Neuroprotection最新文献

{"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}

{"title":"Introductory Chapter: Concept of Neuroprotection - A New Perspective","authors":"R. Chang, Y. Ho","doi":"10.5772/INTECHOPEN.85631","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.85631","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88211288","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":"The Role and Development of the Antagonist of Adenosine A2A in Parkinson’s Disease","authors":"W. Aryati, Nabilah Nurtika Salamah, Rezi Riadhi Syahdi, Arry Yanuar","doi":"10.5772/INTECHOPEN.84272","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.84272","url":null,"abstract":"Adenosine is a neuromodulator that regulates the body’s response to dopamine and another neurotransmitter in the brain that is responsible for motoric, emotion, learning, and memory function. Adenosine is a G-protein-coupled receptor and has four subtypes, which are A 1, A 2A , A 2B , and A 3 . Adenosine A 2A is located in the striatum of the brain. Antagonist interferes with GABA releasing, modulates acetyl-choline and releases dopamine, and also facilitates dopamine receptor’s signaling. Therefore, it can reduce motoric symptoms in Parkinson’s disease. Adenosine A 2A antagonist is also believed to have neuroprotective effects. Several compounds have been reported and have undergone clinical test as selective adenosine A 2A antagonists, including istradefylline, preladenant, tozadenant, vipadenant, ST-1535, and SYN-115. Nonselective adenosine A 2A antagonists from natural compounds are caffeine and theophylline. ,","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"25 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72890883","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}