Acta neurobiologiae experimentalis最新文献_第9页

Vinpocetine ameliorates developmental hyperserotonemia induced behavioral and biochemical changes: role of neuronal function, inflammation, and oxidative stress. 长春西汀改善发育性高血清素血症引起的行为和生化变化:神经元功能，炎症和氧化应激的作用。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2022-03-31 DOI: 10.55782/ane‑2022‑004

Kanishk Luhach, G. Kulkarni, Vijay P. Singh, Bhupesh Sharma

{"title":"Vinpocetine ameliorates developmental hyperserotonemia induced behavioral and biochemical changes: role of neuronal function, inflammation, and oxidative stress.","authors":"Kanishk Luhach, G. Kulkarni, Vijay P. Singh, Bhupesh Sharma","doi":"10.55782/ane‑2022‑004","DOIUrl":"https://doi.org/10.55782/ane‑2022‑004","url":null,"abstract":"Hyperserotonemia, during the early developmental phase, generates behavioral and biochemical phenotypes associated with autism spectrum disorder (ASD) in rats. Phosphodiesterase‑1 (PDE1) inhibitors are known to provide benefits in various brain conditions. We investigated the role of a selective PDE1 inhibitor, vinpocetine on ASD‑related behavioral phenotypes (social behavioral deficits, repetitive behavior, anxiety, and hyperlocomotion) in a developmental hyperserotonemia (DHS) rat model. Also, effects on biochemical markers related with neuronal function brain derived neurotrophic factor (BDNF) and phosphorylated cAMP response element binding protein (pCREB), inflammation interleukins (IL‑6 and IL‑10) and tumor necrosis factor-alpha (TNF‑α), and oxidative stress (TBARS and GSH) were studied in important brain areas (frontal cortex, cerebellum, hippocampus, and striatum). Administration of 5‑methoxytryptamine (5‑MT) to rats prenatally (gestational day 12) and in early developmental stages postnatal day (PND 0 - PND 20), resulted in impaired behavior and brain biochemistry. Administration of vinpocetine daily (10 and 20 mg/kg) to 5‑MT rats from PND 21 to PND 48 resulted in an improvement of behavioral deficits. Also, vinpocetine administration significantly increased the levels of BDNF, ratio of pCREB/ CREB, IL‑10, and GSH, and significantly decreased TNF‑α, IL‑6, and TBARS levels in different brain areas. Finally, our correlation analysis indicated that behavioral outcomes were significantly associated with the biochemical outcome. Vinpocetine, a selective PDE1 inhibitor, rectified important behavioral phenotypes related with ASD, possibly by improving markers of neuronal function, brain inflammation, and brain oxidative stress. Thus, PDE1 could be a potential target for pharmacological interventions and furthering our understanding of ASD pathogenesis.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"82 1 1","pages":"35-51"},"PeriodicalIF":1.4,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70810516","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}

引用次数: 2

Reduced expression of apoptotic proteins in the ischemic rat brain following Sertoli cell transplantation. 支持细胞移植后缺血大鼠脑中凋亡蛋白的表达降低。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2022-03-31 DOI: 10.55782/ane‑2022‑003

Nadia Khoshbaf Khiabanian, M. Bigdeli, S. Khaksar, A. Aliaghaei

{"title":"Reduced expression of apoptotic proteins in the ischemic rat brain following Sertoli cell transplantation.","authors":"Nadia Khoshbaf Khiabanian, M. Bigdeli, S. Khaksar, A. Aliaghaei","doi":"10.55782/ane‑2022‑003","DOIUrl":"https://doi.org/10.55782/ane‑2022‑003","url":null,"abstract":"Sertoli cells (SCs) may be a new candidate to decrease ischemic damage due to their ability to secrete factors that actively protect neurons and inhibit uncontrollable immune responses. Pre‑treatment with these cells was considered in the current study. SCs were injected into the right striatum in rats using the stereotaxic technique. Ten days after injection, middle cerebral artery occlusion surgery was performed. Following these procedures, neurological deficit scores, brain edema, blood‑brain barrier integrity, infarct volume, and the expression of apoptotic factors in the cortex, striatum, and piriform cortex‑amygdala were evaluated. Analysis showed that behavioral deficits, infarct volume, blood‑brain barrier permeability, and edema in the striatal area in the allograft group demonstrated a significant decrease compared to the control group. Additionally, analysis of the expression of caspase‑3 and Bcl‑2 proteins in the striatum indicated a remarkable reduction and increase, respectively, in the allograft group compared to the control group. According to the obtained results, one possible mechanism for the neuroprotection induced by SCs in an ischemic brain is the reduction of apoptotic factors.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"82 1 1","pages":"22-34"},"PeriodicalIF":1.4,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70810359","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}

