IBRO Neuroscience Reports最新文献

{"title":"Design of neural organoids engineered by mechanical forces","authors":"Dang Ngoc Anh Suong ,&nbsp;Keiko Imamura ,&nbsp;Yoshikazu Kato ,&nbsp;Haruhisa Inoue","doi":"10.1016/j.ibneur.2024.01.004","DOIUrl":"10.1016/j.ibneur.2024.01.004","url":null,"abstract":"<div><p>Neural organoids consist of three-dimensional tissue derived from pluripotent stem cells that could recapitulate key features of the human brain. During the past decade, organoid technology has evolved in the field of human brain science by increasing the quality and applicability of its products. Among them, a novel approach involving the design of neural organoids engineered by mechanical forces has emerged. This review describes previous approaches for the generation of neural organoids, the engineering of neural organoids by mechanical forces, and future challenges for the application of mechanical forces in the design of neural organoids.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 190-195"},"PeriodicalIF":1.5,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000034/pdfft?md5=4cbac011e5917c019f138723895f6b8d&pid=1-s2.0-S2667242124000034-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139632929","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":"Pre-adolescence repeat exposure to sub-anesthetic doses of ketamine induces long-lasting behaviors and cognition impairment in male and female rat adults","authors":"Amir Barzegar Behrooz ,&nbsp;Mahdieh Nasiri ,&nbsp;Soheila Adeli ,&nbsp;Maryam Jafarian ,&nbsp;Seyed Khalil Pestehei ,&nbsp;Javad Fahanik Babaei","doi":"10.1016/j.ibneur.2024.01.005","DOIUrl":"10.1016/j.ibneur.2024.01.005","url":null,"abstract":"<div><p>In pre-adolescence, repeated anesthesia may be required for therapeutic interventions. Adult cognitive and neurobehavioral problems may result from preadolescent exposure to anesthetics. This study examined the long-term morphological and functional effects of repeated sub-anesthetic doses of ketamine exposure on male and female rat adults during pre-adolescence. Weaned 48 pre-adolescent rats from eight mothers and were randomly divided into four equal groups: control group and the ketamine group of males and females (20 mg/kg daily for 14 days); then animals received care for 20–30 days. Repeated exposure to sub-anesthetic doses of ketamine on cognitive functions was assayed using Social discrimination and novel object tests. Besides, an elevated plus maze and fear conditioning apparatus were utilized to determine exploratory and anxiety-like behavior in adults. Toluidine blue stain was used to evaluate the number of dead neurons in the hippocampus, and the effects of ketamine on synaptic plasticity were compared in the perforant pathway of the CA1 of the hippocampus. Our study indicates that repeated exposure to sub-anesthetic doses of ketamine during pre-adolescence can result in neurobehavioral impairment in male and female rat adulthood but does not affect anxiety-like behavior. We found a significant quantifiable increase in dark neurons. Recorded electrophysiologically, repeat sub-anesthetic doses of ketamine resulted in hampering long-term potentiation and pair pulse in male adult animals. Our results showed that repeated exposure to sub-anesthetic doses of ketamine during pre-adolescence can induce hippocampus and neuroplasticity changes later in adulthood. This study opens up a new line of inquiry into potential adverse outcomes of repeated anesthesia exposure in pre-adolescent rats.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 211-223"},"PeriodicalIF":1.5,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266724212400006X/pdfft?md5=a521ace097142f22293f72fa5f832f46&pid=1-s2.0-S266724212400006X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139631695","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":"Superoxide dismutase and neurological disorders","authors":"Saravana Babu Chidambaram ,&nbsp;Nikhilesh Anand ,&nbsp;Sudhir Rama Varma ,&nbsp;Srinivasan Ramamurthy ,&nbsp;Chandrasekaran Vichitra ,&nbsp;Ambika Sharma ,&nbsp;Arehally M. Mahalakshmi ,&nbsp;Musthafa Mohamed Essa","doi":"10.1016/j.ibneur.2023.11.007","DOIUrl":"10.1016/j.ibneur.2023.11.007","url":null,"abstract":"<div><p>Superoxide dismutase (SOD) is a common antioxidant enzyme found majorly in living cells. The main physiological role of SOD is detoxification and maintain the redox balance, acts as a first line of