Sonia Sanchez-Bezanilla, Daniel J. Beard, R. Hood, N. Åberg, P. Crock, F. Walker, M. Nilsson, J. Isgaard, L. Ong
Aims We have shown that growth hormone (GH) treatment poststroke increases neuroplasticity in peri-infarct areas and the hippocampus, improving motor and cognitive outcomes. We aimed to explore the mechanisms of GH treatment by investigating how GH modulates pathways known to induce neuroplasticity, focusing on association between brain-derived neurotrophic factor (BDNF) and mammalian target of rapamycin (mTOR) in the peri-infarct area, hippocampus, and thalamus. Methods Recombinant human growth hormone (r-hGH) or saline was delivered (0.25 μl/hr, 0.04 mg/day) to mice for 28 days, commencing 48 hours after photothrombotic stroke. Protein levels of pro-BDNF, total-mTOR, phosphorylated-mTOR, total-p70S6K, and phosporylated-p70S6K within the peri-infarct area, hippocampus, and thalamus were evaluated by western blotting at 30 days poststroke. Results r-hGH treatment significantly increased pro-BDNF in peri-infarct area, hippocampus, and thalamus (p < 0.01). r-hGH treatment significantly increased expression levels of total-mTOR in the peri-infarct area and thalamus (p < 0.05). r-hGH treatment significantly increased expression of total-p70S6K in the hippocampus (p < 0.05). Conclusion r-hGH increases pro-BDNF within the peri-infarct area and regions that are known to experience secondary neurodegeneration after stroke. Upregulation of total-mTOR protein expression in the peri-infarct and thalamus suggests that this might be a pathway that is involved in the neurorestorative effects previously reported in these animals and warrants further investigation. These findings suggest region-specific mechanisms of action of GH treatment and provide further understanding for how GH treatment promotes neurorestorative effects after stroke.
{"title":"Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice","authors":"Sonia Sanchez-Bezanilla, Daniel J. Beard, R. Hood, N. Åberg, P. Crock, F. Walker, M. Nilsson, J. Isgaard, L. Ong","doi":"10.1155/2022/9983042","DOIUrl":"https://doi.org/10.1155/2022/9983042","url":null,"abstract":"Aims We have shown that growth hormone (GH) treatment poststroke increases neuroplasticity in peri-infarct areas and the hippocampus, improving motor and cognitive outcomes. We aimed to explore the mechanisms of GH treatment by investigating how GH modulates pathways known to induce neuroplasticity, focusing on association between brain-derived neurotrophic factor (BDNF) and mammalian target of rapamycin (mTOR) in the peri-infarct area, hippocampus, and thalamus. Methods Recombinant human growth hormone (r-hGH) or saline was delivered (0.25 μl/hr, 0.04 mg/day) to mice for 28 days, commencing 48 hours after photothrombotic stroke. Protein levels of pro-BDNF, total-mTOR, phosphorylated-mTOR, total-p70S6K, and phosporylated-p70S6K within the peri-infarct area, hippocampus, and thalamus were evaluated by western blotting at 30 days poststroke. Results r-hGH treatment significantly increased pro-BDNF in peri-infarct area, hippocampus, and thalamus (p < 0.01). r-hGH treatment significantly increased expression levels of total-mTOR in the peri-infarct area and thalamus (p < 0.05). r-hGH treatment significantly increased expression of total-p70S6K in the hippocampus (p < 0.05). Conclusion r-hGH increases pro-BDNF within the peri-infarct area and regions that are known to experience secondary neurodegeneration after stroke. Upregulation of total-mTOR protein expression in the peri-infarct and thalamus suggests that this might be a pathway that is involved in the neurorestorative effects previously reported in these animals and warrants further investigation. These findings suggest region-specific mechanisms of action of GH treatment and provide further understanding for how GH treatment promotes neurorestorative effects after stroke.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"45 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85858524","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}
Although the cerebellum has been consistently noted in the process of cognition, the pathophysiology of this link is still under exploration. Cerebellar stroke, in which the lesions are focal and limited, provides an appropriate clinical model disease for studying the role of the cerebellum in the cognitive process. This review article targeting the cerebellar stroke population (1) describes a cognitive impairment profile, (2) identifies the cerebellar structural alterations linked to cognition, and (3) reveals possible mechanisms of cerebellar cognition using functional neuroimaging. The data indicates the disruption of the cerebro-cerebellar loop in cerebellar stroke and its contribution to cognitive dysfunctions. And the characteristic of cognitive deficits are mild, span a broad spectrum, dominated by executive impairment. The consideration of these findings could contribute to deeper and more sophisticated insights into the cognitive function of the cerebellum and might provide a novel approach to cognitive rehabilitation. The goal of this review is to spread awareness of cognitive impairments in cerebellar disorders.
