Pub Date : 2020-11-18DOI: 10.20517/2347-8659.2020.54
C. Cordano, C. Ramos, S. Arnow, Andrés Cruz-Herranz, Caroline Guglielmetti, M. Iester, F. Bandini
{"title":"Inflammation in the anterior visual pathway in multiple sclerosis: what do the animal models teach us?","authors":"C. Cordano, C. Ramos, S. Arnow, Andrés Cruz-Herranz, Caroline Guglielmetti, M. Iester, F. Bandini","doi":"10.20517/2347-8659.2020.54","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.54","url":null,"abstract":"","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45027401","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 : 2020-11-13DOI: 10.20517/2347-8659.2020.49
Liesa Regner, B. Labeit, P. Muhle, T. Ruck, R. Dziewas, T. Warnecke, S. Suntrup-Krueger
Cranial nerve involvement is rarely seen in chronic inflammatory demyelinating polyneuropathy (CIDP). We present a patient diagnosed with CIDP who was in a stable medical condition under long-term treatment with intravenous immunoglobulin (IVIG) every five weeks for more than seven years. Following a 12-day delay in the patient’s regular IVIG therapy, he developed acute bilateral vocal cord palsy. The patient had to be intubated and tracheostomized because of acute respiratory distress. Weaning from mechanical ventilation was complicated due to pneumonia. After antibiotic treatment and restarting IVIG therapy vocal cord palsy rapidly improved allowing for subsequent decannulation. Although coincidence between treatment delay and symptom development does not prove definitive causality this case report may serve as a reminder how time critical IVIG therapy can be for sufficient symptom control. Moreover, it provides evidence that IVIG therapy may be effective for the treatment of cranial nerve symptoms in CIDP.
{"title":"Mind the gap: acute bilateral vocal cord palsy in CIDP after extending the IVIG treatment interval?","authors":"Liesa Regner, B. Labeit, P. Muhle, T. Ruck, R. Dziewas, T. Warnecke, S. Suntrup-Krueger","doi":"10.20517/2347-8659.2020.49","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.49","url":null,"abstract":"Cranial nerve involvement is rarely seen in chronic inflammatory demyelinating polyneuropathy (CIDP). We present a patient diagnosed with CIDP who was in a stable medical condition under long-term treatment with intravenous immunoglobulin (IVIG) every five weeks for more than seven years. Following a 12-day delay in the patient’s regular IVIG therapy, he developed acute bilateral vocal cord palsy. The patient had to be intubated and tracheostomized because of acute respiratory distress. Weaning from mechanical ventilation was complicated due to pneumonia. After antibiotic treatment and restarting IVIG therapy vocal cord palsy rapidly improved allowing for subsequent decannulation. Although coincidence between treatment delay and symptom development does not prove definitive causality this case report may serve as a reminder how time critical IVIG therapy can be for sufficient symptom control. Moreover, it provides evidence that IVIG therapy may be effective for the treatment of cranial nerve symptoms in CIDP.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43668393","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 : 2020-11-11DOI: 10.20517/2347-8659.2020.47
Berenice A Silva, Esteban A Miglietta, C. Ferrari
Multiple sclerosis (MS) is a neurodegenerative and inflammatory disease usually presenting with acute demyelinating events that can start as, or progress to, chronic damage. The development of animal experimental models, specific for each stage of MS will aid in the design of new drugs specific for the different forms of the disease. Animal models of experimental autoimmune encephalomyelitis successfully reflect the pathophysiological mechanisms of the early phases of MS. However, few models resemble the features of the progressive forms of MS such as cortical demyelination and meningeal inflammation. Recently, a few auspicious animal models recapitulating many of the characteristics of progressive MS, aimed at a better understanding of the pathology of these forms of the disease, have been developed. In this review, we will summarize the latest developments in animal models reflecting the cortical and meningeal pathological features of progressive MS, as well as their response to drugs specifically targeting these forms.