引用次数: 0

Overexpression of C9orf72 exacerbates Aβ25‑35‑induced oxidative stress and apoptosis in PC12 cells. C9orf72的过表达加剧了Aβ25‑35诱导的PC12细胞氧化应激和凋亡。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2022-03-31 DOI: 10.55782/ane‑2022‑007

Jing Chen, Mingming Zhang, H. Bai, Peiyu Shi, Meng Du, Shijie Zhang, Jiyu Lou

{"title":"Overexpression of C9orf72 exacerbates Aβ25‑35‑induced oxidative stress and apoptosis in PC12 cells.","authors":"Jing Chen, Mingming Zhang, H. Bai, Peiyu Shi, Meng Du, Shijie Zhang, Jiyu Lou","doi":"10.55782/ane‑2022‑007","DOIUrl":"https://doi.org/10.55782/ane‑2022‑007","url":null,"abstract":"Alzheimer's disease (AD) is the most common neurodegenerative disease and is manifested by memory loss and spatial disorientation. There is currently no effective treatment for AD. Abnormalities of the chromosome 9 open reading frame 72 (C9ORF72) gene have been associated with various neurodegenerative diseases. However, its intrinsic roles in AD remain to be elucidated. Here we found that Aβ25‑35 increased the expression of C9orf72 in PC12 cells at both mRNA and protein levels. In Aβ25‑35‑treated PC12 cells, C9orf72 overexpression induced an abnormally condensed and fragmented nucleus and apoptosis, as well as significantly enhanced reactive oxygen species (ROS) levels. Mechanistically, an Aβ25‑35‑induced decrease of superoxide dismutase activity was augmented by C9orf72 overexpression, which in contrast increased malondialdehyde content. Consistently, further apoptotic analysis revealed significant downregulation of Bcl‑2 and Bcl‑xL expression and enhanced cleavage of caspase‑3 with Aβ25‑35 treatment, all of which were exacerbated by C9orf72 overexpression. In addition, tau phosphorylation, another hallmark of AD pathology, was induced by Aβ25‑35 and was remarkably enhanced by C9orf72 overexpression. Our data indicate that C9orf72 plays important roles in intracellular ROS signaling and Aβ25‑35‑induced neuronal apoptosis in AD. These findings provide insights into C9orf72 function in the pathogenesis of many related neurodegenerative diseases and provide a basis for potential therapeutic interventions.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"82 1 1","pages":"77-87"},"PeriodicalIF":1.4,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70810536","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}

引用次数: 1

Blocking of NF‑kB/p38 MAPK pathways mitigates oligodendrocyte pathology in a model of neonatal white matter injury. 阻断NF‑kB/p38 MAPK通路可减轻新生儿白质损伤模型中的少突胶质细胞病理。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2022-03-31 DOI: 10.55782/ane‑2022‑005