{"title":"Cognitive Dysfunction following Cerebellar Stroke: Insights Gained from Neuropsychological and Neuroimaging Research","authors":"Qi Liu, Chang-bin Liu, Yu Chen, Yumei Zhang","doi":"10.1155/2022/3148739","DOIUrl":"https://doi.org/10.1155/2022/3148739","url":null,"abstract":"Although the cerebellum has been consistently noted in the process of cognition, the pathophysiology of this link is still under exploration. Cerebellar stroke, in which the lesions are focal and limited, provides an appropriate clinical model disease for studying the role of the cerebellum in the cognitive process. This review article targeting the cerebellar stroke population (1) describes a cognitive impairment profile, (2) identifies the cerebellar structural alterations linked to cognition, and (3) reveals possible mechanisms of cerebellar cognition using functional neuroimaging. The data indicates the disruption of the cerebro-cerebellar loop in cerebellar stroke and its contribution to cognitive dysfunctions. And the characteristic of cognitive deficits are mild, span a broad spectrum, dominated by executive impairment. The consideration of these findings could contribute to deeper and more sophisticated insights into the cognitive function of the cerebellum and might provide a novel approach to cognitive rehabilitation. The goal of this review is to spread awareness of cognitive impairments in cerebellar disorders.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"8 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87537668","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}
Zhen-Kun Gao, Xin-Ya Shen, Yu Han, Yi-Sha Guo, Mei Yuan, Xia Bi
Myelination is regulated by various glial cells in the central nervous system (CNS), including oligodendrocytes (OLs), microglia, and astrocytes. Myelination of the CNS requires the generation of functionally mature OLs from OPCs. OLs are the myelin-forming cells in the CNS. Microglia play both beneficial and detrimental roles during myelin damage and repair. Astrocyte is responsible for myelin formation and regeneration by direct interaction with oligodendrocyte lineage cells. These glial cells are influenced by experience-dependent activities such as environmental enrichment (EE). To date, there are few studies that have investigated the association between EE and glial cells. EE with a complex combination of sensorimotor, cognitive, and social stimulation has a significant effect on cognitive impairment and brain plasticity. Hence, one mechanism through EE improving cognitive function may rely on the mutual effect of EE and glial cells. The purpose of this paper is to review recent research into the efficacy of EE for myelination and glial cells at cellular and molecular levels and offers critical insights for future research directions of EE and the treatment of EE in cognitive impairment disease.
