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Article: Diet supplement CoQ 10 delays brain atrophy in aged transgenic mice with mutations in the amyloid precursor protein: An in vivo volume MRI study

TitleDiet supplement CoQ 10 delays brain atrophy in aged transgenic mice with mutations in the amyloid precursor protein: An in vivo volume MRI study
Authors
KeywordsAlzheimer's Disease
Antioxidant
App/Ps1 Double Transgenic Mice
Hemispheric Volume
Hippocampal Volume
Issue Date2008
PublisherI O S Press. The Journal's web site is located at http://www.iospress.nl/html/09516433.php
Citation
Biofactors, 2008, v. 32 n. 1-4, p. 169-178 How to Cite?
AbstractWe tested the hypotheses that supplemental intake of the diet supplement Coenzyme Q 10 (CoQ 10) could delay brain atrophy in double transgenic amyloid precursor protein (APP) / presenilin 1 (PS1), single transgenic APP and PS1 as well as wild type mice by volume MR image in vivo. One hundred and twelve mice (28 APP/PS1, 28 APP, 28 PS1 and 28 wild types) were studied. Half of each genotype group (n = 14 per group) was treated with CoQ 10 2400 mg/kg/day, and the other half with placebo for 60 days. Magnetic resonance (MR) images were used to obtain the volumes of the hemispheres and hippocampi. APP / PS1, APP, PS1 and wild type mice treated with CoQ 10 exhibited significantly less atrophy in hemisphere and hippocampus than those receiving placebo. The neuro-protective effect of the CoQ 10 on hemispheric volume, and hippocampal volume was related to genotype; greater in APP/PS1 than APP and PS1 mice and less in wild type mice. Our result indicated that CoQ 10 may have therapeutic potential in the prevention and treatment of MCI and AD. © 2008 - IUBMB/IOS Press and the authors. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/155502
ISSN
2015 Impact Factor: 4.504
2015 SCImago Journal Rankings: 1.683
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Gen_US
dc.contributor.authorJack, CRen_US
dc.contributor.authorYang, XFen_US
dc.contributor.authorYang, ESen_US
dc.date.accessioned2012-08-08T08:33:48Z-
dc.date.available2012-08-08T08:33:48Z-
dc.date.issued2008en_US
dc.identifier.citationBiofactors, 2008, v. 32 n. 1-4, p. 169-178en_US
dc.identifier.issn0951-6433en_US
dc.identifier.urihttp://hdl.handle.net/10722/155502-
dc.description.abstractWe tested the hypotheses that supplemental intake of the diet supplement Coenzyme Q 10 (CoQ 10) could delay brain atrophy in double transgenic amyloid precursor protein (APP) / presenilin 1 (PS1), single transgenic APP and PS1 as well as wild type mice by volume MR image in vivo. One hundred and twelve mice (28 APP/PS1, 28 APP, 28 PS1 and 28 wild types) were studied. Half of each genotype group (n = 14 per group) was treated with CoQ 10 2400 mg/kg/day, and the other half with placebo for 60 days. Magnetic resonance (MR) images were used to obtain the volumes of the hemispheres and hippocampi. APP / PS1, APP, PS1 and wild type mice treated with CoQ 10 exhibited significantly less atrophy in hemisphere and hippocampus than those receiving placebo. The neuro-protective effect of the CoQ 10 on hemispheric volume, and hippocampal volume was related to genotype; greater in APP/PS1 than APP and PS1 mice and less in wild type mice. Our result indicated that CoQ 10 may have therapeutic potential in the prevention and treatment of MCI and AD. © 2008 - IUBMB/IOS Press and the authors. All rights reserved.en_US
dc.languageengen_US
dc.publisherI O S Press. The Journal's web site is located at http://www.iospress.nl/html/09516433.phpen_US
dc.relation.ispartofBioFactorsen_US
dc.subjectAlzheimer's Diseaseen_US
dc.subjectAntioxidanten_US
dc.subjectApp/Ps1 Double Transgenic Miceen_US
dc.subjectHemispheric Volumeen_US
dc.subjectHippocampal Volumeen_US
dc.titleDiet supplement CoQ 10 delays brain atrophy in aged transgenic mice with mutations in the amyloid precursor protein: An in vivo volume MRI studyen_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.doi10.1002/biof.5520320120-
dc.identifier.pmid19096113-
dc.identifier.scopuseid_2-s2.0-58149373850en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-58149373850&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume32en_US
dc.identifier.issue1-4en_US
dc.identifier.spage169en_US
dc.identifier.epage178en_US
dc.identifier.isiWOS:000263247200020-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridLi, G=35767974200en_US
dc.identifier.scopusauthoridJack, CR=18033457700en_US
dc.identifier.scopusauthoridYang, XF=23007172600en_US
dc.identifier.scopusauthoridYang, ES=7202021229en_US

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