defence against Reactive nitrogen species (RNS), Reactive oxygen species (ROS), and other such potentially hazardous molecules. SOD catalyses the conversion of superoxide anion free radicals (O _{2 -}.) into molecular oxygen (O ₂) and hydrogen peroxide (H ₂O ₂) in the cells. Superoxide dismutases (SODs) are expressed in neurons and glial cells throughout the CNS both intracellularly and extracellularly. Endogenous oxidative stress (OS) linked with enlarged production of reactive oxygen metabolites (ROMs), inflammation, deregulation of redox balance, mitochondrial dysfunction and bioenergetic crisis are found to be prerequisite for neuronal loss in neurological diseases. Clinical and genetic studies indicate a direct correlation between mutations in SOD gene and neurodegenerative diseases, like Amyotrophic Lateral Sclerosis (ALS), Huntington’s disease (HD), Parkinson’s Disease (PD) and Alzheimer’s Disease (AD). Therefore, inhibitors of OS are considered as an optimistic approach to prevent neuronal loss. SOD mimetics like Metalloporphyrin Mn (II)-cyclic polyamines, Nitroxides and Mn (III)- Salen complexes are designed and used as therapeutic extensively in the treatment of neurological disorders. SODs and SOD mimetics are promising future therapeutics in the field of various diseases with OS-mediated pathology.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 373-394"},"PeriodicalIF":1.5,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022856/pdfft?md5=c522ce0267a96189fbf83056880c5cf2&pid=1-s2.0-S2667242123022856-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139638818","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":"Chronic chemogenetic activation of hippocampal progenitors enhances adult neurogenesis and modulates anxiety-like behavior and fear extinction learning","authors":"Megha Maheshwari ,&nbsp;Aastha Singla ,&nbsp;Anoop Rawat,&nbsp;Toshali Banerjee,&nbsp;Sthitapranjya Pati,&nbsp;Sneha Shah,&nbsp;Sudipta Maiti,&nbsp;Vidita A. Vaidya","doi":"10.1016/j.ibneur.2024.01.002","DOIUrl":"https://doi.org/10.1016/j.ibneur.2024.01.002","url":null,"abstract":"<div><p>Adult hippocampal neurogenesis is a lifelong process that involves the integration of newborn neurons into the hippocampal network, and plays a role in cognitive function and the modulation of mood-related behavior. Here, we sought to address the impact of chemogenetic activation of adult hippocampal progenitors on distinct stages of progenitor development, including quiescent stem cell activation, progenitor turnover, differentiation and morphological maturation. We find that hM3Dq-DREADD-mediated activation of nestin-positive adult hippocampal progenitors recruits quiescent stem cells, enhances progenitor proliferation, increases doublecortin-positive newborn neuron number, accompanied by an acceleration of differentiation and morphological maturation, associated with increased dendritic complexity. Behavioral analysis indicated anxiolytic behavioral responses in transgenic mice subjected to chemogenetic activation of adult hippocampal progenitors at timepoints when newborn neurons are predicted to integrate into the mature hippocampal network. Furthermore, we noted an enhanced fear memory extinction on a contextual fear memory learning task in transgenic mice subjected to chemogenetic activation of adult hippocampal progenitors. Our findings indicate that hM3Dq-DREAD-mediated chemogenetic activation of adult hippocampal progenitors impacts distinct aspects of hippocampal neurogenesis, associated with the regulation of anxiety-like behavior and fear memory extinction.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 168-181"},"PeriodicalIF":1.5,"publicationDate":"2024-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000022/pdfft?md5=df598fc9ac8daf26f82312f635ce69ae&pid=1-s2.0-S2667242124000022-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139653524","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":"Impact of dihydropyrimidinase-related protein 2 in memory formation on rats and its possible role in neuronal back remodeling","authors":"Arif A. Mekhtiev,&nbsp;Shamsiyya M. Asadova","doi":"10.1016/j.ibneur.2024.01.001","DOIUrl":"https://doi.org/10.1016/j.ibneur.2024.01.001","url":null,"abstract":"<div><p>The article concerns the problem of molecular mechanisms of memory formation. In this study the effects of polyclonal antibodies to serotonin-modulating anticonsolidation protein (SMAP) complex and its component dihydropyrimidinase-related protein 2 (DRP2) have been analyzed. Intra-cerebral administration of polyclonal anti-SMAP antibody significantly enhanced elaboration and strengthened memory formation in two complex behavioral conditioned models. At the same time, intra-cerebral administration of anti-SMAP antibody resulted in an increase of the content of nerve growth factor (NGF) in the water-soluble fraction of the hippocampus while intra-cerebral administration of anti-DRP2 antibody caused a decrease in the content of β-III tubulin (a marker of differentiated neurons) in the hippocampus and in the left parietal cortex of untrained rats. The obtained results indicate that DRP2 might participate in regulation of the processes of back remodeling of mature nerve cells of adult organisms, occurring during training of rats in the behavioral paradigm used in this study under the effects of anti-SMAP and anti-DRP2 antibodies. Conclusion is made that back remodeling (dedifferentiation) of mature nerve cells, apparently, is engaged in memory formation.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 155-161"},"PeriodicalIF":1.5,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000010/pdfft?md5=63251340f7f50ed9a10fb8eba3c48660&pid=1-s2.0-S2667242124000010-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139503976","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":"Dose-dependent changes in orientation amplitude maps in the cat visual cortex after propofol bolus injections","authors":"Svetlana I. Shumikhina ,&nbsp;Sergei A. Kozhukhov ,&nbsp;Igor V. Bondar","doi":"10.1016/j.ibneur.2023.12.010","DOIUrl":"10.1016/j.ibneur.2023.12.010","url":null,"abstract":"<div><p>A general intravenous anesthetic propofol (2,6-diisopropylphenol) is widely used in clinical, veterinary practice and animal experiments. It activates gamma- aminobutyric acid (GABAa) receptors. Though the cerebral cortex is one of the major targets of propofol action, no study of dose dependency of propofol action on cat visual cortex was performed yet. Also, no such investigation was done until now using intrinsic signal optical imaging. Here, we report for the first time on the dependency of optical signal in the visual cortex (area 17/area 18) on the propofol dose. Optical imaging of intrinsic responses to visual stimuli was performed in cats before and after propofol bolus injections at different doses on the background of continuous propofol infusion. Orientation amplitude maps were recorded. We found that amplitude of optical signal significantly decreased after a bolus dose of propofol. The effect was dose- and time-dependent producing stronger suppression of optical signal under the highest bolus propofol doses and short time interval after injection. In each hemisphere, amplitude at cardinal and oblique orientations decreased almost equally. However, surprisingly, amplitude at cardinal orientations in the ipsilateral hemisphere was depressed stronger than in contralateral cortex at most time intervals. As the magnitude of optical signal represents the strength of orientation tuned component, these our data give new insights on the mechanisms of generation of orientation selectivity. Our results also provide new data toward understanding brain dynamics under anesthesia and suggest a recommendation for conducting intrinsic signal optical imaging experiments on cortical functioning under propofol anesthesia.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 224-240"},"PeriodicalIF":1.5,"publicationDate":"2024-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022972/pdfft?md5=aede37d98597ec794ed49c5e4f2988f2&pid=1-s2.0-S2667242123022972-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139457427","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":"Assessing remission in major depressive disorder using a functional-structural data fusion pipeline: A CAN-BIND-1 study","authors":"Sondos Ayyash ,&nbsp;Andrew D. Davis ,&nbsp;Gésine L. Alders ,&nbsp;Glenda MacQueen ,&nbsp;Stephen C. Strother ,&nbsp;Stefanie Hassel ,&nbsp;Mojdeh Zamyadi ,&nbsp;Stephen R. Arnott ,&nbsp;Jacqueline K. Harris ,&nbsp;Raymond W. Lam ,&nbsp;Roumen Milev ,&nbsp;Daniel J. Müller ,&nbsp;Sidney H. Kennedy ,&nbsp;Susan Rotzinger ,&nbsp;Benicio N. Frey ,&nbsp;Luciano Minuzzi ,&nbsp;Geoffrey B. Hall ,&nbsp;CAN-BIND Investigator Team","doi":"10.1016/j.ibneur.2023.12.011","DOIUrl":"10.1016/j.ibneur.2023.12.011","url":null,"abstract":"<div><p>Neural