{"title":"Enriched Environment Effects on Myelination of the Central Nervous System: Role of Glial Cells","authors":"Zhen-Kun Gao, Xin-Ya Shen, Yu Han, Yi-Sha Guo, Mei Yuan, Xia Bi","doi":"10.1155/2022/5766993","DOIUrl":"https://doi.org/10.1155/2022/5766993","url":null,"abstract":"Myelination is regulated by various glial cells in the central nervous system (CNS), including oligodendrocytes (OLs), microglia, and astrocytes. Myelination of the CNS requires the generation of functionally mature OLs from OPCs. OLs are the myelin-forming cells in the CNS. Microglia play both beneficial and detrimental roles during myelin damage and repair. Astrocyte is responsible for myelin formation and regeneration by direct interaction with oligodendrocyte lineage cells. These glial cells are influenced by experience-dependent activities such as environmental enrichment (EE). To date, there are few studies that have investigated the association between EE and glial cells. EE with a complex combination of sensorimotor, cognitive, and social stimulation has a significant effect on cognitive impairment and brain plasticity. Hence, one mechanism through EE improving cognitive function may rely on the mutual effect of EE and glial cells. The purpose of this paper is to review recent research into the efficacy of EE for myelination and glial cells at cellular and molecular levels and offers critical insights for future research directions of EE and the treatment of EE in cognitive impairment disease.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"2014 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86623494","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}
Haipeng Xu, Kelin He, Rong Hu, Yanzhi Ge, Xinyun Li, F. Ni, Bei Que, Yi Chen, Ruijie Ma
Stroke is one of the leading causes of death and disability worldwide. Evidence shows that ischemic stroke (IS) accounts for nearly 80 percent of all strokes and that the etiology, risk factors, and prognosis of this disease differ by gender. Female patients may bear a greater burden than male patients. The immune system may play an important role in the pathophysiology of females with IS. Therefore, it is critical to investigate the key biomarkers and immune infiltration of female IS patients to develop effective treatment methods. Herein, we used weighted gene co-expression network analysis (WGCNA) to determine the key modules and core genes in female IS patients using the GSE22255, GSE37587, and GSE16561 datasets from the GEO database. Subsequently, we performed functional enrichment analysis and built a protein-protein interaction (PPI) network. Ten genes were selected as the true central genes for further investigation. After that, we explored the specific molecular and biological functions of these hub genes to gain a better understanding of the underlying pathogenesis of female IS patients. Moreover, the “Cell type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT)” was used to examine the distribution pattern of immune subtypes in female patients with IS and normal controls, revealing a new potential target for clinical treatment of the disease.
中风是全世界导致死亡和残疾的主要原因之一。有证据表明，缺血性中风(IS)占所有中风的近80%，其病因、危险因素和预后因性别而异。女性患者可能比男性患者承受更大的负担。免疫系统可能在IS女性的病理生理中发挥重要作用。因此，研究女性is患者的关键生物标志物和免疫浸润对制定有效的治疗方法至关重要。本文采用加权基因共表达网络分析(WGCNA)，利用GEO数据库中的GSE22255、GSE37587和GSE16561数据集，确定女性IS患者的关键模块和核心基因。随后，我们进行了功能富集分析，并建立了蛋白质-蛋白质相互作用(PPI)网络。选出10个基因作为真正的中心基因进行进一步研究。之后，我们探索了这些枢纽基因的特定分子和生物学功能，以更好地了解女性IS患者的潜在发病机制。此外，利用“Cell type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT)”检测女性IS患者和正常对照中免疫亚型的分布模式，揭示了临床治疗该疾病的新的潜在靶点。
{"title":"Identifying Key Biomarkers and Immune Infiltration in Female Patients with Ischemic Stroke Based on Weighted Gene Co-Expression Network Analysis","authors":"Haipeng Xu, Kelin He, Rong Hu, Yanzhi Ge, Xinyun Li, F. Ni, Bei Que, Yi Chen, Ruijie Ma","doi":"10.1155/2022/5379876","DOIUrl":"https://doi.org/10.1155/2022/5379876","url":null,"abstract":"Stroke is one of the leading causes of death and disability worldwide. Evidence shows that ischemic stroke (IS) accounts for nearly 80 percent of all strokes and that the etiology, risk factors, and prognosis of this disease differ by gender. Female patients may bear a greater burden than male patients. The immune system may play an important role in the pathophysiology of females with IS. Therefore, it is critical to investigate the key biomarkers and immune infiltration of female IS patients to develop effective treatment methods. Herein, we used weighted gene co-expression network analysis (WGCNA) to determine the key modules and core genes in female IS patients using the GSE22255, GSE37587, and GSE16561 datasets from the GEO database. Subsequently, we performed functional enrichment analysis and built a protein-protein interaction (PPI) network. Ten genes were selected as the true central genes for further investigation. After that, we explored the specific molecular and biological functions of these hub genes to gain a better understanding of the underlying pathogenesis of female IS patients. Moreover, the “Cell type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT)” was used to examine the distribution pattern of immune subtypes in female patients with IS and normal controls, revealing a new potential target for clinical treatment of the disease.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"8 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90823821","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}
