ASN NEURO最新文献

{"title":"Tropomyosin Receptor Kinase B Expressed in Oligodendrocyte Lineage Cells Functions to Promote Myelin Following a Demyelinating Lesion.","authors":"Yangyang Huang,&nbsp;Yeri J Song,&nbsp;Maria Isaac,&nbsp;Shir Miretzky,&nbsp;Ashish Patel,&nbsp;W Geoffrey McAuliffe,&nbsp;Cheryl F Dreyfus","doi":"10.1177/1759091420957464","DOIUrl":"https://doi.org/10.1177/1759091420957464","url":null,"abstract":"<p><p>The levels of brain-derived neurotrophic factor (BDNF) in the corpus callosum have previously been shown to have a critical impact on oligodendrocyte (OLG) lineage cells during cuprizone-elicited demyelination. In particular, BDNF+/- mice exhibit greater losses in myelin protein levels compared to wild-type mice after cuprizone. To investigate whether OLGs may directly mediate these effects of BDNF during a lesion <i>in vivo</i>, we used the cuprizone model of demyelination with inducible conditional male knockout mice to specifically delete the high-affinity tropomyosin receptor kinase B (TrkB) receptor from proteolipid protein + OLGs during cuprizone-elicited demyelination and subsequent remyelination. The loss of TrkB during cuprizone-elicited demyelination results in an increased sensitivity to demyelination as demonstrated by greater deficits in myelin protein levels, greater decreases in numbers of mature OLGs, increased numbers of demyelinated axons, and decreased myelin thickness. When mice are removed from cuprizone, they exhibit a delayed recovery in myelin proteins and myelin. Our data indicate that following a demyelinating lesion, TrkB in OLGs positively regulates myelin protein expression, myelin itself, and remyelination.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"12 ","pages":"1759091420957464"},"PeriodicalIF":4.7,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1759091420957464","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10442809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physical Activity Ameliorates Impaired Hippocampal Neurogenesis in the Tg4-42 Mouse Model of Alzheimer’s Disease","authors":"Anna-Lina Gerberding, S. Zampar, Martina Stazi, D. Liebetanz, O. Wirths","doi":"10.1177/1759091419892692","DOIUrl":"https://doi.org/10.1177/1759091419892692","url":null,"abstract":"There is growing evidence from epidemiological studies that especially midlife physical activity might exert a positive influence on the risk and progression of Alzheimer’s disease. In this study, the Tg4-42 mouse model of Alzheimer’s disease has been utilized to assess the effect of different housing conditions on structural changes in the hippocampus. Focusing on the dentate gyrus, we demonstrate that 6-month-old Tg4-42 mice have a reduced number of newborn neurons in comparison to age-matched wild-type mice. Housing these mice for 4 months with either unlimited or intermittent access to a running wheel resulted in a significant rescue of dentate gyrus neurogenesis. Although neither dentate gyrus volume nor neuron number could be modified in this Alzheimer’s disease mouse model, unrestricted access to a running wheel significantly increased dentate gyrus volume and granule cell number in wild-type mice.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1759091419892692","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45588334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2019 Academic Annual Meeting and the Frontier Seminar on “Glial Cell Function and Disease” (Nantong, China)","authors":"Yu-Feng Wang, Yong-Jing Gao","doi":"10.1177/1759091419863576","DOIUrl":"https://doi.org/10.1177/1759091419863576","url":null,"abstract":"The contribution of glial activities to the functions, diseases, and repair of the central nervous system has received increasing attention in neuroscience studies. To promote the research of glial cells and increase cooperation with peers, the 2019 Academic Annual Meeting and the Frontier Seminar on “Glial Cell Function and Disease” was held in Nantong City, Jiangsu Province, China from May 24 to 26. The meeting was organized by Drs. Yong-Jing Gao and Jia-Wei Zhou of the Chinese Society of Neuroscience Glia Branch. The conference