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Immunotherapy by targeting of VGKC complex for seizure control and prevention of cognitive impairment in a mouse model of epilepsy
Epilepsy is a type of refractory neurologic disorder mental disease, which is associated with cognitive impairments and memory dysfunction. However, the potential mechanisms of epilepsy are not well understood. Previous evidence has identified the voltage gated potassium channel complex (VGKC) as a...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6059666/ https://www.ncbi.nlm.nih.gov/pubmed/29749462 http://dx.doi.org/10.3892/mmr.2018.9004 |
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author | Fan, Zhiliang Feng, Xiaojuan Fan, Zhigang Zhu, Xingyuan Yin, Shaohua |
author_facet | Fan, Zhiliang Feng, Xiaojuan Fan, Zhigang Zhu, Xingyuan Yin, Shaohua |
author_sort | Fan, Zhiliang |
collection | PubMed |
description | Epilepsy is a type of refractory neurologic disorder mental disease, which is associated with cognitive impairments and memory dysfunction. However, the potential mechanisms of epilepsy are not well understood. Previous evidence has identified the voltage gated potassium channel complex (VGKC) as a target in various cohorts of patients with epilepsy. In the present study, the efficacy of an antibody against VGKC (anti-VGKC) for the treatment of epilepsy in mice was investigated. A mouse model of lithium-pilocarpine temporal lobe epilepsy was established and anti-VGKC treatment was administered for 30 days. Memory impairment, anxiety, visual attention, inhibitory control and neuronal loss were measured in the mouse model of lithium-pilocarpine temporal lobe epilepsy. The results revealed that epileptic mice treated with anti-VGKC were able to learn the task and presented attention impairment, even a tendency toward impulsivity and compulsivity. It was also exhibited that anti-VGKC treatment decreased neuronal loss in structures classically associated with attentional performance in hippocampus. Mice who received Anti-VGKC treatment had inhibited motor seizures and hippocampal damage as compared with control mice. In conclusion, these results indicated that anti-VGKC treatment may present benefits for improvements of the condition of motor attention impairment and cognitive competence, which suggests that VGKC may be a potential target for the treatment of epilepsy. |
format | Online Article Text |
id | pubmed-6059666 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-60596662018-07-26 Immunotherapy by targeting of VGKC complex for seizure control and prevention of cognitive impairment in a mouse model of epilepsy Fan, Zhiliang Feng, Xiaojuan Fan, Zhigang Zhu, Xingyuan Yin, Shaohua Mol Med Rep Articles Epilepsy is a type of refractory neurologic disorder mental disease, which is associated with cognitive impairments and memory dysfunction. However, the potential mechanisms of epilepsy are not well understood. Previous evidence has identified the voltage gated potassium channel complex (VGKC) as a target in various cohorts of patients with epilepsy. In the present study, the efficacy of an antibody against VGKC (anti-VGKC) for the treatment of epilepsy in mice was investigated. A mouse model of lithium-pilocarpine temporal lobe epilepsy was established and anti-VGKC treatment was administered for 30 days. Memory impairment, anxiety, visual attention, inhibitory control and neuronal loss were measured in the mouse model of lithium-pilocarpine temporal lobe epilepsy. The results revealed that epileptic mice treated with anti-VGKC were able to learn the task and presented attention impairment, even a tendency toward impulsivity and compulsivity. It was also exhibited that anti-VGKC treatment decreased neuronal loss in structures classically associated with attentional performance in hippocampus. Mice who received Anti-VGKC treatment had inhibited motor seizures and hippocampal damage as compared with control mice. In conclusion, these results indicated that anti-VGKC treatment may present benefits for improvements of the condition of motor attention impairment and cognitive competence, which suggests that VGKC may be a potential target for the treatment of epilepsy. D.A. Spandidos 2018-07 2018-05-09 /pmc/articles/PMC6059666/ /pubmed/29749462 http://dx.doi.org/10.3892/mmr.2018.9004 Text en Copyright: © Fan et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Fan, Zhiliang Feng, Xiaojuan Fan, Zhigang Zhu, Xingyuan Yin, Shaohua Immunotherapy by targeting of VGKC complex for seizure control and prevention of cognitive impairment in a mouse model of epilepsy |
title | Immunotherapy by targeting of VGKC complex for seizure control and prevention of cognitive impairment in a mouse model of epilepsy |
title_full | Immunotherapy by targeting of VGKC complex for seizure control and prevention of cognitive impairment in a mouse model of epilepsy |
title_fullStr | Immunotherapy by targeting of VGKC complex for seizure control and prevention of cognitive impairment in a mouse model of epilepsy |
title_full_unstemmed | Immunotherapy by targeting of VGKC complex for seizure control and prevention of cognitive impairment in a mouse model of epilepsy |
title_short | Immunotherapy by targeting of VGKC complex for seizure control and prevention of cognitive impairment in a mouse model of epilepsy |
title_sort | immunotherapy by targeting of vgkc complex for seizure control and prevention of cognitive impairment in a mouse model of epilepsy |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6059666/ https://www.ncbi.nlm.nih.gov/pubmed/29749462 http://dx.doi.org/10.3892/mmr.2018.9004 |
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