Shan Xiong, Liwei Jiang, Yu Wang, T. Pan, Furong Ma
Auditory deprivation affects normal age-related changes in the central auditory maturation. Cochlear implants (CIs) have already become the best treatment strategy for severe to profound hearing impairment. However, it is still hard to evaluate the speech-language outcomes of the pediatric CI recipients because of hearing-impaired children with limited speech-language abilities. The cortical auditory evoked potential (CAEP) provides a window into the development of the auditory cortical pathways. This preliminary study is aimed at assessing electrophysical characteristics of P1-N1 of electrically CAEP in children with CIs and at exploring whether these changes could be accounted for in auditory and speech outcomes of these patients. CAEP responses were recorded in 48 children with CIs in response to electrical stimulus to determine the presence of the P1-N1 response. Speech perception and speech intelligibility of the implanted children were further evaluated with the categories of auditory performance (CAP) test and speech intelligibility rating (SIR) test, respectively, to explore the relationship between the latency of P1-N1 and auditory and speech performance. This study found that P1 and N1 of the intracochlear CAEP were reliably evoked in children fitted with CIs and that the latency of the P1 as opposed to that of N1 was negative in relation to the wearing time of the cochlear implant. Moreover, the latency of the P1 produced significantly negative scores in both CAP and SIR tests, which indicates that P1 latency may be reflective of the auditory performance and speech intelligibility of pediatric CI recipients. These results suggest that the latency of P1 could be used for the objective assessment of auditory and speech function evaluation in cochlear-implanted children, which would be helpful in clinical decision-making regarding intervention for young hearing-impaired children.
{"title":"The Role of the P1 Latency in Auditory and Speech Performance Evaluation in Cochlear Implanted Children","authors":"Shan Xiong, Liwei Jiang, Yu Wang, T. Pan, Furong Ma","doi":"10.1155/2022/6894794","DOIUrl":"https://doi.org/10.1155/2022/6894794","url":null,"abstract":"Auditory deprivation affects normal age-related changes in the central auditory maturation. Cochlear implants (CIs) have already become the best treatment strategy for severe to profound hearing impairment. However, it is still hard to evaluate the speech-language outcomes of the pediatric CI recipients because of hearing-impaired children with limited speech-language abilities. The cortical auditory evoked potential (CAEP) provides a window into the development of the auditory cortical pathways. This preliminary study is aimed at assessing electrophysical characteristics of P1-N1 of electrically CAEP in children with CIs and at exploring whether these changes could be accounted for in auditory and speech outcomes of these patients. CAEP responses were recorded in 48 children with CIs in response to electrical stimulus to determine the presence of the P1-N1 response. Speech perception and speech intelligibility of the implanted children were further evaluated with the categories of auditory performance (CAP) test and speech intelligibility rating (SIR) test, respectively, to explore the relationship between the latency of P1-N1 and auditory and speech performance. This study found that P1 and N1 of the intracochlear CAEP were reliably evoked in children fitted with CIs and that the latency of the P1 as opposed to that of N1 was negative in relation to the wearing time of the cochlear implant. Moreover, the latency of the P1 produced significantly negative scores in both CAP and SIR tests, which indicates that P1 latency may be reflective of the auditory performance and speech intelligibility of pediatric CI recipients. These results suggest that the latency of P1 could be used for the objective assessment of auditory and speech function evaluation in cochlear-implanted children, which would be helpful in clinical decision-making regarding intervention for young hearing-impaired children.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"49 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84261451","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}
Ming-hao Yang, Zhiqiang Guo, Xueyu Lv, Zhu-Qing Zhang, Wei-dong Wang, Jian Wang, L. Hong, Ying-Na Lin, ChunTing Liu
