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dc.contributor.author
AbdAlla, Said
dc.contributor.author
Langer, Andreas
dc.contributor.author
Fu, Xuebin
dc.contributor.author
Quitterer, Ursula
dc.date.accessioned
2018-11-05T10:10:38Z
dc.date.available
2017-06-11T00:38:10Z
dc.date.available
2018-11-05T10:10:38Z
dc.date.issued
2013-08-16
dc.identifier.issn
1422-0067
dc.identifier.other
10.3390/ijms140816917
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/75310
dc.identifier.doi
10.3929/ethz-b-000075310
dc.description.abstract
Increased generation of reactive oxygen species (ROS) is a significant pathological feature in the brains of patients with Alzheimer’s disease (AD). Experimental evidence indicates that inhibition of brain ROS could be beneficial in slowing the neurodegenerative process triggered by amyloid-beta (Abeta) aggregates. The angiotensin II AT1 receptor is a significant source of brain ROS, and AD patients have an increased brain angiotensin-converting enzyme (ACE) level, which could account for an excessive angiotensin-dependent AT1-induced ROS generation. Therefore, we analyzed the impact of ACE inhibition on signs of neurodegeneration of aged Tg2576 mice as a transgenic animal model of AD. Whole genome microarray gene expression profiling and biochemical analyses demonstrated that the centrally active ACE inhibitor captopril normalized the excessive hippocampal ACE activity of AD mice. Concomitantly, the development of signs of neurodegeneration was retarded by six months of captopril treatment. The neuroprotective profile triggered by captopril was accompanied by reduced amyloidogenic processing of the amyloid precursor protein (APP), and decreased hippocampal ROS, which is known to enhance Abeta generation by increased activation of beta- and gamma-secretases. Taken together, our data present strong evidence that ACE inhibition with a widely used cardiovascular drug could interfere with Abeta-dependent neurodegeneration.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
MDPI
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/3.0/
dc.subject
Alzheimer's disease
en_US
dc.subject
Amyloid precursor protein
en_US
dc.subject
Angiotensin-converting enzyme
en_US
dc.subject
AT1 receptor
en_US
dc.subject
Captopril
en_US
dc.subject
Neurodegeneration
en_US
dc.subject
Tg2576 mouse model
en_US
dc.title
ACE Inhibition with Captopril Retards the Development of Signs of Neurodegeneration in an Animal Model of Alzheimer’s Disease
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 3.0 Unported
ethz.journal.title
International Journal of Molecular Sciences
ethz.journal.volume
14
en_US
ethz.journal.issue
8
en_US
ethz.journal.abbreviated
Int. j. mol. sci.
ethz.pages.start
16917
en_US
ethz.pages.end
16942
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.grant
GRK2 inhibition in cardiovascular disease
en_US
ethz.identifier.wos
ethz.identifier.nebis
004068146
ethz.publication.place
S.l.
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02020 - Dep. Chemie und Angewandte Biowiss. / Dep. of Chemistry and Applied Biosc.::02534 - Institut für Pharmazeutische Wiss. / Institute of Pharmaceutical Sciences::03735 - Quitterer, Ursula M. / Quitterer, Ursula M.
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02020 - Dep. Chemie und Angewandte Biowiss. / Dep. of Chemistry and Applied Biosc.::02534 - Institut für Pharmazeutische Wiss. / Institute of Pharmaceutical Sciences::03735 - Quitterer, Ursula M. / Quitterer, Ursula M.
ethz.grant.agreementno
140679
ethz.grant.fundername
SNF
ethz.grant.funderDoi
10.13039/501100001711
ethz.grant.program
Projektförderung in Biologie und Medizin (Abteilung III)
ethz.date.deposited
2017-06-11T00:39:06Z
ethz.source
ECIT
ethz.identifier.importid
imp593651402d1c926559
ethz.ecitpid
pub:118930
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-25T10:32:25Z
ethz.rosetta.lastUpdated
2018-11-05T10:10:59Z
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true
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true
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