dobbs, S. Dobbs
Aim: To address how common are intestinal inflammation and compromised barrier function in idiopathic parkinsonism (IP), any potential treatment benefits, outcome of not treating, and whether screening is worthwhile. This may provide the missing link between systemic/brain inflammation in IP and implicated gastrointestinal microbiota/specific pathogens. Methods: Search strategy was based on PRISMA guidelines. Fifteen of the 1395 articles (1995-2020) identified met the inclusion criteria. Seven gave results on more than one intestinal modality: inflammation, permeability, integrity, and bacterial translocation. Results: The inter-relationship of IP with intestinal inflammation and bacterial translocation is firmly established, lacking only random sample surveys to meet Level-1 Oxford Centre for Evidence-Based Medicine evidence. Evidence for reduced integrity is limited to 2 small studies of tight-junction proteins in colonic biopsies. No overall conclusion can be drawn from studies of faecal and circulating markers of integrity: evidence based on an assay that recognizes wider zonulin family, not the specific peptide exclusively, was censored. Evidence for increased permeability is Page 2 Umamahesan et al. Neuroimmunol Neuroinflammation 2021;8:[Online First] I http://dx.doi.org/10.20517/2347-8659.2020.57 insubstantial: further work is needed in IP with and without small-intestinal-bacterial-overgrowth and including a non-fermentable sugar absorption test. Concentrations of markers of intestinal inflammation (faecal calprotectin) and bacterial translocation (circulating lipopolysaccharide-binding protein) appear not to change with time-sincediagnosis or IP severity. This is compatible with a pre-presentation insult. There are no longitudinal studies on inflammation or translocation to guide design of interventional studies. Neither are cut-points discriminant for IPfacets, or gradients prognostic for its evolution, defined. Conclusion: Intestinal inflammation and barrier function is a strategic junctional point in the hypothesis for the aetipathogenesis of IP.
目的:探讨肠道炎症和屏障功能受损在特发性帕金森病(IP)中有多常见，任何潜在的治疗益处，不治疗的结果，以及筛查是否值得。这可能提供了IP中全身性/脑部炎症与相关胃肠道微生物群/特定病原体之间缺失的联系。方法:检索策略基于PRISMA指南。确定的1395篇文章(1995-2020)中有15篇符合纳入标准。其中7个给出了不止一种肠道形态的结果:炎症、通透性、完整性和细菌易位。结果:IP与肠道炎症和细菌易位之间的相互关系是明确的，仅缺乏随机抽样调查，以满足牛津循证医学中心的一级证据。完整性降低的证据仅限于结肠活检中紧密连接蛋白的2个小型研究。从粪便和循环完整性标记物的研究中无法得出总体结论:基于识别更广泛的zonulin家族而不是特定肽的检测的证据被删除。渗透率增加的证据见第2页Umamahesan等人。Neuroimmunol Neuroinflammation 2021;8:[Online First] I http://dx.doi.org/10.20517/2347-8659.2020.57不实质性:有或没有小肠-细菌-过度生长的IP需要进一步的工作，包括不可发酵糖吸收测试。肠道炎症标志物(粪便钙保护蛋白)和细菌易位(循环脂多糖结合蛋白)的浓度似乎不随诊断时间或IP严重程度而改变。这与演讲前的侮辱是一致的。没有关于炎症或易位的纵向研究来指导介入性研究的设计。对于ipfacet来说，切点并不是判别性的，对于ipfacet的演化，也没有定义梯度预测。结论:肠道炎症与屏障功能是IP发病机制假说的重要结合点。
{"title":"Intestinal inflammation and compromised barrier function in idiopathic parkinsonism: scenario captured by systematic review","authors":"Chianna Umamahesan, Aisha D. Augustin, B. Hayee, M. Ibrahim, David Taylor, C. Weller, A. Charlett, R. Dobbs, S. Dobbs","doi":"10.20517/2347-8659.2020.57","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.57","url":null,"abstract":"Aim: To address how common are intestinal inflammation and compromised barrier function in idiopathic parkinsonism (IP), any potential treatment benefits, outcome of not treating, and whether screening is worthwhile. This may provide the missing link between systemic/brain inflammation in IP and implicated gastrointestinal microbiota/specific pathogens. Methods: Search strategy was based on PRISMA guidelines. Fifteen of the 1395 articles (1995-2020) identified met the inclusion criteria. Seven gave results on more than one intestinal modality: inflammation, permeability, integrity, and bacterial translocation. Results: The inter-relationship of IP with intestinal inflammation and bacterial translocation is firmly established, lacking only random sample surveys to meet Level-1 Oxford Centre for Evidence-Based Medicine evidence. Evidence for reduced integrity is limited to 2 small studies of tight-junction proteins in colonic biopsies. No overall