Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice
Abstract Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal‐dependent memo...
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| Autor*in: |
Zheng‐Mao Li [verfasserIn] Xiu‐Xiu Liu [verfasserIn] Chen Li [verfasserIn] Zhao‐Cong Wei [verfasserIn] Yi Shi [verfasserIn] Heng‐Yi Song [verfasserIn] Xiang Chen [verfasserIn] Yu Zhang [verfasserIn] Jia‐Wei Li [verfasserIn] Rui‐Fang Zhu [verfasserIn] Ben‐Hui Hu [verfasserIn] Wei‐Feng Ye [verfasserIn] Da Huo [verfasserIn] Guo‐Jun Jiang [verfasserIn] Takuya Sasaki [verfasserIn] Li Zhang [verfasserIn] Feng Han [verfasserIn] Ying‐Mei Lu [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: MedComm - Wiley, 2020, 3(2022), 3, Seite n/a-n/a |
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| Übergeordnetes Werk: |
volume:3 ; year:2022 ; number:3 ; pages:n/a-n/a |
| Links: |
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| DOI / URN: |
10.1002/mco2.128 |
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| Katalog-ID: |
DOAJ022585672 |
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| 520 | |a Abstract Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal‐dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome‐wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy‐related genes, there are changes in synaptic organization pathway node genes, such as Bdnf and Grin1. The synapse‐related proteins by Western blot analysis, such as NMDA receptors (NR1 and NR2B), PSD95, and the phosphorylation of synapsin1, are progressively decreased during epileptic seizures in Cdh5‐CreERT2;CDK5f/f mice. Notably, we found that valproate (VPA) and phenytoin (PHT) augment mRNA expression and protein levels of synapse‐related genes and ameliorate memory impairment in Cdh5‐CreERT2;CDK5f/f mice. Our study elucidates a potential mechanism of memory deficits in epilepsy, and pharmacological reversal of synaptic pathology targeting might provide a new therapeutic intervention for epileptic memory deficits. | ||
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| 700 | 0 | |a Ying‐Mei Lu |e verfasserin |4 aut | |
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10.1002/mco2.128 doi (DE-627)DOAJ022585672 (DE-599)DOAJcc2fbbf9b5a04cb3b613c5a9f6ec71eb DE-627 ger DE-627 rakwb eng Zheng‐Mao Li verfasserin aut Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal‐dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome‐wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy‐related genes, there are changes in synaptic organization pathway node genes, such as Bdnf and Grin1. The synapse‐related proteins by Western blot analysis, such as NMDA receptors (NR1 and NR2B), PSD95, and the phosphorylation of synapsin1, are progressively decreased during epileptic seizures in Cdh5‐CreERT2;CDK5f/f mice. Notably, we found that valproate (VPA) and phenytoin (PHT) augment mRNA expression and protein levels of synapse‐related genes and ameliorate memory impairment in Cdh5‐CreERT2;CDK5f/f mice. Our study elucidates a potential mechanism of memory deficits in epilepsy, and pharmacological reversal of synaptic pathology targeting might provide a new therapeutic intervention for epileptic memory deficits. endothelial CDK5 mechanism memory impairment spontaneous epilepsy synapse‐related proteins Medicine R Xiu‐Xiu Liu verfasserin aut Chen Li verfasserin aut Zhao‐Cong Wei verfasserin aut Yi Shi verfasserin aut Heng‐Yi Song verfasserin aut Xiang Chen verfasserin aut Yu Zhang verfasserin aut Jia‐Wei Li verfasserin aut Rui‐Fang Zhu verfasserin aut Ben‐Hui Hu verfasserin aut Wei‐Feng Ye verfasserin aut Da Huo verfasserin aut Guo‐Jun Jiang verfasserin aut Takuya Sasaki verfasserin aut Li Zhang verfasserin aut Feng Han verfasserin aut Ying‐Mei Lu verfasserin aut In MedComm Wiley, 2020 3(2022), 3, Seite n/a-n/a (DE-627)1698066414 (DE-600)3021470-1 26882663 nnns volume:3 year:2022 number:3 pages:n/a-n/a https://doi.org/10.1002/mco2.128 kostenfrei https://doaj.org/article/cc2fbbf9b5a04cb3b613c5a9f6ec71eb kostenfrei https://doi.org/10.1002/mco2.128 kostenfrei https://doaj.org/toc/2688-2663 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2022 3 n/a-n/a |
