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Article: Coenzyme Q10 attenuates β-amyloid pathology in the aged transgenic mice with Alzheimer presenilin 1 mutation

TitleCoenzyme Q10 attenuates β-amyloid pathology in the aged transgenic mice with Alzheimer presenilin 1 mutation
Authors
KeywordsAβ42
Alzheimer's Disease
Coenzyme Q10
Oxidative Stress
Presenilin 1
Issue Date2008
Citation
Journal Of Molecular Neuroscience, 2008, v. 34 n. 2, p. 165-171 How to Cite?
AbstractOne of the neuropathological features of Alzheimer's disease (AD) is the deposition of senile plaques containing β-amyloid (Aβ). There is limited evidence for the treatment to arrest Aβ pathology of AD. In our present study, we tested the effect of coenzyme Q10 (CoQ10), an endogenous antioxidant and a powerful free radical scavenger, on Aβ in the aged transgenic mice overexpressing Alzheimer presenilin 1-L235P (leucine-to-proline mutation at codon 235, 16-17 months old). The treatment by feeding the transgenic mice with CoQ10 for 60 days (1,200 mg kg -1 day -1) partially attenuated Aβ overproduction and intracellular Aβ deposit in the cortex of the transgenic mice compared with the age-matched untreated transgenic mice. Meanwhile, an increased oxidative stress reaction was detected as evidenced by elevated level of malondialdehyde (MDA) and decreased activity of superoxide dismutase (SOD) in the transgenic mice relative to the wild-type mice, and supplementation of CoQ10 partially decreased MDA level and upregulated the activity of SOD. The results indicate that oxidative stress is enhanced in the brain of the transgenic mice, that this enhancement may further promote Aβ42 overproduction in a vicious formation, and that CoQ10 would be beneficial for the therapy of AD. © 2007 Humana Press Inc.
Persistent Identifierhttp://hdl.handle.net/10722/155460
ISSN
2015 Impact Factor: 2.352
2015 SCImago Journal Rankings: 0.988
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, Xen_US
dc.contributor.authorYang, Yen_US
dc.contributor.authorLi, Gen_US
dc.contributor.authorWang, Jen_US
dc.contributor.authorYang, ESen_US
dc.date.accessioned2012-08-08T08:33:36Z-
dc.date.available2012-08-08T08:33:36Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Molecular Neuroscience, 2008, v. 34 n. 2, p. 165-171en_US
dc.identifier.issn0895-8696en_US
dc.identifier.urihttp://hdl.handle.net/10722/155460-
dc.description.abstractOne of the neuropathological features of Alzheimer's disease (AD) is the deposition of senile plaques containing β-amyloid (Aβ). There is limited evidence for the treatment to arrest Aβ pathology of AD. In our present study, we tested the effect of coenzyme Q10 (CoQ10), an endogenous antioxidant and a powerful free radical scavenger, on Aβ in the aged transgenic mice overexpressing Alzheimer presenilin 1-L235P (leucine-to-proline mutation at codon 235, 16-17 months old). The treatment by feeding the transgenic mice with CoQ10 for 60 days (1,200 mg kg -1 day -1) partially attenuated Aβ overproduction and intracellular Aβ deposit in the cortex of the transgenic mice compared with the age-matched untreated transgenic mice. Meanwhile, an increased oxidative stress reaction was detected as evidenced by elevated level of malondialdehyde (MDA) and decreased activity of superoxide dismutase (SOD) in the transgenic mice relative to the wild-type mice, and supplementation of CoQ10 partially decreased MDA level and upregulated the activity of SOD. The results indicate that oxidative stress is enhanced in the brain of the transgenic mice, that this enhancement may further promote Aβ42 overproduction in a vicious formation, and that CoQ10 would be beneficial for the therapy of AD. © 2007 Humana Press Inc.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Molecular Neuroscienceen_US
dc.subjectAβ42en_US
dc.subjectAlzheimer's Diseaseen_US
dc.subjectCoenzyme Q10en_US
dc.subjectOxidative Stressen_US
dc.subjectPresenilin 1en_US
dc.titleCoenzyme Q10 attenuates β-amyloid pathology in the aged transgenic mice with Alzheimer presenilin 1 mutationen_US
dc.typeArticleen_US
dc.identifier.emailYang, ES:esyang@hkueee.hku.hken_US
dc.identifier.authorityYang, ES=rp00199en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s12031-007-9033-7en_US
dc.identifier.scopuseid_2-s2.0-42949122109en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-42949122109&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume34en_US
dc.identifier.issue2en_US
dc.identifier.spage165en_US
dc.identifier.epage171en_US
dc.identifier.isiWOS:000252483400008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYang, X=23007172600en_US
dc.identifier.scopusauthoridYang, Y=34769311500en_US
dc.identifier.scopusauthoridLi, G=35767974200en_US
dc.identifier.scopusauthoridWang, J=7701331129en_US
dc.identifier.scopusauthoridYang, ES=7202021229en_US

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