Mohamed A. Al-Griw, M. Salter, I. Wood

{"title":"Blocking of NF‑kB/p38 MAPK pathways mitigates oligodendrocyte pathology in a model of neonatal white matter injury.","authors":"Mohamed A. Al-Griw, M. Salter, I. Wood","doi":"10.55782/ane‑2022‑005","DOIUrl":"https://doi.org/10.55782/ane‑2022‑005","url":null,"abstract":"Reactive gliosis and inflammation are risk factors for white matter injury (WMI) development, which are correlated with the development of many neurodevelopmental deficits with no treatment. This study aimed to understand the mechanisms correlated with WMI, with a particular focus on the role of nuclear factor‑kappa B (NF‑kB) and p38 mitogen‑activated protein kinases (MAPKs) pathways. Seven‑day‑old Wistar rats were used to generate cerebellar tissue slices. Slices were cultured and randomly allocated to one of 3 groups and treated as follows: group‑I (control); group‑II (WMI), slices were subjected to 20 min of oxygen‑glucose deprivation (OGD); group‑III (WMI+ blockers), slices were subjected to OGD and treated with the blockers. Results showed that OGD insult triggered a marked increase in the apoptosis among WM elements, as confirmed by TUNEL assay. Immunocytochemical experiments revealed that there was a significant decrease in the percent of MBP+ OLs and NG2+ OPCs, and myelin integrity. There was also a significant increase in the percent of reactive microglia and astrocytes. BrdU immunostaining revealed there was an increase in the percent of proliferating microglia and astrocytes. Q‑RT‑PCR results showed OGD upregulated the expression levels of cytokines (TNF‑α, IL‑1, IL‑6, and IL‑1β) and inducible nitric oxide synthase (iNOS). On the other hand, treatment with BAY11 or SB203580 significantly enhanced the OL survival, restored myelin loss, and reduced microglia and astrocyte reactivity, and downregulated the iNOS and cytokine expression. Our findings demonstrate that blocking of NF‑KB/p38 MAPK pathways alleviated reactive gliosis, inflammation, and OL loss upon WMI. The findings may help to develop therapeutic interventions for WMI.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"82 1 1","pages":"52-64"},"PeriodicalIF":1.4,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70810757","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}

引用次数: 6

LncRNA NEAT1 alleviates ischemic stroke via transcriptional inhibition of NLRP3 mediated by the miR‑10b‑5p/BCL6 axis. LncRNA NEAT1通过miR - 10b - 5p/BCL6轴介导的NLRP3转录抑制来缓解缺血性卒中。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2022-03-31 DOI: 10.55782/ane‑2022‑002

Zhi-Wen Zhou, Xiang Ren, Wen-Sheng Zhou, Ai-Ping Li, Lijun Zheng

{"title":"LncRNA NEAT1 alleviates ischemic stroke via transcriptional inhibition of NLRP3 mediated by the miR‑10b‑5p/BCL6 axis.","authors":"Zhi-Wen Zhou, Xiang Ren, Wen-Sheng Zhou, Ai-Ping Li, Lijun Zheng","doi":"10.55782/ane‑2022‑002","DOIUrl":"https://doi.org/10.55782/ane‑2022‑002","url":null,"abstract":"Cerebral ischemic stroke (CIS) is a significant cause of disability and death. Inflammation usually occurs after CIS and accelerates cellular damage. NLRP3 plays a key role in the formation of CIS‑associated inflammasome. Understanding how NLRP3 is regulated bears great importance. We hypothesized that lncRNA NEAT1 can downregulate NLRP3 expression by regulating the miR‑10b‑5p/BCL6 axis, and thus regulate microglia‑driven inflammation. The expression of NEAT1 was analyzed in CIS patients and an in vitro model of oxygen and glucose deprivation/re‑oxygenation (OGD/R). We assessed the levels of pro‑inflammatory cytokines IL‑18 and IL‑1β with ELISA. Interactions between NEAT1/miR‑10b‑5p and miR‑10b‑5p/BCL6 were determined by luciferase assay. The interaction of BCL6 and NLRP3 was identified by ChIP; RNA, and protein levels were evaluated by qRT‑PCR and western blot, respectively. We found that NEAT1 level was decreased in CIS patients and OGD/R treated cells. OGD/R exerted pro‑inflammasome effects by increasing the expression of inflammasome‑associated proteins and ROS and malondialdehyde (MDA) while inhibiting SOD production. This effect was partially antagonized by NEAT1. We bioinformatically identified interactions between NEAT1/miR‑10b‑5p, BCL6/miR‑10b‑5p, and NLRP3‑promoter/BCL6, and validated them by luciferase assay, qRT‑PCR, and ChIP. NEAT1 inhibited miR‑10b‑5p and upregulated BCL6 by ceRNA mechanism and alleviated OGD/R induced cell damage. We also proved that BCL6 was a repressive transcription factor in the regulation of NLRP3 expression. Thus, lncRNA NEAT1 inhibited inflammasome activation by NLRP3 in microglia via the NEAT1/ miR‑10b‑5p/BCL6/NLRP3 regulatory axis, which alleviated deleterious outcomes of ischemic stroke.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"5 1","pages":"12-21"},"PeriodicalIF":1.4,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70810289","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}