{"title":"Neuroinflammation in cortical and meningeal pathology in multiple sclerosis: understanding from animal models","authors":"Berenice A Silva, Esteban A Miglietta, C. Ferrari","doi":"10.20517/2347-8659.2020.47","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.47","url":null,"abstract":"Multiple sclerosis (MS) is a neurodegenerative and inflammatory disease usually presenting with acute demyelinating events that can start as, or progress to, chronic damage. The development of animal experimental models, specific for each stage of MS will aid in the design of new drugs specific for the different forms of the disease. Animal models of experimental autoimmune encephalomyelitis successfully reflect the pathophysiological mechanisms of the early phases of MS. However, few models resemble the features of the progressive forms of MS such as cortical demyelination and meningeal inflammation. Recently, a few auspicious animal models recapitulating many of the characteristics of progressive MS, aimed at a better understanding of the pathology of these forms of the disease, have been developed. In this review, we will summarize the latest developments in animal models reflecting the cortical and meningeal pathological features of progressive MS, as well as their response to drugs specifically targeting these forms.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45082455","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 : 2020-10-16DOI: 10.20517/2347-8659.2019.29
A. vonderEmbse, Q. Hu, J. DeWitt
Aim: The purpose of this study was to evaluate sex-biased, maladaptive changes to epigenetic regulation critical for development of neuroimmune crosstalk resulting from an early-life toxicant exposure previously associated with increased susceptibility to later-life neurodegeneration. Methods: An evaluation of early-life gene x environment (GxE) interactions was performed in a mouse model of Alzheimer’s disease (Tg) orally exposed to lead acetate (Pb) from postnatal day (PND) 5-9. Following exposure, immunohistochemical analysis was used to evaluate hippocampal expression of DAP12, a marker for perinatal microglia related to microglial-mediated postnatal synaptic pruning of neurons. Altered profiles of three microRNAs critical to homeostatic microglia: neuron signaling (miR-34a, miR-124, miR-132) were measured by
{"title":"Postnatal toxicant exposure in 3xTgAD mice promotes gene x environment-related early alterations to neuroimmune epigenetic profiles","authors":"A. vonderEmbse, Q. Hu, J. DeWitt","doi":"10.20517/2347-8659.2019.29","DOIUrl":"https://doi.org/10.20517/2347-8659.2019.29","url":null,"abstract":"Aim: The purpose of this study was to evaluate sex-biased, maladaptive changes to epigenetic regulation critical for development of neuroimmune crosstalk resulting from an early-life toxicant exposure previously associated with increased susceptibility to later-life neurodegeneration. Methods: An evaluation of early-life gene x environment (GxE) interactions was performed in a mouse model of Alzheimer’s disease (Tg) orally exposed to lead acetate (Pb) from postnatal day (PND) 5-9. Following exposure, immunohistochemical analysis was used to evaluate hippocampal expression of DAP12, a marker for perinatal microglia related to microglial-mediated postnatal synaptic pruning of neurons. Altered profiles of three microRNAs critical to homeostatic microglia: neuron signaling (miR-34a, miR-124, miR-132) were measured by","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47400545","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 : 2020-10-16DOI: 10.20517/2347-8659.2020.41
V. Mundula, Anna Stainer, F. Motta, M. Ciccarelli
Coronavirus disease-19 (COVID-19) is caused by a severe acute respiratory syndrome coronavirus-2 and was declared a pandemic in March 2020. It mainly causes upper respiratory symptoms, but an interstitial viral pneumonia may occur, in severe cases complicated by acute respiratory distress syndrome. Neurological involvement has been reported but has not been well investigated. A 75-year old man presenting with severe COVID-19 related pneumonia developed a severe cognitive impairment and a right temporal hemianopsia, with focal microangiopathy and subacute ischemic alterations detected on brain imaging, interpreted as vasculitic-inflammatory injury. The neurological disorder was diagnosed only after he was extubated. A rehabilitation program was set up, so the patient had a complete cognitive recovery. Our case underlines how COVID-19 can lead to severe neurological sequelae, so neurological examination should be promptly performed when patients display signs of nervous system involvement, in order to prevent further damages.
