Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia

Vascular dementia (VaD) is the second most common type of dementia after Alzheimer’s disease (AD), characterized by progressive cognitive impairment, memory loss, and thinking or speech problems. VaD is usually caused by cerebrovascular disease, during which, cerebrovascular endothelial cells (CECs)...
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Autor*in:	Feixue Wang [verfasserIn] Yu Cao [verfasserIn] Lina Ma [verfasserIn] Hui Pei [verfasserIn] Wolf Dieter Rausch [verfasserIn] Hao Li [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	vascular dementia cerebrovascular endothelial cells endothelial nitric oxide synthase oxidative stress inflammation white matter lesion

Übergeordnetes Werk:	In: Frontiers in Aging Neuroscience - Frontiers Media S.A., 2010, 10(2018)
Übergeordnetes Werk:	volume:10 ; year:2018

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fnagi.2018.00376

Katalog-ID:	DOAJ035278234

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520			\|a Vascular dementia (VaD) is the second most common type of dementia after Alzheimer’s disease (AD), characterized by progressive cognitive impairment, memory loss, and thinking or speech problems. VaD is usually caused by cerebrovascular disease, during which, cerebrovascular endothelial cells (CECs) are vulnerable. CEC dysfunction occurs before the onset of VaD and can eventually lead to dysregulation of cerebral blood flow and blood–brain barrier damage, followed by the activation of glia and inflammatory environment in the brain. White matter, neuronal axons, and synapses are compromised in this process, leading to cognitive impairment. The present review summarizes the mechanisms underlying CEC impairment during hypoperfusion and pathological role of CECs in VaD. Through the comprehensive examination and summarization, endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway, Ras homolog gene family member A (RhoA) signaling pathway, and CEC-derived caveolin-1 (CAV-1) are proposed to serve as targets of new drugs for the treatment of VaD.
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spelling	10.3389/fnagi.2018.00376 doi (DE-627)DOAJ035278234 (DE-599)DOAJ06e741e8d3b64392948cf24b8ca72954 DE-627 ger DE-627 rakwb eng RC321-571 Feixue Wang verfasserin aut Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Vascular dementia (VaD) is the second most common type of dementia after Alzheimer’s disease (AD), characterized by progressive cognitive impairment, memory loss, and thinking or speech problems. VaD is usually caused by cerebrovascular disease, during which, cerebrovascular endothelial cells (CECs) are vulnerable. CEC dysfunction occurs before the onset of VaD and can eventually lead to dysregulation of cerebral blood flow and blood–brain barrier damage, followed by the activation of glia and inflammatory environment in the brain. White matter, neuronal axons, and synapses are compromised in this process, leading to cognitive impairment. The present review summarizes the mechanisms underlying CEC impairment during hypoperfusion and pathological role of CECs in VaD. Through the comprehensive examination and summarization, endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway, Ras homolog gene family member A (RhoA) signaling pathway, and CEC-derived caveolin-1 (CAV-1) are proposed to serve as targets of new drugs for the treatment of VaD. vascular dementia cerebrovascular endothelial cells endothelial nitric oxide synthase oxidative stress inflammation white matter lesion Neurosciences. Biological psychiatry. Neuropsychiatry Yu Cao verfasserin aut Lina Ma verfasserin aut Hui Pei verfasserin aut Wolf Dieter Rausch verfasserin aut Hao Li verfasserin aut In Frontiers in Aging Neuroscience Frontiers Media S.A., 2010 10(2018) (DE-627)629834350 (DE-600)2558898-9 16634365 nnns volume:10 year:2018 https://doi.org/10.3389/fnagi.2018.00376 kostenfrei https://doaj.org/article/06e741e8d3b64392948cf24b8ca72954 kostenfrei https://www.frontiersin.org/article/10.3389/fnagi.2018.00376/full kostenfrei https://doaj.org/toc/1663-4365 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2018
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allfieldsSound	10.3389/fnagi.2018.00376 doi (DE-627)DOAJ035278234 (DE-599)DOAJ06e741e8d3b64392948cf24b8ca72954 DE-627 ger DE-627 rakwb eng RC321-571 Feixue Wang verfasserin aut Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Vascular dementia (VaD) is the second most common type of dementia after Alzheimer’s disease (AD), characterized by progressive cognitive impairment, memory loss, and thinking or speech problems. VaD is usually caused by cerebrovascular disease, during which, cerebrovascular endothelial cells (CECs) are vulnerable. CEC dysfunction occurs before the onset of VaD and can eventually lead to dysregulation of cerebral blood flow and blood–brain barrier damage, followed by the activation of glia and inflammatory environment in the brain. White matter, neuronal axons, and synapses are compromised in this process, leading to cognitive impairment. The present review summarizes the mechanisms underlying CEC impairment during hypoperfusion and pathological role of CECs in VaD. Through the comprehensive examination and summarization, endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway, Ras homolog gene family member A (RhoA) signaling pathway, and CEC-derived caveolin-1 (CAV-1) are proposed to serve as targets of new drugs for the treatment of VaD. vascular dementia cerebrovascular endothelial cells endothelial nitric oxide synthase oxidative stress inflammation white matter lesion Neurosciences. Biological psychiatry. Neuropsychiatry Yu Cao verfasserin aut Lina Ma verfasserin aut Hui Pei verfasserin aut Wolf Dieter Rausch verfasserin aut Hao Li verfasserin aut In Frontiers in Aging Neuroscience Frontiers Media S.A., 2010 10(2018) (DE-627)629834350 (DE-600)2558898-9 16634365 nnns volume:10 year:2018 https://doi.org/10.3389/fnagi.2018.00376 kostenfrei https://doaj.org/article/06e741e8d3b64392948cf24b8ca72954 kostenfrei https://www.frontiersin.org/article/10.3389/fnagi.2018.00376/full kostenfrei https://doaj.org/toc/1663-4365 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2018