引用次数: 3

The effect of Madopar on absence‑like seizures in WAG/Rij rats. 美多巴对WAG/Rij大鼠失神样癫痫发作的影响。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2022-03-31 DOI: 10.55782/ane‑2022‑008

Ali Al-Kaleel, O. Erbaş, H. Aygün

{"title":"The effect of Madopar on absence‑like seizures in WAG/Rij rats.","authors":"Ali Al-Kaleel, O. Erbaş, H. Aygün","doi":"10.55782/ane‑2022‑008","DOIUrl":"https://doi.org/10.55782/ane‑2022‑008","url":null,"abstract":"The aim of this study was to investigate the effect of Madopar on the absence seizures and the anxiety‑like behavior (assessed using the open field test) in Wistar Albino Glaxo/Rijswijk (WAG/Rij) rats. Twenty‑eight male WAG/Rij rats were randomly divided into four groups: group I: control; group II: Madopar 5 mg/kg; group III: Madopar 50 mg/kg; group IV: Madopar 100 mg/kg. A tripolar electrode was attached to all WAG/Rij rats. Electrocorticography (ECoG) recordings were made before and after Madopar (5, 50, and 100 mg/kg) injection for three hours. Anxiety‑related behavior was studied using the open field test for 5 min after the ECoG recordings. Madopar significantly reduced the number and duration of spike‑wave discharges (SWDs) when compared to the control group. The highest dose of Madopar (100 mg/kg) significantly reduced the duration of SWDs when compared to Madopar (5 mg/kg). All Madopar doses did not alter the duration of grooming, but the highest doses of Madopar significantly increased the number of squares crossed in the open field test when compared to the control and Madopar (5 mg/kg) groups. These results revealed that Madopar reduced the absence‑like seizures and the anxiety‑related behavior in WAG/Rij rats. This may emphasize the therapeutic properties of the Madopar/L‑dopa in absence epilepsy.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"130 1","pages":"88-95"},"PeriodicalIF":1.4,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70810660","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}

引用次数: 0

Identification of microRNA/target gene in the dentate gyrus of 7‑day‑old mice following isoflurane exposure. 异氟醚暴露后7日龄小鼠齿状回中microRNA/靶基因的鉴定

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2022-03-31 DOI: 10.55782/ane‑2022‑009

Bing Yang, Chu-Tong Zhang, Le-Fan Liu, Xiao-Lin Wu, H. Hu, Yu Chen, Muneeb Iqbal, Yan-bing Ma, Jin-Song Zhou, X. Xiao, Jianxin Liu