Rumination is a common symptom of major depressive disorder (MDD) and has been characterized as a vulnerability factor for the onset or recurrence of MDD. However, the neurobiological mechanisms underlying rumination and appropriate treatment strategies remain unclear. In the current study, we used resting-state functional magnetic resonance imaging to investigate the effects of body-mind relaxation meditation induction (BMRMI) intervention in MDD with rumination. To this aim, we have recruited 25 MDD and 24 healthy controls (HCs). Changes in functional connectivity (FC) of the anterior cingulate cortex (ACC) subregion and the scores of clinical measurements were examined using correlation analysis. At baseline, MDD showed stronger FC between the right dorsal ACC (dACC) and right superior frontal gyrus than did the HC group. Compared to baseline, the HC group showed a significantly enhanced FC between the right dACC and right superior frontal gyrus, and the MDD group demonstrated a significantly weaker FC between the left dACC and right middle frontal gyrus (MFG) after the intervention. Furthermore, the FC between the right dACC and right superior frontal gyrus was positively associated with rumination scores across all participants at baseline. The above results indicate that BMRMI may regulate self-referential processing and cognitive function through modulating FC of the dACC in MDD with rumination.
{"title":"BMRMI Reduces Depressive Rumination Possibly through Improving Abnormal FC of Dorsal ACC","authors":"Ming-hao Yang, Zhiqiang Guo, Xueyu Lv, Zhu-Qing Zhang, Wei-dong Wang, Jian Wang, L. Hong, Ying-Na Lin, ChunTing Liu","doi":"10.1155/2022/8068988","DOIUrl":"https://doi.org/10.1155/2022/8068988","url":null,"abstract":"Rumination is a common symptom of major depressive disorder (MDD) and has been characterized as a vulnerability factor for the onset or recurrence of MDD. However, the neurobiological mechanisms underlying rumination and appropriate treatment strategies remain unclear. In the current study, we used resting-state functional magnetic resonance imaging to investigate the effects of body-mind relaxation meditation induction (BMRMI) intervention in MDD with rumination. To this aim, we have recruited 25 MDD and 24 healthy controls (HCs). Changes in functional connectivity (FC) of the anterior cingulate cortex (ACC) subregion and the scores of clinical measurements were examined using correlation analysis. At baseline, MDD showed stronger FC between the right dorsal ACC (dACC) and right superior frontal gyrus than did the HC group. Compared to baseline, the HC group showed a significantly enhanced FC between the right dACC and right superior frontal gyrus, and the MDD group demonstrated a significantly weaker FC between the left dACC and right middle frontal gyrus (MFG) after the intervention. Furthermore, the FC between the right dACC and right superior frontal gyrus was positively associated with rumination scores across all participants at baseline. The above results indicate that BMRMI may regulate self-referential processing and cognitive function through modulating FC of the dACC in MDD with rumination.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"85 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84567711","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}
Ke Shang, Xiao Chen, Chang Cheng, Xiang Luo, Shabei Xu, Wei Wang, Chenchen Liu
Introduction The association between arterial tortuosity and acute ischemic stroke (AIS) has been reported, but showing inconsistent results. We hypothesized that tortuosity of extra- and intracranial large arteries might be higher in AIS patients. Furthermore, we explored the correlation between artery tortuosity and white matter hyperintensity (WMH) severity in AIS patients. Methods 166 AIS patients identified as large artery atherosclerosis, and 83 control subjects were enrolled. All subjects received three-dimensional computed tomography angiography (CTA). Arterial tortuosity was evaluated using the tortuosity index. WMHs were evaluated using magnetic resonance imaging in all AIS patients. Results AIS patients showed significantly increased arterial tortuosity index relative to controls, including left carotid artery (CA) (p = 0.001), right CA (p < 0.001), left common carotid artery (CCA) (p < 0.001), right CCA (p < 0.001), left internal carotid artery (p = 0.001), right internal carotid artery (p = 0.01), left extracranial internal carotid artery (EICA) (p < 0.001), right EICA (p = 0.01), and vertebral artery dominance (VAD) (p = 0.001). The tortuosity of all above arteries was associated with the presence of AIS. AIS patients with moderate or severe WMHs had a higher tortuosity index in left CA (p = 0.005), left CCA (p = 0.003), left EICA (p = 0.07), and VAD (p = 0.001). In addition, the tortuosity of left EICA and VAD was associated with WMH severity in AIS patients. Conclusions Increased extra- and intracranial large arteries tortuosity is associated with AIS. The tortuosity of left carotid artery system and vertebral artery may be the independent risk factors for WMH severity in AIS patients. Clinical Trial Registration. This trial is registered with NCT03122002 (http://www.clinicaltrials.gov).
