Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis

β-amyloid (Aβ) deposition, neurofibrillary tangles induced by phosphorylation of tau protein, and neuronal apoptosis are pathological hallmarks of Alzheimer’s disease (AD). The dementia rate in alcoholic abusers were found to be higher than in control people. The present study explored the potential...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Yaqi Wang [verfasserIn] Yi Zhang [verfasserIn] Xiaomin Zhang [verfasserIn] Tingting Yang [verfasserIn] Chengeng Liu [verfasserIn] Peichang Wang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	Alzheimer’s disease alcohol dehydrogenase 1B β-amyloid p75NTR apoptosis

Übergeordnetes Werk:	In: Frontiers in Aging Neuroscience - Frontiers Media S.A., 2010, 11(2019)
Übergeordnetes Werk:	volume:11 ; year:2019

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fnagi.2019.00135

Katalog-ID:	DOAJ004842316

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allfields	10.3389/fnagi.2019.00135 doi (DE-627)DOAJ004842316 (DE-599)DOAJ3e088fdbef504c02851d1ea86ebde7fa DE-627 ger DE-627 rakwb eng RC321-571 Yaqi Wang verfasserin aut Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier β-amyloid (Aβ) deposition, neurofibrillary tangles induced by phosphorylation of tau protein, and neuronal apoptosis are pathological hallmarks of Alzheimer’s disease (AD). The dementia rate in alcoholic abusers were found to be higher than in control people. The present study explored the potential roles of alcohol dehydrogenase 1B (ADH1B) in AD pathology by determining the ADH1B levels in AD patient sera, in the hippocampus of APP/PS-1 AD model mice, and in an AD model cell line treated with Aβ1-42. The results show that ADH1B levels decreased significantly both in the serum of AD patients and in the hippocampus of APP/PS-1 AD model mice. In addition, the apoptotic rate was reduced and viability was significantly increased in AD model cells transfected with ADH1B overexpression vector. The levels of the p75 neurotrophin receptor (p75NTR), an Aβ1-42 receptor, were down-regulated in the ADH1B overexpressing AD model cell and up-regulated in cells transfected with the shRNA vector of ADH1B. Protein levels of cleaved caspase-3 and Bax decreased significantly, whereas Bcl-2 levels increased in cells overexpressing ADH1B. The opposite trend was observed for cleaved caspase-3, Bax, and Bcl-2 levels in cells transfected with the shRNA vector of ADH1B. The levels of reactive oxygen species (ROS) were found to be reduced in ADH1B overexpressing cells and increased when cells were transfected with the shRNA vector of ADH1B. These results indicate that ADH1B might be important in the prevention of AD, especially for abusers of alcohol, and a potential new target of AD treatment. Alzheimer’s disease alcohol dehydrogenase 1B β-amyloid p75NTR apoptosis Neurosciences. Biological psychiatry. Neuropsychiatry Yi Zhang verfasserin aut Xiaomin Zhang verfasserin aut Tingting Yang verfasserin aut Chengeng Liu verfasserin aut Peichang Wang verfasserin aut In Frontiers in Aging Neuroscience Frontiers Media S.A., 2010 11(2019) (DE-627)629834350 (DE-600)2558898-9 16634365 nnns volume:11 year:2019 https://doi.org/10.3389/fnagi.2019.00135 kostenfrei https://doaj.org/article/3e088fdbef504c02851d1ea86ebde7fa kostenfrei https://www.frontiersin.org/article/10.3389/fnagi.2019.00135/full kostenfrei https://doaj.org/toc/1663-4365 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 11 2019
spelling	10.3389/fnagi.2019.00135 doi (DE-627)DOAJ004842316 (DE-599)DOAJ3e088fdbef504c02851d1ea86ebde7fa DE-627 ger DE-627 rakwb eng RC321-571 Yaqi Wang verfasserin aut Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier β-amyloid (Aβ) deposition, neurofibrillary tangles induced by phosphorylation of tau protein, and neuronal apoptosis are pathological hallmarks of Alzheimer’s disease (AD). The dementia rate in alcoholic abusers were found to be higher than in control people. The present study explored the potential roles of alcohol dehydrogenase 1B (ADH1B) in AD pathology by determining the ADH1B levels in AD patient sera, in the hippocampus of APP/PS-1 AD model mice, and in an AD model cell line treated with Aβ1-42. The results show that ADH1B levels decreased significantly