focused on the physiological and pathological functions of astrocytes, microglia, and oligodendrocytes with 25 speakers in two plenary speeches and five sections of more than 180 participants engaged in glial cell research. In the two plenary lectures, Yutian Wang from the University of British Columbia and Xia Zhang from the University of Ottawa presented “Development of NMDAR (N-methyl-D-aspartic acid receptor)-positive allosteric modulators as novel therapeutics for brain disorders” and “Mechanisms underlying cannabinoid regulation of brain function and disease,” respectively. The five sections included microglia and disease, astrocytes and disease, glioma treatment and glial imaging, oligodendrocytes and disease, and glial–neuronal interactions and disease. This meeting allowed extensive and in-depth academic exchanges on the latest research and experimental techniques, represented the highest achievements of Chinese scholars on glial cells, and promoted the cooperation between peers in the fields of glia studies.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1759091419863576","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47851821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum","authors":"","doi":"10.1177/1759091419847891","DOIUrl":"https://doi.org/10.1177/1759091419847891","url":null,"abstract":"","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1759091419847891","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41951843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abstracts of the 2018 Meeting of ArgentineSociety for Research in Neurosciences","authors":"","doi":"10.1177/1759091419834821","DOIUrl":"https://doi.org/10.1177/1759091419834821","url":null,"abstract":"","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1759091419834821","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48790633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intracerebroventricular Infusion of Gangliosides Augments the Adult Neural Stem Cell Pool in Mouse Brain","authors":"Yutaka Itokazu, Dongpei Li, R. Yu","doi":"10.1177/1759091419884859","DOIUrl":"https://doi.org/10.1177/1759091419884859","url":null,"abstract":"We previously reported that ganglioside GD3 is the predominant species in neural stem cells (NSCs) and reduced postnatal NSC pools are observed in both the subventricular zone and dentate gyrus (DG) of GD3-synthase knockout (GD3S-KO) mouse brains. Specifically, deficiency of GD3 in GD3S-KO animals revealed a dramatic reduction in cellularity in the DG of the hippocampus of the developing mouse brain, resulting in severe behavioral deficits in these animals. To further evaluate the functional role of GD3 in postnatal brain, we performed rescue experiments by intracerebroventricular infusion of ganglioside GD3 in adult GD3S-KO animals and found that it could restore the NSC pools and enhance the NSCs for self-renewal. Furthermore, 5xFAD mouse model was utilized, and GD3 restored NSC numbers and GM1 promoted neuronal differentiation. Our results thus demonstrate that exogenously administered gangliosides are capable to restore the function of postnatal NSCs. Since ganglioside expression profiles are associated not only with normal brain development but also with pathogenic mechanisms of diseases, such as Alzheimer’s disease, we anticipate that the administration of exogenous gangliosides, such as GD3 and GM1, may represent a novel and effective strategy for promoting adult neurogenesis in damaged brain for disease treatment.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1759091419884859","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43037955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erythropoietin as a Neuroprotective Molecule: An Overview of Its Therapeutic Potential in Neurodegenerative Diseases","authors":"Federica Rey, A. Balsari, T. Giallongo, S. Ottolenghi, A. D. Di Giulio, M. Samaja, S. Carelli","doi":"10.1177/1759091419871420","DOIUrl":"https://doi.org/10.1177/1759091419871420","url":null,"abstract":"Erythropoietin (EPO) is a cytokine mainly induced in hypoxia conditions. Its major production site is the kidney. EPO primarily