{"title":"Identification of microRNA/target gene in the dentate gyrus of 7‑day‑old mice following isoflurane exposure.","authors":"Bing Yang, Chu-Tong Zhang, Le-Fan Liu, Xiao-Lin Wu, H. Hu, Yu Chen, Muneeb Iqbal, Yan-bing Ma, Jin-Song Zhou, X. Xiao, Jianxin Liu","doi":"10.55782/ane‑2022‑009","DOIUrl":"https://doi.org/10.55782/ane‑2022‑009","url":null,"abstract":"Studies on rodents and nonhuman primates suggest that exposure to anesthetics, particularly in the young brain, is associated with neuronal apoptosis as well as hippocampal‑dependent cognitive dysfunction. Disruption of the development of dentate gyrus may play an important role in anesthetics‑induced neurotoxicity. However, the anesthetics triggered molecular events in the dentate gyrus of the developing brain are poorly understood. By integrating two independent data sets obtained from miRNA‑seq and mRNA‑seq respectively, this study aims to profile the network of miRNA and potential target genes, as well as relevant events occurring in the dentate gyrus of isoflurane exposed 7‑day‑old mice. We found that a single four hours exposure to isoflurane yielded 1059 pairs of differently expressed miRNAs/target genes in the dentate gyrus. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis further indicates that dysregulated miRNAs/target genes have far‑reaching effects on the cellular pathophysiological events, such as cell apoptosis, axon development, and synaptic transmission. Our results would greatly broaden our functional understanding of the role of miRNA/target gene in the context of anesthetics‑induced neurotoxicity.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"82 1 1","pages":"96-105"},"PeriodicalIF":1.4,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70811096","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}

引用次数: 2

Optical coherence tomography reveals heterogeneity of the brain tissue and vasculature in the ischemic region after photothrombotic stroke in mice. 光学相干断层扫描显示小鼠光血栓性中风后缺血区域的脑组织和血管的异质性。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2022-03-31 DOI: 10.55782/ane‑2022‑010

H. Doleżyczek, P. Kasprzycki, J. Włodarczyk, M. Wojtkowski, M. Malinowska

{"title":"Optical coherence tomography reveals heterogeneity of the brain tissue and vasculature in the ischemic region after photothrombotic stroke in mice.","authors":"H. Doleżyczek, P. Kasprzycki, J. Włodarczyk, M. Wojtkowski, M. Malinowska","doi":"10.55782/ane‑2022‑010","DOIUrl":"https://doi.org/10.55782/ane‑2022‑010","url":null,"abstract":"We demonstrate in vivo imaging of the ischemic area in the mouse brain after photostroke using a custom prototype Gaussian‑beam optical coherence tomography (OCT) setup in which the near infrared imaging beam and the green photoinducing light pass through the same objective lens. The goal of our research was analysis of vascularity of the ischemic area during 2‑week progress of stroke and correlating the hypo‑ and hyperreflective OCT scattering areas with the location of activated microglia and astroglia. Angiogenesis, which was assessed using angiomaps, showed that the area of vessels in the ischemic center increased until day 7. OCT imaging revealed a heterogeneous scattering signal pattern in the ischemic area. On structural OCT images, we found presence of a core area of ischemia with a hyporeflective OCT signal and a halo of hyperreflective signal around the core. The core signal decreased in size by 70% by day 14. Immunocytochemistry revealed that the hyporeflective area in the ischemic core was associated with microglia/macrophage activation, whereas the hyperreflective signal from the halo came from activated astrocytes.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"82 1 1","pages":"106-119"},"PeriodicalIF":1.4,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70811251","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}

引用次数: 0

Impact of COVID‑19 infection in patients with neurodegenerative diseases with particular focus on Alzheimer's and Parkinson's disease. COVID - 19感染对神经退行性疾病患者的影响，特别是阿尔茨海默病和帕金森病。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2022-01-01 DOI: 10.55782/ane-2022-040

Prathima Guntipalli, Sirisha Gara, Sujan Poudel, Aakash Hans, Muhammad Abdullah Usman, Deeksha Dhar, Ramya Pakala, Sangam Shah, Sangharsha Thapa, Sudarshan Acharya, Kester J Nedd, Sam Kara