both in the serum of AD patients and in the hippocampus of APP/PS-1 AD model mice. In addition, the apoptotic rate was reduced and viability was significantly increased in AD model cells transfected with ADH1B overexpression vector. The levels of the p75 neurotrophin receptor (p75NTR), an Aβ1-42 receptor, were down-regulated in the ADH1B overexpressing AD model cell and up-regulated in cells transfected with the shRNA vector of ADH1B. Protein levels of cleaved caspase-3 and Bax decreased significantly, whereas Bcl-2 levels increased in cells overexpressing ADH1B. The opposite trend was observed for cleaved caspase-3, Bax, and Bcl-2 levels in cells transfected with the shRNA vector of ADH1B. The levels of reactive oxygen species (ROS) were found to be reduced in ADH1B overexpressing cells and increased when cells were transfected with the shRNA vector of ADH1B. These results indicate that ADH1B might be important in the prevention of AD, especially for abusers of alcohol, and a potential new target of AD treatment. Alzheimer’s disease alcohol dehydrogenase 1B β-amyloid p75NTR apoptosis Neurosciences. Biological psychiatry. Neuropsychiatry Yi Zhang verfasserin aut Xiaomin Zhang verfasserin aut Tingting Yang verfasserin aut Chengeng Liu verfasserin aut Peichang Wang verfasserin aut In Frontiers in Aging Neuroscience Frontiers Media S.A., 2010 11(2019) (DE-627)629834350 (DE-600)2558898-9 16634365 nnns volume:11 year:2019 https://doi.org/10.3389/fnagi.2019.00135 kostenfrei https://doaj.org/article/3e088fdbef504c02851d1ea86ebde7fa kostenfrei https://www.frontiersin.org/article/10.3389/fnagi.2019.00135/full kostenfrei https://doaj.org/toc/1663-4365 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 11 2019
allfields_unstemmed	10.3389/fnagi.2019.00135 doi (DE-627)DOAJ004842316 (DE-599)DOAJ3e088fdbef504c02851d1ea86ebde7fa DE-627 ger DE-627 rakwb eng RC321-571 Yaqi Wang verfasserin aut Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier β-amyloid (Aβ) deposition, neurofibrillary tangles induced by phosphorylation of tau protein, and neuronal apoptosis are pathological hallmarks of Alzheimer’s disease (AD). The dementia rate in alcoholic abusers were found to be higher than in control people. The present study explored the potential roles of alcohol dehydrogenase 1B (ADH1B) in AD pathology by determining the ADH1B levels in AD patient sera, in the hippocampus of APP/PS-1 AD model mice, and in an AD model cell line treated with Aβ1-42. The results show that ADH1B levels decreased significantly both in the serum of AD patients and in the hippocampus of APP/PS-1 AD model mice. In addition, the apoptotic rate was reduced and viability was significantly increased in AD model cells transfected with ADH1B overexpression vector. The levels of the p75 neurotrophin receptor (p75NTR), an Aβ1-42 receptor, were down-regulated in the ADH1B overexpressing AD model cell and up-regulated in cells transfected with the shRNA vector of ADH1B. Protein levels of cleaved caspase-3 and Bax decreased significantly, whereas Bcl-2 levels increased in cells overexpressing ADH1B. The opposite trend was observed for cleaved caspase-3, Bax, and Bcl-2 levels in cells transfected with the shRNA vector of ADH1B. The levels of reactive oxygen species (ROS) were found to be reduced in ADH1B overexpressing cells and increased when cells were transfected with the shRNA vector of ADH1B. These results indicate that ADH1B might be important in the prevention of AD, especially for abusers of alcohol, and a potential new target of AD treatment. Alzheimer’s disease alcohol dehydrogenase 1B β-amyloid p75NTR apoptosis Neurosciences. Biological psychiatry. Neuropsychiatry Yi Zhang verfasserin aut Xiaomin Zhang verfasserin aut Tingting Yang verfasserin aut Chengeng Liu verfasserin aut Peichang Wang verfasserin aut In Frontiers in Aging Neuroscience Frontiers Media S.A., 2010 11(2019) (DE-627)629834350 (DE-600)2558898-9 16634365 nnns volume:11 year:2019 https://doi.org/10.3389/fnagi.2019.00135 kostenfrei https://doaj.org/article/3e088fdbef504c02851d1ea86ebde7fa kostenfrei https://www.frontiersin.org/article/10.3389/fnagi.2019.00135/full kostenfrei https://doaj.org/toc/1663-4365 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 11 2019
