The Experts below are selected from a list of 3915 Experts worldwide ranked by ideXlab platform

David C. Henshall - One of the best experts on this subject based on the ideXlab platform.

  • microRNAs in the Pathophysiology of Epilepsy.
    Neuroscience letters, 2017
    Co-Authors: Gary P. Brennan, David C. Henshall
    Abstract:

    Temporal lobe Epilepsy is a common and often drug-resistant seizure disorder. The underlying pathological processes which give rise to the development of spontaneous seizures include neuroinflammation, cell loss, neurogenesis and dendritic abnormalities and many of these are driven by insult-induced changes in gene expression and gene expression regulation. MicroRNAs are powerful modulators of post-transcriptional gene expression which are dysregulated during epileptogenesis. The advent of locked nucleic acid (LNA) based inhibitory methods and mimic technology has facilitated in vivo functional assessment of these molecules in Epilepsy. Here we review recent advances in our understanding of the role of these short non-coding RNAs in the Pathophysiology of Epilepsy.

  • P2X7 receptor in Epilepsy; role in Pathophysiology and potential targeting for seizure control
    International journal of physiology pathophysiology and pharmacology, 2012
    Co-Authors: Tobias Engel, Alba Jimenez-pacheco, María Teresa Miras-portugal, Miguel Díaz-hernández, David C. Henshall
    Abstract:

    The P2X7 receptor is an ATP-gated non-selective cation-permeable ionotropic receptor selectively expressed in neurons and glia in the brain. Activation of the P2X7 receptor has been found to modulate neuronal excitability in the hippocampus and it has also been linked to microglia activation and neuroinflammatory responses. Accordingly, interest developed on the P2X7 receptor in disorders of the nervous system, including Epilepsy. Studies show that expression of the P2X7 receptor is elevated in damaged regions of the brain after prolonged seizures (status epilepticus) in both neurons and glia. P2X7 receptor expression is also increased in the hippocampus in experimental Epilepsy. Recent data show that mice lacking the P2X7 receptor display altered susceptibility to status epilepticus and that drugs targeting the P2X7 receptor have potent anticonvulsant effects. Together, this suggests that P2X7 receptor ligands may be useful adjunctive treatments for refractory status epilepticus or perhaps pharmacoresistant Epilepsy. This review summarizes the evidence of P2X7 receptor involvement in the Pathophysiology of Epilepsy and the potential of drugs targeting this receptor for seizure control.

Guojun Chen - One of the best experts on this subject based on the ideXlab platform.

  • Increased expression of calponin-3 in epileptic patients and experimental rats.
    Experimental neurology, 2011
    Co-Authors: Yanbing Han, Huan Yin, Qiong Zhu, Jing Luo, Xuefeng Wang, Guojun Chen
    Abstract:

    Abstract Calponin-3 is an actin-interacting protein and is expressed in the brain. Our previous microarray scan has found an up-regulation of calponin-3 gene CNN3 in the temporal lobe of patients with drug-resistant Epilepsy. Here we investigated in epileptic patients the changes of brain and cerebrospinal fluid (CSF) calponin-3 expressions, and assessed calponin-3 expression pattern in a rat model of pilocarpine-induced Epilepsy. We showed that in the temporal neocortices of 30 patients with drug-resistant Epilepsy, both mRNA and protein level of calponin-3 were significantly increased. In addition, the augmentation of CSF calponin-3 from 126 epileptic patients was closely correlated with disease duration. Moreover, in the cortices of temporal lobes of pilocarpine-treated rats, calponin-3 increased along with the time and maintained at significant high levels for up to 2 months, while the up-regulation of hippocampal calponin-3 only occurred at 24 h and 1 week. The elevated calponin-3 suggests that deregulation of actin filament dynamics in axonal and dendritic outgrowth and synaptic rearrangement may contribute to Pathophysiology of Epilepsy. Highlights ►Calponin-3 is an actin-interacting protein. ►Calponin-3 was significantly increased in the cortices and CSF of patients with Epilepsy. ►In a rat model of Epilepsy, cortical and hippocampal calponin-3 was significantly upregulated for up to 2 months. ►Deregulated actin-binding protein may play a role in the Pathophysiology of Epilepsy.

  • Increased expression of placental growth factor in patients with temporal lobe Epilepsy and a rat model.
    Brain research, 2011
    Co-Authors: Jing Luo, Xuefeng Wang, Xiaogang Zhang, Zonggang Yue, Chunlei Zhou, Fenghua Zhao, Guojun Chen
    Abstract:

    Abstract Placental growth factor (PIGF) plays a role in angiogenesis and neuroprotection. It has been suggested that angiogenesis and blood–brain barrier damage are involved in the Pathophysiology of Epilepsy. In this study, we investigated the PIGF expression in the temporal neocortices of 11 patients with pharmaco-resistant temporal lobe Epilepsy (TLE) and 6 non-epileptic controls, using double immunofluorescence labeling, immunohistochemistry and Western blotting. We also assessed PIGF expression pattern in a rat model of TLE induced by lithium chloride-pilocarpine. We found that PIGF expression was significantly elevated in patients with TLE than in control. TLE patients with initial injuries had significantly higher PIGF level than those without initial injuries. In the TLE rat model, PIGF upregulation started at 6 h after status epilepticus and maintained at significant high level for up to 60 days. These results suggest that the augmentation of brain PIGF is associated with development of Epilepsy.

