Neuroprotection最新文献

{"title":"Neurological manifestations with jugular vein thrombosis linked to an inflammatory profile may be a sequela of long COVID","authors":"Elizabeth Mendoza‐Portillo, Estefania Aleman‐Navarro, G. Aleph Prieto, Yvonne Rosenstein, Jose J. Lozano‐Nuevo, Araceli Perez‐Lopez","doi":"10.1002/nep3.24","DOIUrl":"https://doi.org/10.1002/nep3.24","url":null,"abstract":"Abstract More than 670 million cases of coronavirus disease 2019 (COVID‐19) have been recorded worldwide in the 3 years since the start of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) pandemic. About 45% of survivors of COVID‐19 develop a syndrome known as long‐term COVID, in which symptoms persist even months after the acute infection. About 76% of patients with long COVID experience neurological manifestations. Moreover, patients who have survived COVID‐19 have an increased risk of cerebral venous thrombosis. This case report describes a 41‐year‐old woman who developed neurological manifestations associated with jugular vein thrombosis 24 h after administration of the Oxford–AstraZeneca (ChAdOx1 nCoV‐19) vaccine (AstraZeneca‐Serum Institute of India). She had been infected with SARS‐CoV‐2 three months before vaccination. Although initially suspected to be a case of vaccine‐induced immune thrombotic thrombocytopenia (VITT) in view of her recent vaccination, the patient did not have any hallmarks of VITT, such as thrombocytopenia, an increased d ‐dimer level, or antibodies against platelet factor‐4. Moreover, the neurological manifestations were associated with a high concentration of inflammatory cytokines, including interleukin (IL)‐6, IL‐17A, and IL‐21, and elevated neutrophil levels in cerebrospinal fluid, suggesting that inflammatory immune components had a role in the development of thrombotic events and pointing to an alternative diagnosis. In this case, the laboratory results indicated that the neurological manifestations associated with jugular vein thrombosis were not associated with VITT. Therefore, we propose that the thrombosis of the left jugular vein was a sequela of SARS‐CoV‐2 infection.","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":" 39","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135243081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preserving cognitive function in patients with Alzheimer's disease: The Alzheimer's disease neuroprotection research initiative (ADNRI)","authors":"Jie Liu, Heleen van Beusekom, Xian‐Le Bu, Gong Chen, Paulo Henrique Rosado de Castro, Xiaochun Chen, Xiaowei Chen, Andrew N. Clarkson, Tracy D. Farr, Yuhong Fu, Jianping Jia, Jukka Jolkkonen, Woojin Scott Kim, Paula Korhonen, Shen Li, Yajie Liang, Guang‐Hui Liu, Guiyou Liu, Yu‐Hui Liu, Tarja Malm, Xiaobo Mao, Joaquim Miguel Oliveira, Mike M. Modo, Pedro Ramos‐Cabrer, Karsten Ruscher, Weihong Song, Jun Wang, Xuanyue Wang, Yun Wang, Haitao Wu, Lize Xiong, Yi Yang, Keqiang Ye, Jin‐Tai Yu, Xin‐Fu Zhou, Marietta Zille, Colin L. Masters, Piotr Walczak, Boltze Johannes, Xunming Ji, Yan‐Jiang Wang","doi":"10.1002/nep3.23","DOIUrl":"https://doi.org/10.1002/nep3.23","url":null,"abstract":"Abstract The global trend toward aging populations has resulted in an increase in the occurrence of Alzheimer's disease (AD) and associated socioeconomic burdens. Abnormal metabolism of amyloid‐β (Aβ) has been proposed as a significant pathomechanism in AD, supported by results of recent clinical trials using anti‐Aβ antibodies. Nonetheless, the cognitive benefits of the current treatments are limited. The etiology of AD is multifactorial, encompassing Aβ and tau accumulation, neuroinflammation, demyelination, vascular dysfunction, and comorbidities, which collectively lead to widespread neurodegeneration in the brain and cognitive impairment. Hence, solely removing Aβ from the brain may be insufficient to combat neurodegeneration and preserve cognition. To attain effective treatment for AD, it is necessary to (1) conduct extensive research on various mechanisms that cause neurodegeneration, including advances in neuroimaging techniques for earlier detection and a more precise characterization of molecular events at scales ranging from cellular to the full system level; (2) identify neuroprotective intervention targets against different neurodegeneration mechanisms; and (3) discover novel and optimal combinations of neuroprotective intervention strategies to maintain cognitive function in AD patients. The Alzheimer's Disease Neuroprotection Research Initiative's objective