allfieldsGer	10.3389/fnagi.2019.00135 doi (DE-627)DOAJ004842316 (DE-599)DOAJ3e088fdbef504c02851d1ea86ebde7fa DE-627 ger DE-627 rakwb eng RC321-571 Yaqi Wang verfasserin aut Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier β-amyloid (Aβ) deposition, neurofibrillary tangles induced by phosphorylation of tau protein, and neuronal apoptosis are pathological hallmarks of Alzheimer’s disease (AD). The dementia rate in alcoholic abusers were found to be higher than in control people. The present study explored the potential roles of alcohol dehydrogenase 1B (ADH1B) in AD pathology by determining the ADH1B levels in AD patient sera, in the hippocampus of APP/PS-1 AD model mice, and in an AD model cell line treated with Aβ1-42. The results show that ADH1B levels decreased significantly both in the serum of AD patients and in the hippocampus of APP/PS-1 AD model mice. In addition, the apoptotic rate was reduced and viability was significantly increased in AD model cells transfected with ADH1B overexpression vector. The levels of the p75 neurotrophin receptor (p75NTR), an Aβ1-42 receptor, were down-regulated in the ADH1B overexpressing AD model cell and up-regulated in cells transfected with the shRNA vector of ADH1B. Protein levels of cleaved caspase-3 and Bax decreased significantly, whereas Bcl-2 levels increased in cells overexpressing ADH1B. The opposite trend was observed for cleaved caspase-3, Bax, and Bcl-2 levels in cells transfected with the shRNA vector of ADH1B. The levels of reactive oxygen species (ROS) were found to be reduced in ADH1B overexpressing cells and increased when cells were transfected with the shRNA vector of ADH1B. These results indicate that ADH1B might be important in the prevention of AD, especially for abusers of alcohol, and a potential new target of AD treatment. Alzheimer’s disease alcohol dehydrogenase 1B β-amyloid p75NTR apoptosis Neurosciences. Biological psychiatry. Neuropsychiatry Yi Zhang verfasserin aut Xiaomin Zhang verfasserin aut Tingting Yang verfasserin aut Chengeng Liu verfasserin aut Peichang Wang verfasserin aut In Frontiers in Aging Neuroscience Frontiers Media S.A., 2010 11(2019) (DE-627)629834350 (DE-600)2558898-9 16634365 nnns volume:11 year:2019 https://doi.org/10.3389/fnagi.2019.00135 kostenfrei https://doaj.org/article/3e088fdbef504c02851d1ea86ebde7fa kostenfrei https://www.frontiersin.org/article/10.3389/fnagi.2019.00135/full kostenfrei https://doaj.org/toc/1663-4365 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 11 2019
allfieldsSound	10.3389/fnagi.2019.00135 doi (DE-627)DOAJ004842316 (DE-599)DOAJ3e088fdbef504c02851d1ea86ebde7fa DE-627 ger DE-627 rakwb eng RC321-571 Yaqi Wang verfasserin aut Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier β-amyloid (Aβ) deposition, neurofibrillary tangles induced by phosphorylation of tau protein, and neuronal apoptosis are pathological hallmarks of Alzheimer’s disease (AD). The dementia rate in alcoholic abusers were found to be higher than in control people. The present study explored the potential roles of alcohol dehydrogenase 1B (ADH1B) in AD pathology by determining the ADH1B levels in AD patient sera, in the hippocampus of APP/PS-1 AD model mice, and in an AD model cell line treated with Aβ1-42. The results show that ADH1B levels decreased significantly both in the serum of AD patients and in the hippocampus of APP/PS-1 AD model mice. In addition, the apoptotic rate was reduced and viability was significantly increased in AD model cells transfected with ADH1B overexpression vector. The levels of the p75 neurotrophin receptor (p75NTR), an Aβ1-42 receptor, were down-regulated in the ADH1B overexpressing AD model cell and up-regulated in cells transfected with the shRNA vector of ADH1B. Protein levels of cleaved caspase-3 and Bax decreased significantly, whereas Bcl-2 levels increased in cells overexpressing ADH1B. The opposite trend was observed for cleaved caspase-3, Bax, and Bcl-2 levels in cells transfected with the shRNA vector of ADH1B. The levels of reactive oxygen species (ROS) were found to be reduced in ADH1B overexpressing cells and increased when cells were transfected with the shRNA vector of ADH1B. These results indicate that ADH1B might be important in the prevention of AD, especially for abusers of alcohol, and