Ashok K Shetty - One of the best experts on this subject based on the ideXlab platform.

  • chronobiology of limbic seizures potential mechanisms and prospects of chronotherapy for mesial temporal lobe Epilepsy
    Neuroscience & Biobehavioral Reviews, 2019
    Co-Authors: Daniel Leite Goes Gitai, Tiago Gomes De Andrade, Ygor Daniel Ramos Dos Santos, Sahithi Attaluri, Ashok K Shetty
    Abstract:

    Abstract Mesial Temporal Lobe Epilepsy (mTLE) characterized by progressive development of complex partial seizures originating from the hippocampus is the most prevalent and refractory type of Epilepsy. One of the remarkable features of mTLE is the rhythmic pattern of occurrence of spontaneous seizures, implying a dependence on the endogenous clock system for seizure threshold. Conversely, circadian rhythms are affected by Epilepsy too. Comprehending how the circadian system and seizures interact with each other is essential for understanding the Pathophysiology of Epilepsy as well as for developing innovative therapies that are efficacious for better seizure control. In this review, we confer how the temporal dysregulation of the circadian clock in the hippocampus combined with multiple uncoupled oscillators could lead to periodic seizure occurrences and comorbidities. Unraveling these associations with additional research would help in developing chronotherapy for mTLE, based on the chronobiology of spontaneous seizures. Notably, differential dosing of antiepileptic drugs over the circadian period and/or strategies that resynchronize biological rhythms may substantially improve the management of seizures in mTLE patients.

Jing Luo - One of the best experts on this subject based on the ideXlab platform.

  • Increased Placental Growth Factor in Cerebrospinal Fluid of Patients with Epilepsy
    Neurochemical research, 2011
    Co-Authors: Ying Zhang, Qiong Zhu, Jing Luo, Zhenli Guo, Hongxiang Yin, Kebin Zeng, Liang Wang, Xiaogang Zhang
    Abstract:

    Recent studies suggest that angiogenesis and vascular endothelial growth factor (VEGF) are involved in the Pathophysiology of Epilepsy. However, relatively little data are available linking placenta growth factor (PIGF) with Epilepsy. In this study, we assessed concentrations of PIGF in cerebrospinal fluid (CSF) of 60 epileptic patients and 24 non-seizure subjects using sandwich enzyme-linked immunosorbent assays. Epileptic patients in general had higher concentration of CSF-PIGF than controls (7.95 ± 0.88 ng/l vs. 5.87 ± 0.79 ng/l, P 5 years was higher than those in patients with durations of 1–5 years and

  • Increased expression of calponin-3 in epileptic patients and experimental rats.
    Experimental neurology, 2011
    Co-Authors: Yanbing Han, Huan Yin, Qiong Zhu, Jing Luo, Xuefeng Wang, Guojun Chen
    Abstract:

    Abstract Calponin-3 is an actin-interacting protein and is expressed in the brain. Our previous microarray scan has found an up-regulation of calponin-3 gene CNN3 in the temporal lobe of patients with drug-resistant Epilepsy. Here we investigated in epileptic patients the changes of brain and cerebrospinal fluid (CSF) calponin-3 expressions, and assessed calponin-3 expression pattern in a rat model of pilocarpine-induced Epilepsy. We showed that in the temporal neocortices of 30 patients with drug-resistant Epilepsy, both mRNA and protein level of calponin-3 were significantly increased. In addition, the augmentation of CSF calponin-3 from 126 epileptic patients was closely correlated with disease duration. Moreover, in the cortices of temporal lobes of pilocarpine-treated rats, calponin-3 increased along with the time and maintained at significant high levels for up to 2 months, while the up-regulation of hippocampal calponin-3 only occurred at 24 h and 1 week. The elevated calponin-3 suggests that deregulation of actin filament dynamics in axonal and dendritic outgrowth and synaptic rearrangement may contribute to Pathophysiology of Epilepsy. Highlights ►Calponin-3 is an actin-interacting protein. ►Calponin-3 was significantly increased in the cortices and CSF of patients with Epilepsy. ►In a rat model of Epilepsy, cortical and hippocampal calponin-3 was significantly upregulated for up to 2 months. ►Deregulated actin-binding protein may play a role in the Pathophysiology of Epilepsy.