{"title":"Arterial Tortuosity and Its Correlation with White Matter Hyperintensities in Acute Ischemic Stroke","authors":"Ke Shang, Xiao Chen, Chang Cheng, Xiang Luo, Shabei Xu, Wei Wang, Chenchen Liu","doi":"10.1155/2022/4280410","DOIUrl":"https://doi.org/10.1155/2022/4280410","url":null,"abstract":"Introduction The association between arterial tortuosity and acute ischemic stroke (AIS) has been reported, but showing inconsistent results. We hypothesized that tortuosity of extra- and intracranial large arteries might be higher in AIS patients. Furthermore, we explored the correlation between artery tortuosity and white matter hyperintensity (WMH) severity in AIS patients. Methods 166 AIS patients identified as large artery atherosclerosis, and 83 control subjects were enrolled. All subjects received three-dimensional computed tomography angiography (CTA). Arterial tortuosity was evaluated using the tortuosity index. WMHs were evaluated using magnetic resonance imaging in all AIS patients. Results AIS patients showed significantly increased arterial tortuosity index relative to controls, including left carotid artery (CA) (p = 0.001), right CA (p < 0.001), left common carotid artery (CCA) (p < 0.001), right CCA (p < 0.001), left internal carotid artery (p = 0.001), right internal carotid artery (p = 0.01), left extracranial internal carotid artery (EICA) (p < 0.001), right EICA (p = 0.01), and vertebral artery dominance (VAD) (p = 0.001). The tortuosity of all above arteries was associated with the presence of AIS. AIS patients with moderate or severe WMHs had a higher tortuosity index in left CA (p = 0.005), left CCA (p = 0.003), left EICA (p = 0.07), and VAD (p = 0.001). In addition, the tortuosity of left EICA and VAD was associated with WMH severity in AIS patients. Conclusions Increased extra- and intracranial large arteries tortuosity is associated with AIS. The tortuosity of left carotid artery system and vertebral artery may be the independent risk factors for WMH severity in AIS patients. Clinical Trial Registration. This trial is registered with NCT03122002 (http://www.clinicaltrials.gov).","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"31 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82878691","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}
Xiaotong Zhang, Zhaocong Chen, Na Li, Jingfeng Liang, Y. Zou, Huixiang Wu, Z. Kang, Z. Dou, Weihong Qiu
Recently, an increasing number of studies have highlighted the role of the cerebellum in language processing. However, the role of neural reorganization within the cerebellum as well as within the cerebrocerebellar system caused by poststroke aphasia remains unknown. To solve this problem, in the present study, we investigated regional alterations of the cerebellum as well as the functional reorganization of the cerebrocerebellar circuit by combining structural and resting-state functional magnetic resonance imaging (fMRI) techniques. Twenty patients diagnosed with aphasia following left-hemispheric stroke and 20 age-matched healthy controls (HCs) were recruited in this study. The Western Aphasia Battery (WAB) test was used to assess the participants' language ability. Gray matter volume, spontaneous brain activity, functional connectivity, and effective connectivity were examined in each participant. We discovered that gray matter volumes in right cerebellar lobule VI and right Crus I were significantly lower in the patient group, and the brain activity within these regions was significantly correlated with WAB scores. We also discovered decreased functional connectivity within the crossed cerebrocerebellar circuit, which was significantly correlated with WAB scores. Moreover, altered information flow between the cerebellum and the contralateral cerebrum was found. Together, our findings provide evidence for regional alterations within the cerebellum and the reorganization of the cerebrocerebellar system following poststroke aphasia and highlight the important role of the cerebellum in language processing within aphasic individuals after stroke.