is to facilitate coordinated, multidisciplinary efforts to develop systemic neuroprotective strategies to combat AD. The aim is to achieve mitigation of the full spectrum of pathological processes underlying AD, with the goal of halting or even reversing cognitive decline.","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136237396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Join us on an amazing journey towards next-generation treatments for CNS disorders: Launch of Neuroprotection, a new high-quality journal in translational neuroscience.","authors":"Xuming Ji, Piotr Walczak, Heleen M M van Beusekom, Ana I Casas, Andrew Clarkson, Tracy Farr, Jukka Jolkkonen, Yajie Liang, Michel M Modo, Paulo H Rosado-de-Castro, Karsten Ruscher, Yan-Jiang Wang, Haitao Wu, Marietta Zille, Shen Li, Johannes Boltze","doi":"10.1002/nep3.8","DOIUrl":"10.1002/nep3.8","url":null,"abstract":"Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China Department of Diagnostic Radiology and Nuclear Medicine, Center for Advanced Imaging Research, University of Maryland, Baltimore, Maryland, USA Department of Cardiology, Erasmus MC Rotterdam, University Medical Center Rotterdam, Rotterdam, The Netherlands Department of Neurology, Center for Translational Neuro‐ and Behavioral Sciences (C‐TNBS), University Clinics Essen, Essen, Germany Department of Anatomy, Brain Health Research Center and Brain Research New Zealand, Dunedin, New Zealand Medical School, Queen's Medical Centre, University of Nottingham, Nottingham, UK A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA Department of Radiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, USA Department of Anatomy and Department of Radiology, School of Medicine, Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil Laboratory for Experimental Brain Research, University of Lund, Lund, Sweden Department of Neurology, Daping Hospital, Center for Clinical Neuroscience, Chongqing, China Department of Neurobiology, Beijing Institute of Basic Medical Sciences, Beijing, China Department of Pharmaceutical Sciences, Division of Pharmacology and Toxicology, University of Vienna, Vienna, Austria Department of Neurology and Psychiatry, Beijing Shijitan Hospital, Capital Medical University, Beijing, China School of Life Sciences, University of Warwick, Coventry, UK","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"1 1","pages":"5-8"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10494522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10232621","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}

{"title":"3D printing-based frugal manufacturing of glass pipettes for minimally invasive delivery of therapeutics to the brain.","authors":"Guanda Qiao, David Gulisashvili, Anna Jablonska, Guiling Zhao, Miroslaw Janowski, Piotr Walczak, Yajie Liang","doi":"10.1002/nep3.20","DOIUrl":"10.1002/nep3.20","url":null,"abstract":"<p><strong>Objective: </strong>Intracerebral delivery of agents in liquid form is usually achieved through commercially available and durable metal needles. However, their size and texture may contribute to mechanical brain damage. Glass pipettes with a thin tip may significantly reduce injection-associated brain damage but require access to prohibitively expensive programmable pipette pullers. This study is to remove the economic barrier to the application of minimally invasive delivery of therapeutics to the brain, such as chemical compounds, viral vectors, and cells.</p><p><strong>Methods: </strong>We took advantage of the rapid development of free educational online resources and emerging low-cost 3D printers by designing an affordable pipette puller (APP) to remove the cost obstacle.</p><p><strong>Results: </strong>We showed that our APP could produce glass pipettes with a sharp tip opening down to 20 μm or less, which is sufficiently thin for the delivery of therapeutics into the brain. A pipeline from pipette pulling to brain injection using low-cost and open-source equipment was established to facilitate the application of the APP.</p><p><strong>Conclusion: </strong>In the spirit of frugal science, our device may democratize glass pipette-puling and substantially promote the application of minimally invasive and precisely controlled delivery of therapeutics to the brain for finding more effective therapies of brain diseases.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"1 1","pages":"58-65"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10538625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41170632","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}