  • Increased expression of placental growth factor in patients with temporal lobe Epilepsy and a rat model.
    Brain research, 2011
    Co-Authors: Jing Luo, Xuefeng Wang, Xiaogang Zhang, Zonggang Yue, Chunlei Zhou, Fenghua Zhao, Guojun Chen
    Abstract:

    Abstract Placental growth factor (PIGF) plays a role in angiogenesis and neuroprotection. It has been suggested that angiogenesis and blood–brain barrier damage are involved in the Pathophysiology of Epilepsy. In this study, we investigated the PIGF expression in the temporal neocortices of 11 patients with pharmaco-resistant temporal lobe Epilepsy (TLE) and 6 non-epileptic controls, using double immunofluorescence labeling, immunohistochemistry and Western blotting. We also assessed PIGF expression pattern in a rat model of TLE induced by lithium chloride-pilocarpine. We found that PIGF expression was significantly elevated in patients with TLE than in control. TLE patients with initial injuries had significantly higher PIGF level than those without initial injuries. In the TLE rat model, PIGF upregulation started at 6 h after status epilepticus and maintained at significant high level for up to 60 days. These results suggest that the augmentation of brain PIGF is associated with development of Epilepsy.

Xuefeng Wang - One of the best experts on this subject based on the ideXlab platform.

  • Increased expression of calponin-3 in epileptic patients and experimental rats.
    Experimental neurology, 2011
    Co-Authors: Yanbing Han, Huan Yin, Qiong Zhu, Jing Luo, Xuefeng Wang, Guojun Chen
    Abstract:

    Abstract Calponin-3 is an actin-interacting protein and is expressed in the brain. Our previous microarray scan has found an up-regulation of calponin-3 gene CNN3 in the temporal lobe of patients with drug-resistant Epilepsy. Here we investigated in epileptic patients the changes of brain and cerebrospinal fluid (CSF) calponin-3 expressions, and assessed calponin-3 expression pattern in a rat model of pilocarpine-induced Epilepsy. We showed that in the temporal neocortices of 30 patients with drug-resistant Epilepsy, both mRNA and protein level of calponin-3 were significantly increased. In addition, the augmentation of CSF calponin-3 from 126 epileptic patients was closely correlated with disease duration. Moreover, in the cortices of temporal lobes of pilocarpine-treated rats, calponin-3 increased along with the time and maintained at significant high levels for up to 2 months, while the up-regulation of hippocampal calponin-3 only occurred at 24 h and 1 week. The elevated calponin-3 suggests that deregulation of actin filament dynamics in axonal and dendritic outgrowth and synaptic rearrangement may contribute to Pathophysiology of Epilepsy. Highlights ►Calponin-3 is an actin-interacting protein. ►Calponin-3 was significantly increased in the cortices and CSF of patients with Epilepsy. ►In a rat model of Epilepsy, cortical and hippocampal calponin-3 was significantly upregulated for up to 2 months. ►Deregulated actin-binding protein may play a role in the Pathophysiology of Epilepsy.

  • Increased expression of placental growth factor in patients with temporal lobe Epilepsy and a rat model.
    Brain research, 2011
    Co-Authors: Jing Luo, Xuefeng Wang, Xiaogang Zhang, Zonggang Yue, Chunlei Zhou, Fenghua Zhao, Guojun Chen
    Abstract:

    Abstract Placental growth factor (PIGF) plays a role in angiogenesis and neuroprotection. It has been suggested that angiogenesis and blood–brain barrier damage are involved in the Pathophysiology of Epilepsy. In this study, we investigated the PIGF expression in the temporal neocortices of 11 patients with pharmaco-resistant temporal lobe Epilepsy (TLE) and 6 non-epileptic controls, using double immunofluorescence labeling, immunohistochemistry and Western blotting. We also assessed PIGF expression pattern in a rat model of TLE induced by lithium chloride-pilocarpine. We found that PIGF expression was significantly elevated in patients with TLE than in control. TLE patients with initial injuries had significantly higher PIGF level than those without initial injuries. In the TLE rat model, PIGF upregulation started at 6 h after status epilepticus and maintained at significant high level for up to 60 days. These results suggest that the augmentation of brain PIGF is associated with development of Epilepsy.

  • Decreased expression of thyroid receptor-associated protein 220 in temporal lobe tissue of patients with refractory Epilepsy.
    Biochemical and biophysical research communications, 2006
    Co-Authors: Xuefeng Wang, Yun Gong, Feng-ying Liu, Ji-jun Sun, Guo-ming Luan, Yuping Wang
    Abstract:

    Purpose: TRAP220 (thyroid hormone receptor-associated protein) functions as a coactivator for nuclear receptors and stimulates transcription by recruiting the TRAP mediator complex to hormone responsive promoter regions. Thus, TRAP220 enhances the function of thyroid/steroid hormone receptors such as thyroid hormone and oestrogen receptors. This study investigated the expression of TRAP220 mRNA and protein level in epileptic brains comparing with human control. Methods: We examined the expression of TRAP220 mRNA and protein levels in temporal lobes from patients with chronic pharmacoresistant Epilepsy who have undergone surgery. Results: Expression of TRAP220 mRNA and protein was shown to be decreased significantly in the temporal cortex of the patients with Epilepsy. Conclusions: Our work showed that a decrease in TRAP220 mRNA and protein levels may be involved in the Pathophysiology of Epilepsy and may be associated with impairment of the brain caused by frequent seizures.