a potential new target of AD treatment. Alzheimer’s disease alcohol dehydrogenase 1B β-amyloid p75NTR apoptosis Neurosciences. Biological psychiatry. Neuropsychiatry Yi Zhang verfasserin aut Xiaomin Zhang verfasserin aut Tingting Yang verfasserin aut Chengeng Liu verfasserin aut Peichang Wang verfasserin aut In Frontiers in Aging Neuroscience Frontiers Media S.A., 2010 11(2019) (DE-627)629834350 (DE-600)2558898-9 16634365 nnns volume:11 year:2019 https://doi.org/10.3389/fnagi.2019.00135 kostenfrei https://doaj.org/article/3e088fdbef504c02851d1ea86ebde7fa kostenfrei https://www.frontiersin.org/article/10.3389/fnagi.2019.00135/full kostenfrei https://doaj.org/toc/1663-4365 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 11 2019
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source	In Frontiers in Aging Neuroscience 11(2019) volume:11 year:2019
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topic_facet	Alzheimer’s disease alcohol dehydrogenase 1B β-amyloid p75NTR apoptosis Neurosciences. Biological psychiatry. Neuropsychiatry
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container_title	Frontiers in Aging Neuroscience
authorswithroles_txt_mv	Yaqi Wang @@aut@@ Yi Zhang @@aut@@ Xiaomin Zhang @@aut@@ Tingting Yang @@aut@@ Chengeng Liu @@aut@@ Peichang Wang @@aut@@
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callnumber-first	R - Medicine
author	Yaqi Wang
spellingShingle	Yaqi Wang misc RC321-571 misc Alzheimer’s disease misc alcohol dehydrogenase 1B misc β-amyloid misc p75NTR misc apoptosis misc Neurosciences. Biological psychiatry. Neuropsychiatry Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis
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topic_title	RC321-571 Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis Alzheimer’s disease alcohol dehydrogenase 1B β-amyloid p75NTR apoptosis
topic	misc RC321-571 misc Alzheimer’s disease misc alcohol dehydrogenase 1B misc β-amyloid misc p75NTR misc apoptosis misc Neurosciences. Biological psychiatry. Neuropsychiatry
topic_unstemmed	misc RC321-571 misc Alzheimer’s disease misc alcohol dehydrogenase 1B misc β-amyloid misc p75NTR misc apoptosis misc Neurosciences. Biological psychiatry. Neuropsychiatry
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title	Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis
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title_full	Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis
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title_sort	alcohol dehydrogenase 1b suppresses β-amyloid-induced neuron apoptosis
callnumber	RC321-571
title_auth	Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis
abstract	β-amyloid (Aβ) deposition, neurofibrillary tangles induced by phosphorylation of tau protein, and neuronal apoptosis are pathological hallmarks of Alzheimer’s disease (AD). The dementia rate in alcoholic abusers were found to be higher than in control people. The present study explored the potential roles of alcohol dehydrogenase 1B (ADH1B) in AD pathology by determining the ADH1B levels in AD patient sera, in the hippocampus of APP/PS-1 AD model mice, and in an AD model cell line treated with Aβ1-42. The results show that ADH1B levels decreased significantly both in the serum of AD patients and in the hippocampus of APP/PS-1 AD model mice. In addition, the apoptotic rate was reduced and viability was significantly increased in AD model cells transfected with ADH1B overexpression vector. The levels of the p75 neurotrophin receptor (p75NTR), an Aβ1-42 receptor, were down-regulated in the ADH1B overexpressing AD model cell and up-regulated in cells transfected with the shRNA vector of ADH1B. Protein levels of cleaved caspase-3 and Bax decreased significantly, whereas Bcl-2 levels increased in cells overexpressing ADH1B. The opposite trend was observed for cleaved caspase-3, Bax, and Bcl-2 levels in cells transfected with the shRNA vector of ADH1B. The levels of reactive oxygen species (ROS) were found to be reduced in ADH1B overexpressing cells and increased when cells were transfected with the shRNA vector of ADH1B. These results indicate that ADH1B might be important in the prevention of AD, especially for abusers of alcohol, and a potential new target of AD treatment.