{"title":"Two-month acute microangiopathic brain injury follow-up in severe COVID-19: a case report","authors":"V. Mundula, Anna Stainer, F. Motta, M. Ciccarelli","doi":"10.20517/2347-8659.2020.41","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.41","url":null,"abstract":"Coronavirus disease-19 (COVID-19) is caused by a severe acute respiratory syndrome coronavirus-2 and was declared a pandemic in March 2020. It mainly causes upper respiratory symptoms, but an interstitial viral pneumonia may occur, in severe cases complicated by acute respiratory distress syndrome. Neurological involvement has been reported but has not been well investigated. A 75-year old man presenting with severe COVID-19 related pneumonia developed a severe cognitive impairment and a right temporal hemianopsia, with focal microangiopathy and subacute ischemic alterations detected on brain imaging, interpreted as vasculitic-inflammatory injury. The neurological disorder was diagnosed only after he was extubated. A rehabilitation program was set up, so the patient had a complete cognitive recovery. Our case underlines how COVID-19 can lead to severe neurological sequelae, so neurological examination should be promptly performed when patients display signs of nervous system involvement, in order to prevent further damages.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44460651","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 : 2020-10-16DOI: 10.20517/2347-8659.2020.43
Zahraa I Khamis, Nancy Al-Akkary, Timothy Hua, Sophia A. Draughon, Yan Li, Q. Sang
Human primary brain cancer is one of the most lethal and clinically challenging malignancies. The failure of conventional therapies to alleviate its poor outcome has prompted efforts to find innovative treatments. Recent breakthroughs in immunotherapy across a variety of solid tumors have set immune-based therapeutics as a pillar for brain cancer treatment. However, the unique features of brain malignancies including intratumoral heterogeneity, immunosuppressive microenvironment, and impervious blood-brain barrier, thwart the success of immunotherapeutic approaches. Yet, seminal findings regarding tumor-driven enrichment of specific immune cells granted the field novel insights to harness the immune cells to fight cancer. This review discusses the anatomical, microenvironmental, and immunobiological features of the human brain and presents an overview of immunotherapies tested for primary brain cancer patients with a special emphasis on registered phase 2, 3, and combinatorial clinical trials. Immune checkpoint inhibitors, immune cell-based therapies, cancer vaccines, oncolytic viral therapy, and combination therapies are investigated in clinical settings for the treatment of human brain tumors. Despite their occasional adverse effects, immune-targeted therapies provide a promising opportunity for primary brain cancer patients to enhance survival and improve prognosis. Page 2 Khamis et al. Neuroimmunol Neuroinflammation 2020;7:[Online First] I http://dx.doi.org/10.20517/2347-8659.2020.43
{"title":"Clinical investigations of immunotherapy for human primary brain tumors","authors":"Zahraa I Khamis, Nancy Al-Akkary, Timothy Hua, Sophia A. Draughon, Yan Li, Q. Sang","doi":"10.20517/2347-8659.2020.43","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.43","url":null,"abstract":"Human primary brain cancer is one of the most lethal and clinically challenging malignancies. The failure of conventional therapies to alleviate its poor outcome has prompted efforts to find innovative treatments. Recent breakthroughs in immunotherapy across a variety of solid tumors have set immune-based therapeutics as a pillar for brain cancer treatment. However, the unique features of brain malignancies including intratumoral heterogeneity, immunosuppressive microenvironment, and impervious blood-brain barrier, thwart the success of immunotherapeutic approaches. Yet, seminal findings regarding tumor-driven enrichment of specific immune cells granted the field novel insights to harness the immune cells to fight cancer. This review discusses the anatomical, microenvironmental, and immunobiological features of the human brain and presents an overview of immunotherapies tested for primary brain cancer patients with a special emphasis on registered phase 2, 3, and combinatorial clinical trials. Immune checkpoint inhibitors, immune cell-based therapies, cancer vaccines, oncolytic viral therapy, and combination therapies are investigated in clinical settings for the treatment of human brain tumors. Despite their occasional adverse effects, immune-targeted therapies provide a promising opportunity for primary brain cancer patients to enhance survival and improve prognosis. Page 2 Khamis et al. Neuroimmunol Neuroinflammation 2020;7:[Online First] I http://dx.doi.org/10.20517/2347-8659.2020.43","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45538672","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 : 2020-10-16DOI: 10.20517/2347-8659.2020.15
