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Increased heat shock transcription factor 1 in the cerebellum reverses the deficiency of Purkinje cells in Alzheimer's disease

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.brainres.2013.04.059 Byline: Yu-Qing Jiang, Xiu-Li Wang, Xue-Hong Cao, Zeng-You Ye, Li Li, Wen-Qing Cai Abstract: Alzheimer's disease (AD) is one of the most debilitating neurodegenerative nerve diseases, seri... Full description

Journal Title: Brain Research June 26, 2013, Vol.1518, p.105(7)
Main Author: Jiang, Yu - Qing
Other Authors: Wang, Xiu - Li , Cao, Xue - Hong , Ye, Zeng - You , Li, Li , Cai, Wen - Qing
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Cengage Learning, Inc.
ID: ISSN: 0006-8993
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recordid: gale_ofa341655956
title: Increased heat shock transcription factor 1 in the cerebellum reverses the deficiency of Purkinje cells in Alzheimer's disease
format: Article
creator:
  • Jiang, Yu - Qing
  • Wang, Xiu - Li
  • Cao, Xue - Hong
  • Ye, Zeng - You
  • Li, Li
  • Cai, Wen - Qing
subjects:
  • Alzheimer's Disease
  • Brain
  • Amyloid Beta-protein
ispartof: Brain Research, June 26, 2013, Vol.1518, p.105(7)
description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.brainres.2013.04.059 Byline: Yu-Qing Jiang, Xiu-Li Wang, Xue-Hong Cao, Zeng-You Ye, Li Li, Wen-Qing Cai Abstract: Alzheimer's disease (AD) is one of the most debilitating neurodegenerative nerve diseases, seriously affecting one's ability to carry out daily activities. AD is both progressive and incurable, but molecular studies have begun to shed light on the mechanisms that underlie it. Immunochemical staining showed that cell bodies of Purkinje cells in the cerebellum were significantly reduced in AD rats compared with normal rats. Heat shock protein 70 (HSP70) was found to prevent polyglutamine aggregation in Huntington's disease and spinocerebellar ataxias (SCAs) and to relieve symptoms in SCAs and Parkinson's disease. Recently, AD-related phenotypes were found to be suppressed in HSP70 transgenic rats. However, the effects of other HSPs and the mechanisms of HSP-triggered changes in AD are unknown. In this study, we found that expression levels of HSP60, -70, and -90 were downregulated in the cerebella of rats with AD. Furthermore, heat shock factor 1 (HSF1), a key transcription factor for the expression of HSP genes, was found to be greatly decreased in the cerebella of AD rats. Even more interesting, injection of lentivirus vector-HSF1 into the cerebella of AD rats significantly increased HSF1 and HSP expression levels and induced an increase in the number of Purkinje cell bodies. Our findings provide novel evidence that low expression of HSPs in AD rats is dependent on the low expression of HSF1, and increased expression of HSF1 contributes to the reversal of cerebellar Purkinje cell deficiency in AD. Therefore, increasing HSF1 expression is a potential new strategy for the treatment of AD. Author Affiliation: (a) Third Hospital of Hebei Medical University, Shijiazhuang 050051, China (b) School of Biology and Pharmaceutical Engineering, Wuhan Polytechnic University, Wuhan, Hubei 430023, China (c) Baylor College of Medicine, Houston, TX 77030, USA (d) Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA (e) Dalian Medical University, Dalian, Liaoning 116044, China (f) Hebei Medical University, Shijiazhuang 050017, China Article History: Accepted 25 April 2013
language: English
source: Cengage Learning, Inc.
identifier: ISSN: 0006-8993
fulltext: fulltext
issn:
  • 0006-8993
  • 00068993
url: Link