abstractGer	β-amyloid (Aβ) deposition, neurofibrillary tangles induced by phosphorylation of tau protein, and neuronal apoptosis are pathological hallmarks of Alzheimer’s disease (AD). The dementia rate in alcoholic abusers were found to be higher than in control people. The present study explored the potential roles of alcohol dehydrogenase 1B (ADH1B) in AD pathology by determining the ADH1B levels in AD patient sera, in the hippocampus of APP/PS-1 AD model mice, and in an AD model cell line treated with Aβ1-42. The results show that ADH1B levels decreased significantly both in the serum of AD patients and in the hippocampus of APP/PS-1 AD model mice. In addition, the apoptotic rate was reduced and viability was significantly increased in AD model cells transfected with ADH1B overexpression vector. The levels of the p75 neurotrophin receptor (p75NTR), an Aβ1-42 receptor, were down-regulated in the ADH1B overexpressing AD model cell and up-regulated in cells transfected with the shRNA vector of ADH1B. Protein levels of cleaved caspase-3 and Bax decreased significantly, whereas Bcl-2 levels increased in cells overexpressing ADH1B. The opposite trend was observed for cleaved caspase-3, Bax, and Bcl-2 levels in cells transfected with the shRNA vector of ADH1B. The levels of reactive oxygen species (ROS) were found to be reduced in ADH1B overexpressing cells and increased when cells were transfected with the shRNA vector of ADH1B. These results indicate that ADH1B might be important in the prevention of AD, especially for abusers of alcohol, and a potential new target of AD treatment.
abstract_unstemmed	β-amyloid (Aβ) deposition, neurofibrillary tangles induced by phosphorylation of tau protein, and neuronal apoptosis are pathological hallmarks of Alzheimer’s disease (AD). The dementia rate in alcoholic abusers were found to be higher than in control people. The present study explored the potential roles of alcohol dehydrogenase 1B (ADH1B) in AD pathology by determining the ADH1B levels in AD patient sera, in the hippocampus of APP/PS-1 AD model mice, and in an AD model cell line treated with Aβ1-42. The results show that ADH1B levels decreased significantly both in the serum of AD patients and in the hippocampus of APP/PS-1 AD model mice. In addition, the apoptotic rate was reduced and viability was significantly increased in AD model cells transfected with ADH1B overexpression vector. The levels of the p75 neurotrophin receptor (p75NTR), an Aβ1-42 receptor, were down-regulated in the ADH1B overexpressing AD model cell and up-regulated in cells transfected with the shRNA vector of ADH1B. Protein levels of cleaved caspase-3 and Bax decreased significantly, whereas Bcl-2 levels increased in cells overexpressing ADH1B. The opposite trend was observed for cleaved caspase-3, Bax, and Bcl-2 levels in cells transfected with the shRNA vector of ADH1B. The levels of reactive oxygen species (ROS) were found to be reduced in ADH1B overexpressing cells and increased when cells were transfected with the shRNA vector of ADH1B. These results indicate that ADH1B might be important in the prevention of AD, especially for abusers of alcohol, and a potential new target of AD treatment.
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title_short	Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis
url	https://doi.org/10.3389/fnagi.2019.00135 https://doaj.org/article/3e088fdbef504c02851d1ea86ebde7fa https://www.frontiersin.org/article/10.3389/fnagi.2019.00135/full https://doaj.org/toc/1663-4365
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Alcohol Dehydrogenase 1B Suppresses β-Amyloid-Induced Neuron Apoptosis

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