{"title":"Impact of COVID‑19 infection in patients with neurodegenerative diseases with particular focus on Alzheimer's and Parkinson's disease.","authors":"Prathima Guntipalli, Sirisha Gara, Sujan Poudel, Aakash Hans, Muhammad Abdullah Usman, Deeksha Dhar, Ramya Pakala, Sangam Shah, Sangharsha Thapa, Sudarshan Acharya, Kester J Nedd, Sam Kara","doi":"10.55782/ane-2022-040","DOIUrl":"https://doi.org/10.55782/ane-2022-040","url":null,"abstract":"Neurodegenerative disorders (NDD) are chronic neurological diseases characterized by loss and/or damage to neurons along with the myelin sheath, and patients are at higher risk of severe infection with the SARS‑CoV‑2. A comprehensive literature search was performed using relevant terms and inclusion‑exclusion criteria. Recent articles, subjects older than 50 years, and articles written in the English language were included, whereas letters to the editor and articles related to pregnant women were excluded from the review study. COVID‑19 appears to damage angiotensin‑II receptors which cause natural killer cells to lose the ability to clear virus‑infected cells, owing to worse outcomes in patients with NDD. COVID‑19 can worsen the symptoms of Alzheimer's disease. In addition, COVID‑19 worsens drug‑responsive motor symptoms in Parkinson's disease (PD) and other symptoms like fatigue and urinary complaints. Vitamin D is essential in decreasing pro‑inflammatory and increasing anti‑inflammatory cytokines in ongoing COVID‑19 infections and reducing angiotensin receptors and, hence, decreasing COVID‑19 infection severity. Telemedicine shows promise for patients with NDD but is yet to overcome legal issues and personal barriers. COVID‑19 has a significant effect on neurodegenerative conditions, which appears partly to the nature of the NDD and the neuro‑invasive capabilities of the SARS‑CoV‑2. The protective role of vitamin D in patients with NDD further supports this hypothesis. Modifications in current health care, like the telemedicine platform, are required to address the increased risk of serious infection in this population. Further studies will be required to clarify conflicting reports in many fields.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"82 4","pages":"424-432"},"PeriodicalIF":1.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9222509","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}

引用次数: 0

The effect of taxifolin on oxidative sciatic nerve damage induced by cobalt chloride in rats: a biochemical and histopathological evaluation. 杉木素对氯化钴致大鼠坐骨神经氧化损伤的生物化学和组织病理学影响。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2022-01-01 DOI: 10.55782/ane-2022-024

Ceyda Tanoğlu, Alevtina Ersoy, Taha Abdulkadir Çoban, Gülce Naz Yazıcı, Renad Mammadov, Bahadır Süleyman

{"title":"The effect of taxifolin on oxidative sciatic nerve damage induced by cobalt chloride in rats: a biochemical and histopathological evaluation.","authors":"Ceyda Tanoğlu, Alevtina Ersoy, Taha Abdulkadir Çoban, Gülce Naz Yazıcı, Renad Mammadov, Bahadır Süleyman","doi":"10.55782/ane-2022-024","DOIUrl":"https://doi.org/10.55782/ane-2022-024","url":null,"abstract":"Cobalt is a trace element that increases lipid peroxidation and malondialdehyde levels and reduces the antioxidant defense mechanisms of nerve cells. High levels of cobalt exposure may cause peripheral neuropathy, but the mechanism behind this has not yet been elucidated. Taxifolin is a flavonoid whose antioxidant and anti‑inflammatory properties are well‑known. We aimed to investigate the effect of taxifolin on cobalt‑induced oxidative sciatic nerve damage. Eighteen albino male Wistar rats were assigned to three groups: Control, Cobalt, and Taxifolin + Cobalt groups. Total oxidant and total antioxidant status and levels of malondialdehyde, total glutathione, and superoxide dismutase were measured to determine the effect of taxifolin on cobalt‑induced sciatic nerve injury. The following statistically significant effect of taxifolin was observed: It prevented cobalt‑induced oxidative sciatic nerve damage by reducing malondialdehyde levels and total oxidant status and increasing total antioxidant status, total glutathione levels, and superoxide dismutase levels. In a histopathological analysis, we observed similar findings in Control and Taxifolin + Cobalt groups. We determined that taxifolin is effective in preventing cobalt‑induced oxidative damage in sciatic nerve injury.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"82 3","pages":"254-262"},"PeriodicalIF":1.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33498381","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}

引用次数: 1