Neuroprotection最新文献

{"title":"Mechanisms of glutamate metabolic function and dysfunction in vascular dementia","authors":"Jiawen Wang, Yingmei Zhang, Ning Tian, Dongshan Ya, Jiaxin Yang, Yanlin Jiang, Xiaoxia Li, Xiaohui Lin, Bin Yang, Qing-hun Li, Rujia Liao","doi":"10.1002/nep3.32","DOIUrl":"https://doi.org/10.1002/nep3.32","url":null,"abstract":"As the global population ages, research on the pathogenesis and treatment options for older patients with dementia has become increasingly important. Vascular dementia (VaD), the second most frequent type of dementia, is characterized by vascular impairment caused by inadequate blood supply to the brain. VaD is a complex neurological disorder involving multiple cells and signaling pathways, and its prevention and treatment pose clinical challenges with significant behavioral implications. Glutamate, the most abundant amino acid in the brain, plays a critical role as an excitatory neurotransmitter, impacting cognitive function, learning, and memory. Abnormal glutamate metabolism has been closely linked to dementia, and reduced blood flow to the brain can lead to excessive glutamate accumulation, resulting in neuronal death. This article highlights the connection between VaD and glutamate metabolism, aiming to identify better methods for preventing and treating VaD via regulating glutamate metabolism.","PeriodicalId":505813,"journal":{"name":"Neuroprotection","volume":"46 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140425494","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":"Intracranial pressure is elevated at 24 h post‐stroke in mice","authors":"K. Warren, Rebecca J. Hood, Fredrick R. Walker, Neil J. Spratt","doi":"10.1002/nep3.36","DOIUrl":"https://doi.org/10.1002/nep3.36","url":null,"abstract":"It has long been assumed that post‐stroke intracranial pressure (ICP) elevation occurs because of large infarct and edema volumes. However, we have repeatedly shown ICP elevation at 24 h post‐stroke in the presence of little to no edema in rats. Biological processes are often conserved across species and types of injury. Therefore, we aimed to determine if an ICP rise occurs at 24 h post‐stroke in the presence of small infarct and edema volumes in mice.Mice were randomized by random number table to either photothrombotic stroke or sham surgery (n = 15). Epidural ICP was recorded using a fiber optic catheter at 1 h post‐stroke (baseline) and between 23 and 24 h post‐stroke.ICP was significantly higher at 24 h compared to baseline in stroke animals (n = 6; 10.71 ± 6.45 mmHg vs. 3.74 ± 2.20 mmHg, respectively; p = 0.03). ICP at 24 h was also significantly higher in stroke mice compared to sham (n = 6; 3.45 ± 1.43 mmHg; p = 0.02). There was no change in ICP in sham mice (p = 0.9). Edema volumes in stroke animals were small (0.04 ± 0.04 mm3) and unlikely to have caused significant ICP elevation.This study provides evidence of an edema‐independent ICP elevation following small ischemic stroke in mice. The occurrence of this rise supports our findings in other species and suggests it is caused by a previously undescribed mechanism.","PeriodicalId":505813,"journal":{"name":"Neuroprotection","volume":"34 14","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140432914","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":"Mesenchymal stem cell‐derived exosomes: Shaping the next era of stroke treatment","authors":"Arshi Waseem, Saudamini, Rizwanul Haque, Miroslaw Janowski, Syed S. Raza","doi":"10.1002/nep3.30","DOIUrl":"https://doi.org/10.1002/nep3.30","url":null,"abstract":"Exosome‐based treatments are gaining traction as a viable approach to addressing the various issues faced by an ischemic stroke. These extracellular vesicles, mainly produced by mesenchymal stem cells, exhibit many properties with substantial therapeutic potential. Exosomes are particularly appealing for stroke therapy because of their low immunogenicity, effective cargo transport, and ability to cross the blood–brain barrier. Their diverse effects include neuroprotection, angiogenesis stimulation, inflammatory response modulation, and cell death pathway attenuation, synergistically promoting neuronal survival, tissue regeneration, and functional recovery. Exosomes also show potential as diagnostic indicators for early stroke identification and customized treatment options. Despite these promising qualities, current exosome‐based therapeutics have some limitations. The heterogeneity of exosome release among cell types, difficulty in standardization and isolation techniques, and complications linked to dosage and targeted administration necessitates extensive investigation. It is critical to thoroughly understand exosomal processes and their complicated interactions within the cellular milieu. To improve the practicality and efficacy of exosome‐based medicines, research efforts must focus on improving production processes, developing robust evaluation criteria, and developing large‐scale isolation techniques. Altogether, exosomes’ multifunctional properties offer a new route for transforming stroke treatment and significantly improving patient outcomes.","PeriodicalId":505813,"journal":{"name":"Neuroprotection","volume":"6 37","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139194899","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":"Lists of Reviewers","authors":"","doi":"10.1002/nep3.33","DOIUrl":"https://doi.org/10.1002/nep3.33","url":null,"abstract":"","PeriodicalId":505813,"journal":{"name":"Neuroprotection","volume":"31 21-22","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139193790","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":"Mononuclear