network-level changes underlying symptom remission in major depressive disorder (MDD) are often studied from a single perspective. Multimodal approaches to assess neuropsychiatric disorders are evolving, as they offer richer information about brain networks. A <em>FATCAT-awFC</em> pipeline was developed to integrate a computationally intense data fusion method with a toolbox, to produce a faster and more intuitive pipeline for combining functional connectivity with structural connectivity (denoted as anatomically weighted functional connectivity (<em>awFC</em>)). Ninety-three participants from the Canadian Biomarker Integration Network for Depression study (CAN-BIND-1) were included. Patients with MDD were treated with 8 weeks of escitalopram and adjunctive aripiprazole for another 8 weeks. Between-group connectivity (SC, FC, <em>awFC</em>) comparisons contrasted remitters (REM) with non-remitters (NREM) at baseline and 8 weeks. Additionally, a longitudinal study analysis was performed to compare connectivity changes across time for REM, from baseline to week-8. Association between cognitive variables and connectivity were also assessed. REM were distinguished from NREM by lower <em>awFC</em> within the default mode, frontoparietal, and ventral attention networks. Compared to REM at baseline, REM at week-8 revealed increased <em>awFC</em> within the dorsal attention network and decreased awFC within the frontoparietal network. A medium effect size was observed for most results. <em>AwFC</em> in the frontoparietal network was associated with neurocognitive index and cognitive flexibility for the NREM group at week-8. In conclusion, the <em>FATCAT-awFC</em> pipeline has the benefit of providing insight on the ‘full picture’ of connectivity changes for REMs and NREMs while making for an easy intuitive approach.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 135-146"},"PeriodicalIF":1.5,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022996/pdfft?md5=35645af27b50a928e289812dc83b6088&pid=1-s2.0-S2667242123022996-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139395386","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":"Neuroprotective effects of alpha-pinene against behavioral deficits in ketamine-induced mice model of schizophrenia: Focusing on oxidative stress status","authors":"Akbar Hajizadeh Moghaddam ,&nbsp;Fatemeh Malekzadeh Estalkhi ,&nbsp;Sedigheh Khanjani Jelodar ,&nbsp;Tabarek Ahmed Hasan ,&nbsp;Soroush Farhadi-Pahnedari ,&nbsp;Mohammad Karimian","doi":"10.1016/j.ibneur.2023.12.012","DOIUrl":"10.1016/j.ibneur.2023.12.012","url":null,"abstract":"<div><p>Schizophrenia (SCZ) is a profound neurological disorder that affects approximately 1% of the global population. Alpha-pinene (α-pinene) is a natural and active monoterpene found in coniferous tree oil, primarily pine, with diverse pharmacological characteristics, including antioxidative, anxiolytic, and antidepressant properties. This research study delves into the neuroprotective effects of α-pinene on oxidative stress, memory deficits, and depressive and anxiety-like behaviors in a ketamine-induced mice model of SCZ using male mice. The mice were randomly divided into six groups: vehicle, control, positive control, ketamine, α-pinene at 50 mg/kg, and α-pinene at 100 mg/kg. Treatment of the ketamine-induced mice model of SCZ with α-pinene yielded significant improvements in depressive and anxiety-like behaviors and cognitive impairments. Furthermore, it significantly elevated glutathione (GSH) levels, total antioxidant capacity (TAC), dopamine levels, catalase (CAT), and superoxide dismutase (SOD) activities while markedly reducing malondialdehyde (MDA) levels. The current study establishes that α-pinene treatment effectively mitigates oxidative damage, cognitive deficits, and depressive and anxiogenic-like behaviors in the brains of ketamine-treated mice. Therefore, α-pinene treatment is an efficacious approach to forestall the neurobehavioral and neurobiochemical adverse effects of the ketamine-induced SCZ model of mice.