language	English
source	In Frontiers in Aging Neuroscience 10(2018) volume:10 year:2018
sourceStr	In Frontiers in Aging Neuroscience 10(2018) volume:10 year:2018
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	vascular dementia cerebrovascular endothelial cells endothelial nitric oxide synthase oxidative stress inflammation white matter lesion Neurosciences. Biological psychiatry. Neuropsychiatry
isfreeaccess_bool	true
container_title	Frontiers in Aging Neuroscience
authorswithroles_txt_mv	Feixue Wang @@aut@@ Yu Cao @@aut@@ Lina Ma @@aut@@ Hui Pei @@aut@@ Wolf Dieter Rausch @@aut@@ Hao Li @@aut@@
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callnumber-first	R - Medicine
author	Feixue Wang
spellingShingle	Feixue Wang misc RC321-571 misc vascular dementia misc cerebrovascular endothelial cells misc endothelial nitric oxide synthase misc oxidative stress misc inflammation misc white matter lesion misc Neurosciences. Biological psychiatry. Neuropsychiatry Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia
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topic_title	RC321-571 Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia vascular dementia cerebrovascular endothelial cells endothelial nitric oxide synthase oxidative stress inflammation white matter lesion
topic	misc RC321-571 misc vascular dementia misc cerebrovascular endothelial cells misc endothelial nitric oxide synthase misc oxidative stress misc inflammation misc white matter lesion misc Neurosciences. Biological psychiatry. Neuropsychiatry
topic_unstemmed	misc RC321-571 misc vascular dementia misc cerebrovascular endothelial cells misc endothelial nitric oxide synthase misc oxidative stress misc inflammation misc white matter lesion misc Neurosciences. Biological psychiatry. Neuropsychiatry
topic_browse	misc RC321-571 misc vascular dementia misc cerebrovascular endothelial cells misc endothelial nitric oxide synthase misc oxidative stress misc inflammation misc white matter lesion misc Neurosciences. Biological psychiatry. Neuropsychiatry
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title	Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia
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title_full	Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia
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title_sort	dysfunction of cerebrovascular endothelial cells: prelude to vascular dementia
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title_auth	Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia
abstract	Vascular dementia (VaD) is the second most common type of dementia after Alzheimer’s disease (AD), characterized by progressive cognitive impairment, memory loss, and thinking or speech problems. VaD is usually caused by cerebrovascular disease, during which, cerebrovascular endothelial cells (CECs) are vulnerable. CEC dysfunction occurs before the onset of VaD and can eventually lead to dysregulation of cerebral blood flow and blood–brain barrier damage, followed by the activation of glia and inflammatory environment in the brain. White matter, neuronal axons, and synapses are compromised in this process, leading to cognitive impairment. The present review summarizes the mechanisms underlying CEC impairment during hypoperfusion and pathological role of CECs in VaD. Through the comprehensive examination and summarization, endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway, Ras homolog gene family member A (RhoA) signaling pathway, and CEC-derived caveolin-1 (CAV-1) are proposed to serve as targets of new drugs for the treatment of VaD.
abstractGer	Vascular dementia (VaD) is the second most common type of dementia after Alzheimer’s disease (AD), characterized by progressive cognitive impairment, memory loss, and thinking or speech problems. VaD is usually caused by cerebrovascular disease, during which, cerebrovascular endothelial cells (CECs) are vulnerable. CEC dysfunction occurs before the onset of VaD and can eventually lead to dysregulation of cerebral blood flow and blood–brain barrier damage, followed by the activation of glia and inflammatory environment in the brain. White matter, neuronal axons, and synapses are compromised in this process, leading to cognitive impairment. The present review summarizes the mechanisms underlying CEC impairment during hypoperfusion and pathological role of CECs in VaD. Through the comprehensive examination and summarization, endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway, Ras homolog gene family member A (RhoA) signaling pathway, and CEC-derived caveolin-1 (CAV-1) are proposed to serve as targets of new drugs for the treatment of VaD.
abstract_unstemmed	Vascular dementia (VaD) is the second most common type of dementia after Alzheimer’s disease (AD), characterized by progressive cognitive impairment, memory loss, and thinking or speech problems. VaD is usually caused by cerebrovascular disease, during which, cerebrovascular endothelial cells (CECs) are vulnerable. CEC dysfunction occurs before the onset of VaD and can eventually lead to dysregulation of cerebral blood flow and blood–brain barrier damage, followed by the activation of glia and inflammatory environment in the brain. White matter, neuronal axons, and synapses are compromised in this process, leading to cognitive impairment. The present review summarizes the mechanisms underlying CEC impairment during hypoperfusion and pathological role of CECs in VaD. Through the comprehensive examination and summarization, endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway, Ras homolog gene family member A (RhoA) signaling pathway, and CEC-derived caveolin-1 (CAV-1) are proposed to serve as targets of new drugs for the treatment of VaD.
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title_short	Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia
url	https://doi.org/10.3389/fnagi.2018.00376 https://doaj.org/article/06e741e8d3b64392948cf24b8ca72954 https://www.frontiersin.org/article/10.3389/fnagi.2018.00376/full https://doaj.org/toc/1663-4365
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