{"title":"Exploiting moderate hypoxia to benefit patients with brain disease: Molecular mechanisms and translational research in progress.","authors":"Hannelore Ehrenreich,&nbsp;Max Gassmann,&nbsp;Luise Poustka,&nbsp;Martin Burtscher,&nbsp;Peter Hammermann,&nbsp;Anna-Leena Sirén,&nbsp;Klaus-Armin Nave,&nbsp;Kamilla Miskowiak","doi":"10.1002/nep3.15","DOIUrl":"https://doi.org/10.1002/nep3.15","url":null,"abstract":"<p><p>Hypoxia is increasingly recognized as an important physiological driving force. A specific transcriptional program, induced by a decrease in oxygen (O₂) availability, for example, inspiratory hypoxia at high altitude, allows cells to adapt to lower O₂ and limited energy metabolism. This transcriptional program is partly controlled by and partly independent of hypoxia-inducible factors. Remarkably, this same transcriptional program is stimulated in the brain by extensive motor-cognitive exercise, leading to a relative decrease in O₂ supply, compared to the acutely augmented O₂ requirement. We have coined the term \"functional hypoxia\" for this important demand-responsive, relative reduction in O₂ availability. Functional hypoxia seems to be critical for enduring adaptation to higher physiological challenge that includes substantial \"brain hardware upgrade,\" underlying advanced performance. Hypoxia-induced erythropoietin expression in the brain likely plays a decisive role in these processes, which can be imitated by recombinant human erythropoietin treatment. This article review presents hints of how inspiratory O₂ manipulations can potentially contribute to enhanced brain function. It thereby provides the ground for exploiting moderate inspiratory plus functional hypoxia to treat individuals with brain disease. Finally, it sketches a planned multistep pilot study in healthy volunteers and first patients, about to start, aiming at improved performance upon motor-cognitive training under inspiratory hypoxia.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"1 1","pages":"9-19"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7615021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10170540","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}

{"title":"Ex vivo 100 μm isotropic diffusion MRI-based tractography of connectivity changes in the end-stage R6/2 mouse model of Huntington's disease.","authors":"Ashwinee Manivannan, Lesley M Foley, T Kevin Hitchens, Ivan Rattray, Gillian P Bates, Michel Modo","doi":"10.1002/nep3.14","DOIUrl":"10.1002/nep3.14","url":null,"abstract":"<p><strong>Background: </strong>Huntington's disease is a progressive neurodegenerative disorder. Brain atrophy, as measured by volumetric magnetic resonance imaging (MRI), is a downstream consequence of neurodegeneration, but microstructural changes within brain tissue are expected to precede this volumetric decline. The tissue microstructure can be assayed non-invasively using diffusion MRI, which also allows a tractographic analysis of brain connectivity.</p><p><strong>Methods: </strong>We here used ex vivo diffusion MRI (11.7 T) to measure microstructural changes in different brain regions of end-stage (14 weeks of age) wild type and R6/2 mice (male and female) modeling Huntington's disease. To probe the microstructure of different brain regions, reduce partial volume effects and measure connectivity between different regions, a 100 μm isotropic voxel resolution was acquired.</p><p><strong>Results: </strong>Although fractional anisotropy did not reveal any difference between wild-type controls and R6/2 mice, mean, axial, and radial diffusivity were increased in female R6/2 mice and decreased in male R6/2 mice. Whole brain streamlines were only reduced in male R6/2 mice, but streamline density was increased. Region-to-region tractography indicated reductions in connectivity between the cortex, hippocampus, and thalamus with the striatum, as well as within the basal ganglia (striatum-globus pallidus-subthalamic nucleus-substantia nigra-thalamus).</p><p><strong>Conclusions: </strong>Biological sex and left/right hemisphere affected tractographic results, potentially reflecting different stages of disease progression. This proof-of-principle study indicates that diffusion MRI and tractography potentially provide novel biomarkers that connect volumetric changes across different brain regions. In a translation setting, these measurements constitute a novel tool to assess the therapeutic impact of interventions such as neuroprotective agents in transgenic models, as well as patients with Huntington's disease.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"1 1","pages":"66-83"},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10516267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41156258","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}