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10.1002/mco2.128 doi (DE-627)DOAJ022585672 (DE-599)DOAJcc2fbbf9b5a04cb3b613c5a9f6ec71eb DE-627 ger DE-627 rakwb eng Zheng‐Mao Li verfasserin aut Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal‐dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome‐wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy‐related genes, there are changes in synaptic organization pathway node genes, such as Bdnf and Grin1. The synapse‐related proteins by Western blot analysis, such as NMDA receptors (NR1 and NR2B), PSD95, and the phosphorylation of synapsin1, are progressively decreased during epileptic seizures in Cdh5‐CreERT2;CDK5f/f mice. Notably, we found that valproate (VPA) and phenytoin (PHT) augment mRNA expression and protein levels of synapse‐related genes and ameliorate memory impairment in Cdh5‐CreERT2;CDK5f/f mice. Our study elucidates a potential mechanism of memory deficits in epilepsy, and pharmacological reversal of synaptic pathology targeting might provide a new therapeutic intervention for epileptic memory deficits. endothelial CDK5 mechanism memory impairment spontaneous epilepsy synapse‐related proteins Medicine R Xiu‐Xiu Liu verfasserin aut Chen Li verfasserin aut Zhao‐Cong Wei verfasserin aut Yi Shi verfasserin aut Heng‐Yi Song verfasserin aut Xiang Chen verfasserin aut Yu Zhang verfasserin aut Jia‐Wei Li verfasserin aut Rui‐Fang Zhu verfasserin aut Ben‐Hui Hu verfasserin aut Wei‐Feng Ye verfasserin aut Da Huo verfasserin aut Guo‐Jun Jiang verfasserin aut Takuya Sasaki verfasserin aut Li Zhang verfasserin aut Feng Han verfasserin aut Ying‐Mei Lu verfasserin aut In MedComm Wiley, 2020 3(2022), 3, Seite n/a-n/a (DE-627)1698066414 (DE-600)3021470-1 26882663 nnns volume:3 year:2022 number:3 pages:n/a-n/a https://doi.org/10.1002/mco2.128 kostenfrei https://doaj.org/article/cc2fbbf9b5a04cb3b613c5a9f6ec71eb kostenfrei https://doi.org/10.1002/mco2.128 kostenfrei https://doaj.org/toc/2688-2663 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2022 3 n/a-n/a |
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10.1002/mco2.128 doi (DE-627)DOAJ022585672 (DE-599)DOAJcc2fbbf9b5a04cb3b613c5a9f6ec71eb DE-627 ger DE-627 rakwb eng Zheng‐Mao Li verfasserin aut Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal‐dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome‐wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy‐related genes, there are changes in synaptic organization pathway node genes, such as Bdnf and Grin1. The synapse‐related proteins by Western blot analysis, such as NMDA receptors (NR1 and NR2B), PSD95, and the phosphorylation of synapsin1, are progressively decreased during epileptic seizures in Cdh5‐CreERT2;CDK5f/f mice. Notably, we found that valproate (VPA) and phenytoin (PHT) augment mRNA expression and protein levels of synapse‐related genes and ameliorate memory impairment in Cdh5‐CreERT2;CDK5f/f mice. Our study elucidates a potential mechanism of memory deficits in epilepsy, and pharmacological reversal of synaptic pathology targeting might provide a new therapeutic intervention for epileptic memory deficits. endothelial CDK5 mechanism memory impairment spontaneous epilepsy synapse‐related proteins Medicine R Xiu‐Xiu Liu verfasserin aut Chen Li verfasserin aut Zhao‐Cong Wei verfasserin aut Yi Shi verfasserin aut Heng‐Yi Song verfasserin aut Xiang Chen verfasserin aut Yu Zhang verfasserin aut Jia‐Wei Li verfasserin aut Rui‐Fang Zhu verfasserin aut Ben‐Hui Hu verfasserin aut Wei‐Feng Ye verfasserin aut Da Huo verfasserin aut Guo‐Jun Jiang verfasserin aut Takuya Sasaki verfasserin aut Li Zhang verfasserin aut Feng Han verfasserin aut Ying‐Mei Lu verfasserin aut In MedComm Wiley, 2020 3(2022), 3, Seite n/a-n/a (DE-627)1698066414 (DE-600)3021470-1 26882663 nnns volume:3 year:2022 number:3 pages:n/a-n/a https://doi.org/10.1002/mco2.128 kostenfrei https://doaj.org/article/cc2fbbf9b5a04cb3b613c5a9f6ec71eb kostenfrei https://doi.org/10.1002/mco2.128 kostenfrei https://doaj.org/toc/2688-2663 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2022 3 n/a-n/a |