cell therapy of neonatal hypoxic‐ischemic encephalopathy in preclinical versus clinical studies: A systematic analysis of therapeutic efficacy and study design","authors":"Alexander M. Scrutton, Francesca Ollis, Johannes Boltze","doi":"10.1002/nep3.29","DOIUrl":"https://doi.org/10.1002/nep3.29","url":null,"abstract":"Hypoxic‐ischemic encephalopathy (HIE) is a devastating condition affecting around 8.5 in 1000 newborns globally. Therapeutic hypothermia (TH) can reduce mortality and, to a limited extent, disability after HIE. Nevertheless, there is a need for new and effective treatment strategies. Cell‐based treatments using mononuclear cells (MNCs), which can be sourced from umbilical cord blood, are currently being investigated. Despite promising preclinical results, there is currently no strong indicator for the clinical efficacy of the approach. This analysis aimed to provide potential explanations for this discrepancy.A systematic review and meta‐analysis were conducted according to the Preferred Reporting Items for Systematic Reviews and Meta‐Analysis guidelines. Preclinical and clinical studies were retrieved from PubMed, Web of Science, Scopus, and clinicaltrials.gov using a predefined search strategy. A total of 17 preclinical and 7 clinical studies were included. We analyzed overall MNC efficacy in preclinical trials, the methodological quality of preclinical trials, and relevant design features in preclinical versus clinical trials.There was evidence for MNC therapeutic efficacy in preclinical models of HIE. The methodological quality of preclinical studies was not optimal, and statistical design quality was particularly poor. However, methodological quality was above the standard in other fields. There were significant differences in preclinical versus clinical study design including the use of TH as a baseline treatment (only in clinical studies) and much higher MNC doses being applied in preclinical studies.Based on the analyzed data, it is unlikely that therapeutic effect size is massively overestimated in preclinical studies. It is more plausible that the many design differences between preclinical and clinical trials are responsible for the so far lacking proof of the efficacy of MNC treatments in HIE. Additional preclinical and clinical research is required to optimize the application of MNC for experimental HIE treatment.","PeriodicalId":505813,"journal":{"name":"Neuroprotection","volume":"52 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139192515","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":"Activation of neurogenesis in the hippocampus is a novel therapeutic target for Alzheimer's disease","authors":"Akihiko Taguchi, Yuka Okinaka, Akiko Takeda, Takayuki Okamoto, Johannes Boltze, Carsten Claussen, Sheraz Gul","doi":"10.1002/nep3.25","DOIUrl":"https://doi.org/10.1002/nep3.25","url":null,"abstract":"Targeting single mechanisms of physiological (aging) and pathological (neurodegeneration) loss of function in the brain may not be sufficient. Cell–cell interactions between transplanted adult stem cells and resident cells via gap junctions have the potential to support the aging or diseased brain. These cell–cell interactions can also increase hippocampal neurogenesis. This may be a novel therapeutic strategy for Alzheimer's disease and other neurodegenerative diseases that could be applied alongside any established treatments.","PeriodicalId":505813,"journal":{"name":"Neuroprotection","volume":"29 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139253722","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":"Attenuation of amyotrophic lateral sclerosis via stem cell and extracellular vesicle therapy: An updated review","authors":"Gavin Lockard, Jonah Gordon, Samantha Schimmel, Bassel El Sayed, M. Monsour, S. Garbuzova-Davis, C. Borlongan","doi":"10.1002/nep3.26","DOIUrl":"https://doi.org/10.1002/nep3.26","url":null,"abstract":"Amyotrophic lateral sclerosis (ALS) is a rapidly fatal neurological disease characterized by upper and lower motor neuron degeneration. Though typically idiopathic, familial forms of ALS are commonly composed of a superoxide dismutase 1 (SOD1) mutation. Basic science frequently utilizes SOD1 models in vitro and in vivo to replicate ALS conditions. Therapies are sparse; those that exist in the market extend life minimally, thus driving the demand for research to identify novel therapeutics. Transplantation of stem cells is a promising approach for many diseases and has shown efficacy in SOD1 models and clinical trials. The underlying mechanism for stem cell therapy presents an exciting venue for research investigations. Most notably, the paracrine actions of stem cell‐derived extracellular vesicles (EVs) have been suggested as a potent mitigating factor. This literature review focuses on the most recent preclinical research investigating cell‐free methods for treating ALS. Various avenues are being explored, differing on the EV contents (protein, microRNA, etc.) and on the cell target (astrocyte, endothelial cell, motor neuron‐like cells, etc.), and both molecular and behavioral outcomes are being examined. Unfortunately, EVs may also play a role in propagating ALS pathology. Nonetheless, the overarching goal remains clear: to identify efficient cell‐free techniques to attenuate the deadly consequences of ALS.","PeriodicalId":505813,"journal":{"name":"Neuroprotection","volume":"61 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139258900","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}