acts on the erythroid progenitor cells in the bone marrow. More and more studies are highlighting its secondary functions, with a crucial focus on its role in the central nervous system. Here, EPO may interact with up to four distinct isoforms of its receptor (erythropoietin receptor [EPOR]), activating different signaling cascades with roles in neuroprotection and neurogenesis. Indeed, the EPO/EPOR axis has been widely studied in the neurodegenerative diseases field. Its potential therapeutic effects have been evaluated in multiple disorders, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, spinal cord injury, as well as brain ischemia, hypoxia, and hyperoxia. EPO is showing great promise by counteracting secondary neuroinflammatory processes, reactive oxygen species imbalance, and cell death in these diseases. Multiple studies have been performed both in vitro and in vivo, characterizing the mechanisms through which EPO exerts its neurotrophic action. In some cases, clinical trials involving EPO have been performed, highlighting its therapeutic potential. Together, all these works indicate the potential beneficial effects of EPO.","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"79 4","pages":""},"PeriodicalIF":4.7,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1759091419871420","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41275118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2018 Reviewer Thank You","authors":"Hiroko Baba, Anita Bandrowski, Devin Binder, Megan Bosch, Denis Bragin, Jun Cai, Fioravante Capone, Sraboni Chaudhury, Shih-Cheng Chen, Nicholas Colangelo, Carol Colton, Colin Combs, Marek Czosnyka, Glyn Dawson, Fernanda De Felice, Therese Dipaolo","doi":"10.1177/1759091419834384","DOIUrl":"https://doi.org/10.1177/1759091419834384","url":null,"abstract":"Hiroko Baba Anita Bandrowski Devin Binder Megan Bosch Denis Bragin Jun Cai Fioravante Capone Sraboni Chaudhury Shih-Cheng Chen Nicholas Colangelo Carol Colton Colin Combs Marek Czosnyka Glyn Dawson Fernanda De Felice Therese Dipaolo Jeffery Dunn Jeffrey Dupree Douglas Feinstein Todd Fiacco Babette Fuss Luis Garcia-Garcia Cristina Ghiani Stephen Glatt Kirby Gottschalk Alexander Gow Judith Grinspan Gaylia Harry Cecilia Hedin-Pereira Sukant Khurana Jolanta Kotlinska Steven Levison Jun Li David Loane Mychael Lourenco Wendy Macklin Jose Madrigal Frank Middleton Alexander Mongin Chris Naus Andre Obenaus Antonio Oliveira Donna Osterhout Christina Alves Peixoto William Pembroke David Picketts Peter Ponsaerts Matthew Rasband Fabiola Ribeiro Laurie Sanders Susanne Schmid Pankaj Seth Thomas Seyfried Carolyn Smith Ameer Taha Sui-Seng Tee Serge Thal Seema Tiwari-Woodruff E Tronci Louis-Eric Trudeau Michael Vitek Jonathan Vogelgsang Melissa Vondran Gherman Wiederschain Talene Yacoubian Yonghua Zhang ASN Neuro Volume 11: 1 ! The Author(s) 2019 Article reuse guidelines: sagepub.com/journals-permissions DOI: 10.1177/1759091419834384 journals.sagepub.com/home/asn","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1759091419834384","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47434298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered Brain Expression of Insulin and Insulin-Like Growth Factors in Frontotemporal Lobar Degeneration: Another Degenerative Disease Linked to Dysregulation of Insulin Metabolic Pathways.","authors":"Connie J Liou, Ming Tong, Jean P Vonsattel, Suzanne M de la Monte","doi":"10.1177/1759091419839515","DOIUrl":"10.1177/1759091419839515","url":null,"abstract":"<p><strong>Background: </strong>Frontotemporal lobar degeneration (FTLD) is the third most common dementing neurodegenerative disease with nearly 80% having no known etiology.</p><p><strong>Objective: </strong>Growing evidence that neurodegeneration can be linked to dysregulated metabolism prompted us to measure a panel of trophic factors, receptors, and molecules that modulate brain metabolic function in FTLD.