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10.1002/mco2.128 doi (DE-627)DOAJ022585672 (DE-599)DOAJcc2fbbf9b5a04cb3b613c5a9f6ec71eb DE-627 ger DE-627 rakwb eng Zheng‐Mao Li verfasserin aut Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal‐dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome‐wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy‐related genes, there are changes in synaptic organization pathway node genes, such as Bdnf and Grin1. The synapse‐related proteins by Western blot analysis, such as NMDA receptors (NR1 and NR2B), PSD95, and the phosphorylation of synapsin1, are progressively decreased during epileptic seizures in Cdh5‐CreERT2;CDK5f/f mice. Notably, we found that valproate (VPA) and phenytoin (PHT) augment mRNA expression and protein levels of synapse‐related genes and ameliorate memory impairment in Cdh5‐CreERT2;CDK5f/f mice. Our study elucidates a potential mechanism of memory deficits in epilepsy, and pharmacological reversal of synaptic pathology targeting might provide a new therapeutic intervention for epileptic memory deficits. endothelial CDK5 mechanism memory impairment spontaneous epilepsy synapse‐related proteins Medicine R Xiu‐Xiu Liu verfasserin aut Chen Li verfasserin aut Zhao‐Cong Wei verfasserin aut Yi Shi verfasserin aut Heng‐Yi Song verfasserin aut Xiang Chen verfasserin aut Yu Zhang verfasserin aut Jia‐Wei Li verfasserin aut Rui‐Fang Zhu verfasserin aut Ben‐Hui Hu verfasserin aut Wei‐Feng Ye verfasserin aut Da Huo verfasserin aut Guo‐Jun Jiang verfasserin aut Takuya Sasaki verfasserin aut Li Zhang verfasserin aut Feng Han verfasserin aut Ying‐Mei Lu verfasserin aut In MedComm Wiley, 2020 3(2022), 3, Seite n/a-n/a (DE-627)1698066414 (DE-600)3021470-1 26882663 nnns volume:3 year:2022 number:3 pages:n/a-n/a https://doi.org/10.1002/mco2.128 kostenfrei https://doaj.org/article/cc2fbbf9b5a04cb3b613c5a9f6ec71eb kostenfrei https://doi.org/10.1002/mco2.128 kostenfrei https://doaj.org/toc/2688-2663 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2022 3 n/a-n/a |
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10.1002/mco2.128 doi (DE-627)DOAJ022585672 (DE-599)DOAJcc2fbbf9b5a04cb3b613c5a9f6ec71eb DE-627 ger DE-627 rakwb eng Zheng‐Mao Li verfasserin aut Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal‐dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome‐wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy‐related genes, there are changes in synaptic organization pathway node genes, such as Bdnf and Grin1. The synapse‐related proteins by Western blot analysis, such as NMDA receptors (NR1 and NR2B), PSD95, and the phosphorylation of synapsin1, are progressively decreased during epileptic seizures in Cdh5‐CreERT2;CDK5f/f mice. Notably, we found that valproate (VPA) and phenytoin (PHT) augment mRNA expression and protein levels of synapse‐related genes and ameliorate memory impairment in Cdh5‐CreERT2;CDK5f/f mice. Our study elucidates a potential mechanism of memory deficits in epilepsy, and pharmacological reversal of synaptic pathology targeting might provide a new therapeutic intervention for epileptic memory deficits. endothelial CDK5 mechanism memory impairment spontaneous epilepsy synapse‐related proteins Medicine R Xiu‐Xiu Liu verfasserin aut Chen Li verfasserin aut Zhao‐Cong Wei verfasserin aut Yi Shi verfasserin aut Heng‐Yi Song verfasserin aut Xiang Chen verfasserin aut Yu Zhang verfasserin aut Jia‐Wei Li verfasserin aut Rui‐Fang Zhu verfasserin aut Ben‐Hui Hu verfasserin aut Wei‐Feng Ye verfasserin aut Da Huo verfasserin aut Guo‐Jun Jiang verfasserin aut Takuya Sasaki verfasserin aut Li Zhang verfasserin aut Feng Han verfasserin aut Ying‐Mei Lu verfasserin aut In MedComm Wiley, 2020 3(2022), 3, Seite n/a-n/a (DE-627)1698066414 (DE-600)3021470-1 26882663 nnns volume:3 year:2022 number:3 pages:n/a-n/a https://doi.org/10.1002/mco2.128 kostenfrei https://doaj.org/article/cc2fbbf9b5a04cb3b613c5a9f6ec71eb kostenfrei https://doi.org/10.1002/mco2.128 kostenfrei https://doaj.org/toc/2688-2663 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2022 3 n/a-n/a |
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Zheng‐Mao Li @@aut@@ Xiu‐Xiu Liu @@aut@@ Chen Li @@aut@@ Zhao‐Cong Wei @@aut@@ Yi Shi @@aut@@ Heng‐Yi Song @@aut@@ Xiang Chen @@aut@@ Yu Zhang @@aut@@ Jia‐Wei Li @@aut@@ Rui‐Fang Zhu @@aut@@ Ben‐Hui Hu @@aut@@ Wei‐Feng Ye @@aut@@ Da Huo @@aut@@ Guo‐Jun Jiang @@aut@@ Takuya Sasaki @@aut@@ Li Zhang @@aut@@ Feng Han @@aut@@ Ying‐Mei Lu @@aut@@ |
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Zheng‐Mao Li |
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Zheng‐Mao Li misc endothelial CDK5 misc mechanism misc memory impairment misc spontaneous epilepsy misc synapse‐related proteins misc Medicine misc R Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice |
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Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice endothelial CDK5 mechanism memory impairment spontaneous epilepsy synapse‐related proteins |
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Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice |
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Zheng‐Mao Li Xiu‐Xiu Liu Chen Li Zhao‐Cong Wei Yi Shi Heng‐Yi Song Xiang Chen Yu Zhang Jia‐Wei Li Rui‐Fang Zhu Ben‐Hui Hu Wei‐Feng Ye Da Huo Guo‐Jun Jiang Takuya Sasaki Li Zhang Feng Han Ying‐Mei Lu |
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decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial cdk5‐deficient mice |
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Decreased synapse‐associated proteins are associated with the onset of epileptic memory impairment in endothelial CDK5‐deficient mice |
| abstract |
Abstract Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal‐dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome‐wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy‐related genes, there are changes in synaptic organization pathway node genes, such as Bdnf and Grin1. The synapse‐related proteins by Western blot analysis, such as NMDA receptors (NR1 and NR2B), PSD95, and the phosphorylation of synapsin1, are progressively decreased during epileptic seizures in Cdh5‐CreERT2;CDK5f/f mice. Notably, we found that valproate (VPA) and phenytoin (PHT) augment mRNA expression and protein levels of synapse‐related genes and ameliorate memory impairment in Cdh5‐CreERT2;CDK5f/f mice. Our study elucidates a potential mechanism of memory deficits in epilepsy, and pharmacological reversal of synaptic pathology targeting might provide a new therapeutic intervention for epileptic memory deficits. |
| abstractGer |
Abstract Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal‐dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome‐wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy‐related genes, there are changes in synaptic organization pathway node genes, such as Bdnf and Grin1. The synapse‐related proteins by Western blot analysis, such as NMDA receptors (NR1 and NR2B), PSD95, and the phosphorylation of synapsin1, are progressively decreased during epileptic seizures in Cdh5‐CreERT2;CDK5f/f mice. Notably, we found that valproate (VPA) and phenytoin (PHT) augment mRNA expression and protein levels of synapse‐related genes and ameliorate memory impairment in Cdh5‐CreERT2;CDK5f/f mice. Our study elucidates a potential mechanism of memory deficits in epilepsy, and pharmacological reversal of synaptic pathology targeting might provide a new therapeutic intervention for epileptic memory deficits. |
| abstract_unstemmed |
Abstract Accumulating evidence indicates that epilepsy has a higher risk of inducing memory impairment and dementia. However, the underlying onset mechanism remains unclear. Here, we found that mice with spontaneous epilepsy induced by endothelial CDK5 deficiency exhibited hippocampal‐dependent memory impairment at 6 months of age, but not at 2 months of age. Moreover, the persistent epileptic seizures induce aberrant changes in phosphorylation of CaMKII protein in the hippocampus of spontaneous epileptic mice. Using genome‐wide RNA sequencing and intergenic interaction analysis of STRING, we found that in addition to epilepsy‐related genes, there are changes in synaptic organization pathway node genes, such as Bdnf and Grin1. The synapse‐related proteins by Western blot analysis, such as NMDA receptors (NR1 and NR2B), PSD95, and the phosphorylation of synapsin1, are progressively decreased during epileptic seizures in Cdh5‐CreERT2;CDK5f/f mice. Notably, we found that valproate (VPA) and phenytoin (PHT) augment mRNA expression and protein levels of synapse‐related genes and ameliorate memory impairment in Cdh5‐CreERT2;CDK5f/f mice. Our study elucidates a potential mechanism of memory deficits in epilepsy, and pharmacological reversal of synaptic pathology targeting might provide a new therapeutic intervention for epileptic memory deficits. |
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Xiu‐Xiu Liu Chen Li Zhao‐Cong Wei Yi Shi Heng‐Yi Song Xiang Chen Yu Zhang Jia‐Wei Li Rui‐Fang Zhu Ben‐Hui Hu Wei‐Feng Ye Da Huo Guo‐Jun Jiang Takuya Sasaki Li Zhang Feng Han Ying‐Mei Lu |
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