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 182-189"},"PeriodicalIF":1.5,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022984/pdfft?md5=3a7e8ebe08b1d757d31cc9a69f904dd3&pid=1-s2.0-S2667242123022984-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139393513","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":"Antipsychotic effect of diosgenin in ketamine-induced murine model of schizophrenia: Involvement of oxidative stress and cholinergic transmission","authors":"Benneth Ben-Azu ,&nbsp;Olusegun G. Adebayo ,&nbsp;Aliance Romain Fokoua ,&nbsp;Benjamin Oritsemuelebi ,&nbsp;Emmanuel O. Chidebe ,&nbsp;Chukwuebuka B. Nwogueze ,&nbsp;Lenatababari Kumanwee ,&nbsp;God'swill E. Uyere ,&nbsp;Micheal T. Emuakpeje","doi":"10.1016/j.ibneur.2023.12.008","DOIUrl":"https://doi.org/10.1016/j.ibneur.2023.12.008","url":null,"abstract":"<div><p>A decrease in the levels of antioxidant arsenals exacerbate generation of reactive oxygen/nitrogen species, leading to neurochemical dysfunction, with significant impact on the pathogenesis of psychotic disorders such as schizophrenia. This study examined the preventive and reversal effects of diosgenin, a phyto-steroidal saponin with antioxidant functions in mice treated with ketamine which closely replicates schizophrenia-like symptoms in human and laboratory animals. In the preventive phase, adult mice cohorts were clustered into 5 groups (<em>n</em> = 9). Groups 1 and 2 received saline (10 mL/kg, <em>i.p.),</em> groups 3 and 4 were pretreated with diosgenin (25 and 50 mg/kg), and group 5 received risperidone (0.5 mg/kg) orally for 14 days. Mice in groups 2–5 additionally received a daily dose of ketamine (20 mg/kg, <em>i.p.</em>) or saline (10 mL/kg/day, <em>i.p.</em>). In the reversal phase, mice received intraperitoneal injection of ketamine or saline for 14 consecutive days prior to diosgenin (25 and 50 mg/kg/<em>p.o.</em>/day) and risperidone (0.5 mg/kg/<em>p.o</em>./day) treatment from days 8–14. Mice were assessed for behavioral changes. Oxidative, nitrergic markers, and cholinergic (acetylcholinesterase activity) transmission were examined in the striatum, prefrontal-cortex and hippocampus. Diosgenin prevented and reversed hyperlocomotion, cognitive and social deficits in mice treated with ketamine relative to ketamine groups. The increased acetylcholinesterase, malondialdehyde and nitrite levels produced by ketamine were reduced by diosgenin in the striatum, prefrontal-cortex and hippocampus, but did not reverse striatal nitrite level. Diosgenin increased glutathione, and catalase levels, except for hippocampal catalase activity when compared with ketamine controls. Conclusively, these biochemical changes might be related to the behavioral deficits in ketamine-treated mice, which were prevented and reversed by diosgenin.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 86-97"},"PeriodicalIF":1.5,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022960/pdfft?md5=ac5ff5382981927d22ab5b98683fe104&pid=1-s2.0-S2667242123022960-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139109164","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":"Pericyte derivation and transplantation for blood-CNS barrier reconstitution in CNS disorders","authors":"Hyun Woo Kim ,&nbsp;Kenneth Lap Kei Wu ,&nbsp;Kin-Wai Tam ,&nbsp;Ying-Shing Chan ,&nbsp;Daisy Kwok-Yan Shum","doi":"10.1016/j.ibneur.2023.12.007","DOIUrl":"10.1016/j.ibneur.2023.12.007","url":null,"abstract":"<div><p>Disruption of the blood-central nervous system barrier (BCB) is increasingly recognized as a pathological factor in diseases and trauma of the central nervous system. Despite the neuropathological impact, current treatment modalities do not target the BCB; strategies to reconstitute the impaired BCB have been restricted to nutritional and dietary remedies. As an integral cell type in the neurovascular unit, pericytes are crucial to the development, maintenance, and repair of the BCB. As such, pericytes are well poised as cellular agents for reconstitution of the impaired BCB. Here, we summarize recent revelations regarding the role of BCB disruption in diseases and trauma of the central nervous system and highlight how pericytes are harnessed to provide targeted therapeutic effect in each case. This review will also address how recent advances in pericyte derivation strategies can serve to overcome practical hurdles in the clinical use of pericytes.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"16 ","pages":"Pages 147-154"},"PeriodicalIF":1.5,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242123022947/pdfft?md5=01c4f5ba064fc7c52c2774956a7bbebc&pid=1-s2.0-S2667242123022947-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139395006","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}