conclusion can be drawn from studies of faecal and circulating markers of integrity: evidence based on an assay that recognizes wider zonulin family, not the specific peptide exclusively, was censored. Evidence for increased permeability is Page 2 Umamahesan et al. Neuroimmunol Neuroinflammation 2021;8:[Online First] I http://dx.doi.org/10.20517/2347-8659.2020.57 insubstantial: further work is needed in IP with and without small-intestinal-bacterial-overgrowth and including a non-fermentable sugar absorption test. Concentrations of markers of intestinal inflammation (faecal calprotectin) and bacterial translocation (circulating lipopolysaccharide-binding protein) appear not to change with time-sincediagnosis or IP severity. This is compatible with a pre-presentation insult. There are no longitudinal studies on inflammation or translocation to guide design of interventional studies. Neither are cut-points discriminant for IPfacets, or gradients prognostic for its evolution, defined. Conclusion: Intestinal inflammation and barrier function is a strategic junctional point in the hypothesis for the aetipathogenesis of IP.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44714876","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}
Pub Date : 2021-01-01Epub Date: 2021-03-21DOI: 10.20517/2347-8659.2020.34
Nadia Al-Sammarraie, Swapan K Ray
Spinal cord injury (SCI) is a debilitating injury that results from traumatic or non-traumatic insults to the spinal cord, causing significant impairment of the patient's activity and quality of life. Bone morphogenic proteins (BMPs) are a group of polyfunctional cytokines belonging to the transforming growth factor beta superfamily that regulates a wide variety of cellular functions in healthy and disease states. Recent studies suggest that dysregulation of BMP signaling is involved in neuronal demyelination and death after traumatic SCI. The focus of this article is to describe our current understanding of the role of BMP signaling in the regulation of cell fate, proliferation, apoptosis, autophagy, and inflammation in traumatic SCI. First, we will describe the expression of BMPs and pattern of BMP signaling before and after traumatic SCI in rodent models and in vitro. Next, we will discuss the role of BMP in the regulation of neuronal and glial cell differentiation, survival, functional recovery from traumatic SCI, and the gap in knowledge in this area that requires further investigation to improve SCI prognosis.
{"title":"Bone morphogenic protein signaling in spinal cord injury.","authors":"Nadia Al-Sammarraie, Swapan K Ray","doi":"10.20517/2347-8659.2020.34","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.34","url":null,"abstract":"<p><p>Spinal cord injury (SCI) is a debilitating injury that results from traumatic or non-traumatic insults to the spinal cord, causing significant impairment of the patient's activity and quality of life. Bone morphogenic proteins (BMPs) are a group of polyfunctional cytokines belonging to the transforming growth factor beta superfamily that regulates a wide variety of cellular functions in healthy and disease states. Recent studies suggest that dysregulation of BMP signaling is involved in neuronal demyelination and death after traumatic SCI. The focus of this article is to describe our current understanding of the role of BMP signaling in the regulation of cell fate, proliferation, apoptosis, autophagy, and inflammation in traumatic SCI. First, we will describe the expression of BMPs and pattern of BMP signaling before and after traumatic SCI in rodent models and <i>in vitro</i>. Next, we will discuss the role of BMP in the regulation of neuronal and glial cell differentiation, survival, functional recovery from traumatic SCI, and the gap in knowledge in this area that requires further investigation to improve SCI prognosis.</p>","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8052099/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38886055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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