N. Papagiannakis, L. Stefanis
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive motor disturbances and affects more than 1% of the worldwide population. Diagnosis of PD relies on clinical history and physical examination, but misdiagnosis is common in early stages. Despite considerable progress in understanding PD pathophysiology, including genetic and biochemical causes, diagnostic approaches lack accuracy and interventions are restricted to symptomatic treatments. Identification of biomarkers for PD may allow early and more precise diagnosis and monitoring of dopamine replacement strategies and disease-modifying treatments. Increasing evidence suggests that autophagic dysregulation causes the accumulation of abnormal proteins, such as aberrant α-synuclein, a protein critical to PD pathogenesis. Mutations in the GBA gene are a major PD risk factor and β-glucocerebrosidase (GCase) is also emerging as an important molecule in PD pathogenesis. Consequently, proteins involved in the autophagy-lysosome pathway and GCase protein levels and activity are prime targets for the research and development of new PD biomarkers. The studies so far in PD biological material have yielded some consistent results, particularly regarding the levels of Hsc70, a component of the chaperonemediated autophagy pathway, and the enzymatic activity of GCase in GBA mutation carriers. In the future, larger longitudinal studies, corroborating previous research on possible biomarker candidates, as well as extending the search for possible candidates for other lysosomal components, may yield more definitive results.
{"title":"Autophagy-lysosome pathway as a source of candidate biomarkers for Parkinson’s disease","authors":"N. Papagiannakis, L. Stefanis","doi":"10.20517/2347-8659.2020.15","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.15","url":null,"abstract":"Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive motor disturbances and affects more than 1% of the worldwide population. Diagnosis of PD relies on clinical history and physical examination, but misdiagnosis is common in early stages. Despite considerable progress in understanding PD pathophysiology, including genetic and biochemical causes, diagnostic approaches lack accuracy and interventions are restricted to symptomatic treatments. Identification of biomarkers for PD may allow early and more precise diagnosis and monitoring of dopamine replacement strategies and disease-modifying treatments. Increasing evidence suggests that autophagic dysregulation causes the accumulation of abnormal proteins, such as aberrant α-synuclein, a protein critical to PD pathogenesis. Mutations in the GBA gene are a major PD risk factor and β-glucocerebrosidase (GCase) is also emerging as an important molecule in PD pathogenesis. Consequently, proteins involved in the autophagy-lysosome pathway and GCase protein levels and activity are prime targets for the research and development of new PD biomarkers. The studies so far in PD biological material have yielded some consistent results, particularly regarding the levels of Hsc70, a component of the chaperonemediated autophagy pathway, and the enzymatic activity of GCase in GBA mutation carriers. In the future, larger longitudinal studies, corroborating previous research on possible biomarker candidates, as well as extending the search for possible candidates for other lysosomal components, may yield more definitive results.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48428087","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 : 2020-10-16DOI: 10.20517/2347-8659.2020.35
L. Zuroff, J. Benjamins, A. Bar-Or, R. Lisak
Multiple sclerosis (MS) is a lifelong inflammatory demyelinating disease of the central nervous system (CNS). While there has been substantial progress in the development of therapeutic strategies for relapsing disease, the field has lagged behind in its understanding and management of progressive stages of the disease, including secondary progressive and primary progressive MS, respectively. It is now thought that distinct but temporally overlapping mechanisms underlie relapsing and progressive aspects of the disease. Relapsing disease is characterized by waves of peripheral immune cell activation and CNS infiltration leading to focal destruction of the white matter, while progressive disease is thought to be driven by chronic, low-grade multifocal inflammation contained within the CNS