{"title":"Regional Alteration within the Cerebellum and the Reorganization of the Cerebrocerebellar System following Poststroke Aphasia","authors":"Xiaotong Zhang, Zhaocong Chen, Na Li, Jingfeng Liang, Y. Zou, Huixiang Wu, Z. Kang, Z. Dou, Weihong Qiu","doi":"10.1155/2022/3481423","DOIUrl":"https://doi.org/10.1155/2022/3481423","url":null,"abstract":"Recently, an increasing number of studies have highlighted the role of the cerebellum in language processing. However, the role of neural reorganization within the cerebellum as well as within the cerebrocerebellar system caused by poststroke aphasia remains unknown. To solve this problem, in the present study, we investigated regional alterations of the cerebellum as well as the functional reorganization of the cerebrocerebellar circuit by combining structural and resting-state functional magnetic resonance imaging (fMRI) techniques. Twenty patients diagnosed with aphasia following left-hemispheric stroke and 20 age-matched healthy controls (HCs) were recruited in this study. The Western Aphasia Battery (WAB) test was used to assess the participants' language ability. Gray matter volume, spontaneous brain activity, functional connectivity, and effective connectivity were examined in each participant. We discovered that gray matter volumes in right cerebellar lobule VI and right Crus I were significantly lower in the patient group, and the brain activity within these regions was significantly correlated with WAB scores. We also discovered decreased functional connectivity within the crossed cerebrocerebellar circuit, which was significantly correlated with WAB scores. Moreover, altered information flow between the cerebellum and the contralateral cerebrum was found. Together, our findings provide evidence for regional alterations within the cerebellum and the reorganization of the cerebrocerebellar system following poststroke aphasia and highlight the important role of the cerebellum in language processing within aphasic individuals after stroke.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"1 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80437744","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}
Peripheral nerve injury can lead to partial or complete loss of limb function, and nerve transfer is an effective surgical salvage for patients with these injuries. The inability of deprived cortical regions representing damaged nerves to overcome corresponding maladaptive plasticity after the reinnervation of muscle fibers and sensory receptors is thought to be correlated with lasting and unfavorable functional recovery. However, the concept of central nervous system plasticity is rarely elucidated in classical textbooks involving peripheral nerve injury, let alone peripheral nerve transfer. This article is aimed at providing a comprehensive understanding of central nervous system plasticity involving peripheral nerve injury by reviewing studies mainly in human or nonhuman primate and by highlighting the functional and structural modifications in the central nervous system after peripheral nerve transfer. Hopefully, it will help surgeons perform successful nerve transfer under the guidance of modern concepts in neuroplasticity.