{"title":"Monocytes in neonatal stroke and hypoxic‐ischemic encephalopathy: Pathophysiological mechanisms and therapeutic possibilities","authors":"P. M. Pimentel-Coelho","doi":"10.1002/nep3.22","DOIUrl":"https://doi.org/10.1002/nep3.22","url":null,"abstract":"Neonatal arterial ischemic stroke (NAIS) and neonatal hypoxic‐ischemic encephalopathy (HIE) are common causes of neurological impairments in infants, for which treatment options are very limited. NAIS and HIE induce an innate immune response that involves the recruitment of peripheral immune cells, including monocytes, into the brain. Monocytes and monocyte‐derived cells have the potential to contribute to both harmful and beneficial pathophysiological processes, such as neuroinflammation and brain repair, but their roles in NAIS and HIE remain poorly understood. Furthermore, recent evidence indicates that monocyte‐derived macrophages can persist in the brain for several months following NAIS and HIE in mice, with possible long‐lasting consequences that are still unknown. This review provides a comprehensive overview of the mechanisms of monocyte infiltration and their potential functions in the ischemic brain, focusing on HIE and NAIS. Therapeutic strategies targeting monocytes and the possibility of using monocytes for cell‐based therapies are also discussed.","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82270533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liquid–liquid phase separation in synaptopathies","authors":"Huihui Jiang, Haitao Wu","doi":"10.1002/nep3.21","DOIUrl":"https://doi.org/10.1002/nep3.21","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"130 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88436025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aspects of xenobiotics and their receptors in stroke","authors":"Aishika Datta, Bijoyani Ghosh, Deepaneeta Sarmah, Antra Chaudhary, Anupom Borah, P. Bhattacharya","doi":"10.1002/nep3.9","DOIUrl":"https://doi.org/10.1002/nep3.9","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89674252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current Therapeutic Approaches from Imidazoline and Opioid Receptors Modulators in Neuroprotection","authors":"L. Mititelu-Tarțău, M. Bogdan, V. Gheorman, L. Foia, Ancuța Goriuc, G. Rusu, B. R. Buca, L. Pavel, A. Cristofor, C. Tartau, G. Popa","doi":"10.5772/INTECHOPEN.81951","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.81951","url":null,"abstract":"Due to brain plasticity, the nervous system is capable of manifesting behavioral variations, adapted to the influences from both external and internal environment. Multiple neurotransmitters are involved in the mediation of pathological processes at the molecular, cellular, regional, and interregional levels participating in cerebral plasticity, their intervention being responsible for various structural, functional, and behavioral disturbances. The current therapeutic strategies in neuroprotection aim at blocking on different levels, the molecular cascades of the pathophysiological mechanisms responsible for neuronal dysfunctions and ultimately for neuronal death. Different agents influencing these neurotransmitters have demonstrated beneficial effects in neurogenesis and neuroprotection, proved in experimental animal models of focal and global ischemic injuries. Serotonin, dopamine, glutamate, N-methyl-D-aspartate, and nitric oxide have been shown to play a significant role in modulating nervous system injuries. The imidazoline system is one of the important systems involved in human brain functioning. Experimental investigations have revealed the cytoprotective effects of imidazoline I2 receptor ligands against neuronal injury induced by hypoxia in experimental animals. The neuroprotective effects were also highlighted for kappa and delta receptors, whose agonists demonstrated the ability to reduce architectural lesions and to recover neuronal functions of animals with experimentally induced brain ischemia.","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87002104","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}