schliessen

Filtern

 

Bibliotheken

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

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... Full description

Journal Title: Brain Research 26 June 2013, Vol.1519, pp.105-111
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:
Hsp
ID: ISSN: 0006-8993 ; E-ISSN: 1872-6240 ; DOI: 10.1016/j.brainres.2013.04.059
Link: https://www.sciencedirect.com/science/article/pii/S0006899313006446
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: elsevier_sdoi_10_1016_j_brainres_2013_04_059
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
  • Hsf1
  • Hsp
  • Lentivirus Vector
  • Purkinje Cell
  • Anatomy & Physiology
ispartof: Brain Research, 26 June 2013, Vol.1519, pp.105-111
description: 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.
language: eng
source:
identifier: ISSN: 0006-8993 ; E-ISSN: 1872-6240 ; DOI: 10.1016/j.brainres.2013.04.059
fulltext: fulltext
issn:
  • 0006-8993
  • 00068993
  • 1872-6240
  • 18726240
url: Link


@attributes
ID1110437995
RANK0.07
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
LOCALfalse
PrimoNMBib
record
control
sourcerecordiddoi_10_1016_j_brainres_2013_04_059
sourceidelsevier_s
recordidTN_elsevier_sdoi_10_1016_j_brainres_2013_04_059
sourcesystemOther
dbid
0--K
1--M
2.FO
3.~1
41B1
51P~
61RT
71~.
8457
94G.
107-5
118P~
129JM
13AABNK
14AAEDT
15AAKOC
16AAOAW
17AAQFI
18AAXLA
19ABCQJ
20ABFNM
21ABTEW
22ABYKQ
23ACDAQ
24ACIUM
25ACRLP
26AEKER
27AEVXI
28AFKWA
29AFTJW
30AFXIZ
31AGUBO
32AGWIK
33AGYEJ
34AIKHN
35AITUG
36AJBFU
37AJOXV
38AJUYK
39AMFUW
40BLXMC
41EO8
42EO9
43EP2
44EP3
45FDB
46FIRID
47FNPLU
48G-Q
49GBLVA
50J1W
51KOM
52MOBAO
53OAUVE
54OP~
55P-8
56P-9
57PC.
58Q38
59RPZ
60SCC
61SDF
62SDG
63SES
64SSN
65SSZ
66T5K
67Z5R
68~G-
pqid1366576432
display
typearticle
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, 26 June 2013, Vol.1519, pp.105-111
identifier
subjectAlzheimer'S Disease ; Hsf1 ; Hsp ; Lentivirus Vector ; Purkinje Cell ; Anatomy & Physiology
descriptionAlzheimer'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.
languageeng
source
version4
lds50peer_reviewed
links
openurl$$Topenurl_article
openurlfulltext$$Topenurlfull_article
backlink$$Uhttps://www.sciencedirect.com/science/article/pii/S0006899313006446$$EView_record_in_ScienceDirect_(Access_to_full_text_may_be_restricted)
search
creatorcontrib
0Jiang, Yu-Qing
1Wang, Xiu-Li
2Cao, Xue-Hong
3Ye, Zeng-You
4Li, Li
5Cai, Wen-Qing
titleIncreased heat shock transcription factor 1 in the cerebellum reverses the deficiency of Purkinje cells in Alzheimer's disease
description

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.

subject
0Alzheimer'S Disease
1Hsf1
2Hsp
3Lentivirus Vector
4Purkinje Cell
5Anatomy & Physiology
general
0English
1Elsevier B.V
210.1016/j.brainres.2013.04.059
3ScienceDirect (Elsevier B.V.)
4ScienceDirect Journals (Elsevier)
sourceidelsevier_s
recordidelsevier_sdoi_10_1016_j_brainres_2013_04_059
issn
00006-8993
100068993
21872-6240
318726240
rsrctypearticle
creationdate2013
addtitleBrain Research
searchscope
0elsevier_full
1elsevier2
scope
0elsevier_full
1elsevier2
lsr44$$EView_record_in_ScienceDirect_(Access_to_full_text_may_be_restricted)
tmp01ScienceDirect Journals (Elsevier)
tmp02
0--K
1--M
2.FO
3.~1
41B1
51P~
61RT
71~.
8457
94G.
107-5
118P~
129JM
13AABNK
14AAEDT
15AAKOC
16AAOAW
17AAQFI
18AAXLA
19ABCQJ
20ABFNM
21ABTEW
22ABYKQ
23ACDAQ
24ACIUM
25ACRLP
26AEKER
27AEVXI
28AFKWA
29AFTJW
30AFXIZ
31AGUBO
32AGWIK
33AGYEJ
34AIKHN
35AITUG
36AJBFU
37AJOXV
38AJUYK
39AMFUW
40BLXMC
41EO8
42EO9
43EP2
44EP3
45FDB
46FIRID
47FNPLU
48G-Q
49GBLVA
50J1W
51KOM
52MOBAO
53OAUVE
54OP~
55P-8
56P-9
57PC.
58Q38
59RPZ
60SCC
61SDF
62SDG
63SES
64SSN
65SSZ
66T5K
67Z5R
68~G-
startdate20130626
enddate20130626
lsr40Brain Research, 26 June 2013, Vol.1519, pp.105-111
doi10.1016/j.brainres.2013.04.059
citationpf 105 pt 111 vol 1519
lsr30VSR-Enriched:[pqid]
sort
titleIncreased heat shock transcription factor 1 in the cerebellum reverses the deficiency of Purkinje cells in Alzheimer's disease
authorJiang, Yu-Qing ; Wang, Xiu-Li ; Cao, Xue-Hong ; Ye, Zeng-You ; Li, Li ; Cai, Wen-Qing
creationdate20130626
lso0120130626
facets
frbrgroupid4168745765544113803
frbrtype5
newrecords20190904
languageeng
topic
0Alzheimer'S Disease
1Hsf1
2Hsp
3Lentivirus Vector
4Purkinje Cell
5Anatomy & Physiology
collectionScienceDirect (Elsevier B.V.)
prefilterarticles
rsrctypearticles
creatorcontrib
0Jiang, Yu-Qing
1Wang, Xiu-Li
2Cao, Xue-Hong
3Ye, Zeng-You
4Li, Li
5Cai, Wen-Qing
jtitleBrain Research
creationdate2013
toplevelpeer_reviewed
delivery
delcategoryRemote Search Resource
fulltextfulltext
addata
aulast
0Jiang
1Wang
2Cao
3Ye
4Li
5Cai
aufirst
0Yu-Qing
1Xiu-Li
2Xue-Hong
3Zeng-You
4Li
5Wen-Qing
auinitY
auinit1Y
au
0Jiang, Yu-Qing
1Wang, Xiu-Li
2Cao, Xue-Hong
3Ye, Zeng-You
4Li, Li
5Cai, Wen-Qing
atitleIncreased heat shock transcription factor 1 in the cerebellum reverses the deficiency of Purkinje cells in Alzheimer's disease
jtitleBrain Research
risdate20130626
volume1519
spage105
epage111
pages105-111
issn0006-8993
eissn1872-6240
formatjournal
genrearticle
ristypeJOUR
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.

pubElsevier B.V
doi10.1016/j.brainres.2013.04.059
lad01Brain Research
date2013-06-26