</p><p><strong>Methods: </strong>Postmortem frontal (Brodmann's area [BA]8/9 and BA24) and temporal (BA38) lobe homogenates were used to measure immunoreactivity to Tau, phosphorylated tau (pTau), ubiquitin, 4-hydroxynonenal (HNE), transforming growth factor-beta 1 (TGF-β1) and its receptor (TGF-β1R), brain-derived neurotrophic factor (BDNF), nerve growth factor, neurotrophin-3, neurotrophin-4, tropomyosin receptor kinase, and insulin and insulin-like growth factor-1 (IGF-1) and insulin-like growth factor-2 (IGF-2) and their receptors by direct-binding enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>FTLD brains had significantly elevated pTau, ubiquitin, TGF-β1, and HNE immunoreactivity relative to control. In addition, BDNF and neurotrophin-4 were respectively reduced in BA8/9 and BA38, while neurotrophin-3 and nerve growth factor were upregulated in BA38, and tropomyosin receptor kinase was elevated in BA24. Lastly, insulin and insulin receptor expressions were elevated in the frontal lobe, IGF-1 was increased in BA24, IGF-1R was upregulated in all three brain regions, and IGF-2 receptor was reduced in BA24 and BA38.</p><p><strong>Conclusions: </strong>Aberrantly increased levels of pTau, ubiquitin, HNE, and TGF-β1, marking neurodegeneration, oxidative stress, and neuroinflammation, overlap with altered expression of insulin/IGF signaling ligand and receptors in frontal and temporal lobe regions targeted by FTLD. Dysregulation of insulin-IGF signaling networks could account for brain hypometabolism and several characteristic neuropathologic features that characterize FTLD but overlap with Alzheimer's disease, Parkinson's disease, and Dementia with Lewy Body Disease.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"11 ","pages":"1759091419839515"},"PeriodicalIF":4.7,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/20/ca/10.1177_1759091419839515.PMC6535914.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9194784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic and Structural Imaging at 7 Tesla After Repetitive Mild Traumatic Brain Injury in Immature Rats.","authors":"Emin Fidan, Lesley M Foley, Lee Ann New, Henry Alexander, Patrick M Kochanek, T Kevin Hitchens, Hülya Bayır","doi":"10.1177/1759091418770543","DOIUrl":"10.1177/1759091418770543","url":null,"abstract":"<p><p>Mild traumatic brain injury (mTBI) in children is a common and serious public health problem. Traditional neuroimaging findings in children who sustain mTBI are often normal, putting them at risk for repeated mTBI (rmTBI). There is a need for more sensitive imaging techniques capable of detecting subtle neurophysiological alterations after injury. We examined neurochemical and white matter changes using diffusion tensor imaging of the whole brain and proton magnetic resonance spectroscopy of the hippocampi at 7 Tesla in 18-day-old male rats at 7 days after mTBI and rmTBI. Traumatic axonal injury was assessed by beta-amyloid precursor protein accumulation using immunohistochemistry. A significant decrease in fractional anisotropy and increase in axial and radial diffusivity were observed in several brain regions, especially in white matter regions, after a single mTBI versus sham and more prominently after rmTBI. In addition, we observed accumulation of beta-amyloid precursor protein in the external capsule after mTBI and rmTBI. mTBI and rmTBI reduced the N-acetylaspartate/creatine ratio (NAA/Cr) and increased the myoinositol/creatine ratio (Ins/Cr) versus sham. rmTBI exacerbated the reduction in NAA/Cr versus mTBI. The choline/creatine (Cho/Cr) and (lipid/Macro Molecule 1)/creatine (Lip/Cr) ratios were also decreased after rmTBI versus sham. Diffusion tensor imaging findings along with the decrease in Cho and Lip after rmTBI may reflect damage to axonal membrane. NAA and Ins are altered at 7 days after mTBI and rmTBI likely reflecting neuro-axonal damage and glial response, respectively. These findings may be relevant to understanding the extent of disability following mTBI and rmTBI in the immature brain and may identify possible therapeutic targets.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"10 ","pages":"1759091418770543"},"PeriodicalIF":4.7,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5944144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10009735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}