compartment. Specifically, peripheral B cells, T cells, and myeloid cells take up residence within niches of the inflamed CNS, such as the leptomeninges and the Virchow-Robin spaces, where complex interactions between peripheral and CNS resident cells serve to maintain these cellular aggregates and further propagate CNS injury. In particular, immune infiltrates within the meninges are tightly associated with a specific form of cortical injury, termed subpial cortical demyelination, which is thought to be a key pathologic driver of disease progression. Cortical injury in the MS brain likely occurs via a combination of multiple immune-mediated and degenerative processes, perhaps including the production of diffusible toxic mediators by peripheral immune cells retained within the meninges. A better understanding of the interplay between peripheral immune and CNS resident cells is not only relevant to our concept of the disease process, but also represents a novel target for therapeutic intervention that is more specific to progressive disease biology. This review will focus on the role of Page 2 Zuroff et al. Neuroimmunol Neuroinflammation 2020;7:[Online First] I http://dx.doi.org/10.20517/2347-8659.2020.35 CNS-compartmentalized inflammation in the development of cortical injury in MS, with a particular emphasis on the importance of immune-CNS crosstalk in disease progression.
{"title":"Inflammatory mechanisms underlying cortical injury in progressive multiple sclerosis","authors":"L. Zuroff, J. Benjamins, A. Bar-Or, R. Lisak","doi":"10.20517/2347-8659.2020.35","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.35","url":null,"abstract":"Multiple sclerosis (MS) is a lifelong inflammatory demyelinating disease of the central nervous system (CNS). While there has been substantial progress in the development of therapeutic strategies for relapsing disease, the field has lagged behind in its understanding and management of progressive stages of the disease, including secondary progressive and primary progressive MS, respectively. It is now thought that distinct but temporally overlapping mechanisms underlie relapsing and progressive aspects of the disease. Relapsing disease is characterized by waves of peripheral immune cell activation and CNS infiltration leading to focal destruction of the white matter, while progressive disease is thought to be driven by chronic, low-grade multifocal inflammation contained within the CNS compartment. Specifically, peripheral B cells, T cells, and myeloid cells take up residence within niches of the inflamed CNS, such as the leptomeninges and the Virchow-Robin spaces, where complex interactions between peripheral and CNS resident cells serve to maintain these cellular aggregates and further propagate CNS injury. In particular, immune infiltrates within the meninges are tightly associated with a specific form of cortical injury, termed subpial cortical demyelination, which is thought to be a key pathologic driver of disease progression. Cortical injury in the MS brain likely occurs via a combination of multiple immune-mediated and degenerative processes, perhaps including the production of diffusible toxic mediators by peripheral immune cells retained within the meninges. A better understanding of the interplay between peripheral immune and CNS resident cells is not only relevant to our concept of the disease process, but also represents a novel target for therapeutic intervention that is more specific to progressive disease biology. This review will focus on the role of Page 2 Zuroff et al. Neuroimmunol Neuroinflammation 2020;7:[Online First] I http://dx.doi.org/10.20517/2347-8659.2020.35 CNS-compartmentalized inflammation in the development of cortical injury in MS, with a particular emphasis on the importance of immune-CNS crosstalk in disease progression.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47836074","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 : 2020-09-27DOI: 10.20517/2347-8659.2019.005
G. Crozier-Shaw, Hazel Denton, S. Morris
Worldwide, spinal cord injury (SCI) affects around 500,000 people each year and results in significant morbidity. The primary insult to the spinal cord occurs at the time of the initial injury, which may result from a contusion, laceration or more rarely a transection. Secondary damage in SCI is more insidious and subacute; it is the result of a combination of an inflammatory response, vascular changes and ionic dysregulation. Early clinical intervention is vital after the acute, primary insult to ensure the best possible outcomes for these patients. Current evidence on the demographics and mechanisms, underlying basic science and management strategies of spinal cord injuries are outlined.