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titleIncreased heat shock transcription factor 1 in the cerebellum reverses the deficiency of Purkinje cells in Alzheimer's disease
creatorJiang, Yu - Qing ; Wang, Xiu - Li ; Cao, Xue - Hong ; Ye, Zeng - You ; Li, Li ; Cai, Wen - Qing
ispartofBrain Research, June 26, 2013, Vol.1518, p.105(7)
identifierISSN: 0006-8993
subjectAlzheimer's Disease ; Brain ; Amyloid Beta-protein
descriptionTo link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.brainres.2013.04.059 Byline: Yu-Qing Jiang, Xiu-Li Wang, Xue-Hong Cao, Zeng-You Ye, Li Li, Wen-Qing Cai Abstract: Alzheimer's disease (AD) is one of the most debilitating neurodegenerative nerve diseases, seriously affecting one's ability to carry out daily activities. AD is both progressive and incurable, but molecular studies have begun to shed light on the mechanisms that underlie it. Immunochemical staining showed that cell bodies of Purkinje cells in the cerebellum were significantly reduced in AD rats compared with normal rats. Heat shock protein 70 (HSP70) was found to prevent polyglutamine aggregation in Huntington's disease and spinocerebellar ataxias (SCAs) and to relieve symptoms in SCAs and Parkinson's disease. Recently, AD-related phenotypes were found to be suppressed in HSP70 transgenic rats. However, the effects of other HSPs and the mechanisms of HSP-triggered changes in AD are unknown. In this study, we found that expression levels of HSP60, -70, and -90 were downregulated in the cerebella of rats with AD. Furthermore, heat shock factor 1 (HSF1), a key transcription factor for the expression of HSP genes, was found to be greatly decreased in the cerebella of AD rats. Even more interesting, injection of lentivirus vector-HSF1 into the cerebella of AD rats significantly increased HSF1 and HSP expression levels and induced an increase in the number of Purkinje cell bodies. Our findings provide novel evidence that low expression of HSPs in AD rats is dependent on the low expression of HSF1, and increased expression of HSF1 contributes to the reversal of cerebellar Purkinje cell deficiency in AD. Therefore, increasing HSF1 expression is a potential new strategy for the treatment of AD. Author Affiliation: (a) Third Hospital of Hebei Medical University, Shijiazhuang 050051, China (b) School of Biology and Pharmaceutical Engineering, Wuhan Polytechnic University, Wuhan, Hubei 430023, China (c) Baylor College of Medicine, Houston, TX 77030, USA (d) Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA (e) Dalian Medical University, Dalian, Liaoning 116044, China (f) Hebei Medical University, Shijiazhuang 050017, China Article History: Accepted 25 April 2013
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titleIncreased heat shock transcription factor 1 in the cerebellum reverses the deficiency of Purkinje cells in Alzheimer's disease.
descriptionTo link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.brainres.2013.04.059 Byline: Yu-Qing Jiang, Xiu-Li Wang, Xue-Hong Cao, Zeng-You Ye, Li Li, Wen-Qing Cai Abstract: Alzheimer's disease (AD) is one of the most debilitating neurodegenerative nerve diseases, seriously affecting one's ability to carry out daily activities. AD is both progressive and incurable, but molecular studies have begun to shed light on the mechanisms that underlie it. Immunochemical staining showed that cell bodies of Purkinje cells in the cerebellum were significantly reduced in AD rats compared with normal rats. Heat shock protein 70 (HSP70) was found to prevent polyglutamine aggregation in Huntington's disease and spinocerebellar ataxias (SCAs) and to relieve symptoms in SCAs and Parkinson's disease. Recently, AD-related phenotypes were found to be suppressed in HSP70 transgenic rats. However, the effects of other HSPs and the mechanisms of HSP-triggered changes in AD are unknown. In this study, we found that expression levels of HSP60, -70, and -90 were downregulated in the cerebella of rats with AD. Furthermore, heat shock factor 1 (HSF1), a key transcription factor for the expression of HSP genes, was found to be greatly decreased in the cerebella of AD rats. Even more interesting, injection of lentivirus vector-HSF1 into the cerebella of AD rats significantly increased HSF1 and HSP expression levels and induced an increase in the number of Purkinje cell bodies. Our findings provide novel evidence that low expression of HSPs in AD rats is dependent on the low expression of HSF1, and increased expression of HSF1 contributes to the reversal of cerebellar Purkinje cell deficiency in AD. Therefore, increasing HSF1 expression is a potential new strategy for the treatment of AD. Author Affiliation: (a) Third Hospital of Hebei Medical University, Shijiazhuang 050051, China (b) School of Biology and Pharmaceutical Engineering, Wuhan Polytechnic University, Wuhan, Hubei 430023, China (c) Baylor College of Medicine, Houston, TX 77030, USA (d) Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA (e) Dalian Medical University, Dalian, Liaoning 116044, China (f) Hebei Medical University, Shijiazhuang 050017, China Article History: Accepted 25 April 2013
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abstractTo link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.brainres.2013.04.059 Byline: Yu-Qing Jiang, Xiu-Li Wang, Xue-Hong Cao, Zeng-You Ye, Li Li, Wen-Qing Cai Abstract: Alzheimer's disease (AD) is one of the most debilitating neurodegenerative nerve diseases, seriously affecting one's ability to carry out daily activities. AD is both progressive and incurable, but molecular studies have begun to shed light on the mechanisms that underlie it. Immunochemical staining showed that cell bodies of Purkinje cells in the cerebellum were significantly reduced in AD rats compared with normal rats. Heat shock protein 70 (HSP70) was found to prevent polyglutamine aggregation in Huntington's disease and spinocerebellar ataxias (SCAs) and to relieve symptoms in SCAs and Parkinson's disease. Recently, AD-related phenotypes were found to be suppressed in HSP70 transgenic rats. However, the effects of other HSPs and the mechanisms of HSP-triggered changes in AD are unknown. In this study, we found that expression levels of HSP60, -70, and -90 were downregulated in the cerebella of rats with AD. Furthermore, heat shock factor 1 (HSF1), a key transcription factor for the expression of HSP genes, was found to be greatly decreased in the cerebella of AD rats. Even more interesting, injection of lentivirus vector-HSF1 into the cerebella of AD rats significantly increased HSF1 and HSP expression levels and induced an increase in the number of Purkinje cell bodies. Our findings provide novel evidence that low expression of HSPs in AD rats is dependent on the low expression of HSF1, and increased expression of HSF1 contributes to the reversal of cerebellar Purkinje cell deficiency in AD. Therefore, increasing HSF1 expression is a potential new strategy for the treatment of AD. Author Affiliation: (a) Third Hospital of Hebei Medical University, Shijiazhuang 050051, China (b) School of Biology and Pharmaceutical Engineering, Wuhan Polytechnic University, Wuhan, Hubei 430023, China (c) Baylor College of Medicine, Houston, TX 77030, USA (d) Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA (e) Dalian Medical University, Dalian, Liaoning 116044, China (f) Hebei Medical University, Shijiazhuang 050017, China Article History: Accepted 25 April 2013
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