{"title":"Plasticity of the Central Nervous System Involving Peripheral Nerve Transfer","authors":"Jun Shen","doi":"10.1155/2022/5345269","DOIUrl":"https://doi.org/10.1155/2022/5345269","url":null,"abstract":"Peripheral nerve injury can lead to partial or complete loss of limb function, and nerve transfer is an effective surgical salvage for patients with these injuries. The inability of deprived cortical regions representing damaged nerves to overcome corresponding maladaptive plasticity after the reinnervation of muscle fibers and sensory receptors is thought to be correlated with lasting and unfavorable functional recovery. However, the concept of central nervous system plasticity is rarely elucidated in classical textbooks involving peripheral nerve injury, let alone peripheral nerve transfer. This article is aimed at providing a comprehensive understanding of central nervous system plasticity involving peripheral nerve injury by reviewing studies mainly in human or nonhuman primate and by highlighting the functional and structural modifications in the central nervous system after peripheral nerve transfer. Hopefully, it will help surgeons perform successful nerve transfer under the guidance of modern concepts in neuroplasticity.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"64 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89330226","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}
Hao Yu, Fei Xu, Xiangmei Hu, Yanni Tu, Qiuyu Zhang, Zheng Ye, T. Hua
Surround suppression (SS) is a phenomenon that a neuron's response to visual stimuli within the classical receptive field (cRF) is suppressed by a concurrent stimulation in the surrounding receptive field (sRF) beyond the cRF. Studies show that SS affects neuronal response contrast sensitivity in the primary visual cortex (V1). However, the underlying mechanisms remain unclear. Here, we examined SS effect on the contrast sensitivity of cats' V1 neurons with different preferred SFs using external noise-masked visual stimuli and perceptual template model (PTM) analysis at the system level. The contrast sensitivity was evaluated by the inverted threshold contrast of neurons in response to circular gratings of different contrasts in the cRF with or without an annular grating in the sRF. Our results showed that SS significantly reduced the contrast sensitivity of cats' V1 neurons. The SS-induced reduction of contrast sensitivity was not correlated with SS strength but was dependent on neuron's preferred SF, with a larger reduction for neurons with low preferred SFs than those with high preferred SFs. PTM analysis of threshold versus external noise contrast (TvC) functions indicated that SS decreased contrast sensitivity by increasing both the internal additive noise and impact of external noise for neurons with low preferred SFs, but improving only internal additive noise for neurons with high preferred SFs. Furthermore, the SS effect on the contrast-response function of low- and high-SF neurons also exhibited different mechanisms in contrast gain and response gain. Collectively, these results suggest that the mechanisms of SS effect on neuronal contrast sensitivity may depend on neuronal populations with different SFs.
{"title":"Mechanisms of Surround Suppression Effect on the Contrast Sensitivity of V1 Neurons in Cats","authors":"Hao Yu, Fei Xu, Xiangmei Hu, Yanni Tu, Qiuyu Zhang, Zheng Ye, T. Hua","doi":"10.1155/2022/5677655","DOIUrl":"https://doi.org/10.1155/2022/5677655","url":null,"abstract":"Surround suppression (SS) is a phenomenon that a neuron's response to visual stimuli within the classical receptive field (cRF) is suppressed by a concurrent stimulation in the surrounding receptive field (sRF) beyond the cRF. Studies show that SS affects neuronal response contrast sensitivity in the primary visual cortex (V1). However, the underlying mechanisms remain unclear. Here, we examined SS effect on the contrast sensitivity of cats' V1 neurons with different preferred SFs using external noise-masked visual stimuli and perceptual template model (PTM) analysis at the system level. The contrast sensitivity was evaluated by the inverted threshold contrast of neurons in response to circular gratings of different contrasts in the cRF with or without an annular grating in the sRF. Our results showed that SS significantly reduced the contrast sensitivity of cats' V1 neurons. The SS-induced reduction of contrast sensitivity was not correlated with SS strength but was dependent on neuron's preferred SF, with a larger reduction for neurons with low preferred SFs than those with high preferred SFs. PTM analysis of threshold versus external noise contrast (TvC) functions indicated that SS decreased contrast sensitivity by increasing both the internal additive noise and impact of external noise for neurons with low preferred SFs, but improving only internal additive noise for neurons with high preferred SFs. Furthermore, the SS effect on the contrast-response function of low- and high-SF neurons also exhibited different mechanisms in contrast gain and response gain. Collectively, these results suggest that the mechanisms of SS effect on neuronal contrast sensitivity may depend on neuronal populations with different SFs.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"123 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85669508","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}
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