{"title":"Management strategies in acute traumatic spinal cord injury: a narrative review","authors":"G. Crozier-Shaw, Hazel Denton, S. Morris","doi":"10.20517/2347-8659.2019.005","DOIUrl":"https://doi.org/10.20517/2347-8659.2019.005","url":null,"abstract":"Worldwide, spinal cord injury (SCI) affects around 500,000 people each year and results in significant morbidity. The primary insult to the spinal cord occurs at the time of the initial injury, which may result from a contusion, laceration or more rarely a transection. Secondary damage in SCI is more insidious and subacute; it is the result of a combination of an inflammatory response, vascular changes and ionic dysregulation. Early clinical intervention is vital after the acute, primary insult to ensure the best possible outcomes for these patients. Current evidence on the demographics and mechanisms, underlying basic science and management strategies of spinal cord injuries are outlined.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43658853","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 : 2020-09-12DOI: 10.20517/2347-8659.2020.20
R. Davis, K. McCracken, D. Buck, J. Curtis
Aim: Psychosocial stress negatively affects both physical and mental health; and stress-related psychiatric disorders are more common in women. Interestingly, preclinical studies have predominately investigated the effects of psychosocial stress on male mice. These studies suggest that adverse effects of psychosocial stress are due in part to the disruption of inflammatory signaling; however, the extent to which these findings translate to females remains unclear, particularly in the context of female-mediated aggression. Methods: We investigated the effects of acute (2 h) and repeated social defeat (RSD; 2 h/day × 6 days) on proinflammatory cytokine/chemokine expression in male and female C57BL/6J mice: importantly, the CD-1 aggressor mice were the same sex as the subject mice. Results: The effects on these inflammatory factors were dependent on the duration of social defeat, sex, and tissue. A single bout of social defeat reduced brain IL-1β levels in females only, whereas liver IL-1β and CXCL10 levels increased only in males. RSD decreased brain IL-1β levels in males only; while liver IL-1β and CCL2 levels decreased only in females. RSD led to increased exploratory activity in females; behavioral changes were not
{"title":"Social defeat affects inflammatory signaling and exploratory behavior in mice in a sex-dependent manner","authors":"R. Davis, K. McCracken, D. Buck, J. Curtis","doi":"10.20517/2347-8659.2020.20","DOIUrl":"https://doi.org/10.20517/2347-8659.2020.20","url":null,"abstract":"Aim: Psychosocial stress negatively affects both physical and mental health; and stress-related psychiatric disorders are more common in women. Interestingly, preclinical studies have predominately investigated the effects of psychosocial stress on male mice. These studies suggest that adverse effects of psychosocial stress are due in part to the disruption of inflammatory signaling; however, the extent to which these findings translate to females remains unclear, particularly in the context of female-mediated aggression. Methods: We investigated the effects of acute (2 h) and repeated social defeat (RSD; 2 h/day × 6 days) on proinflammatory cytokine/chemokine expression in male and female C57BL/6J mice: importantly, the CD-1 aggressor mice were the same sex as the subject mice. Results: The effects on these inflammatory factors were dependent on the duration of social defeat, sex, and tissue. A single bout of social defeat reduced brain IL-1β levels in females only, whereas liver IL-1β and CXCL10 levels increased only in males. RSD decreased brain IL-1β levels in males only; while liver IL-1β and CCL2 levels decreased only in females. RSD led to increased exploratory activity in females; behavioral changes were not","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48245813","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}
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