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Article: Coenzyme Q10 reduces β-amyloid plaque in an APP/PS1 transgenic mouse model of Alzheimer's disease

TitleCoenzyme Q10 reduces β-amyloid plaque in an APP/PS1 transgenic mouse model of Alzheimer's disease
Authors
Issue Date2010
Citation
Journal Of Molecular Neuroscience, 2010, v. 41 n. 1, p. 110-113 How to Cite?
AbstractWe previously reported that coenzyme Q10 (CoQ10) could reduce intracellular deposition in an aged transgenic mouse model. Here, we further tested the effect of CoQ10 on amyloid plaque in an amyloid precursor protein/presenilin 1 transgenic mouse model of Alzheimer's disease (AD). By using immunohistochemistry and magnetic resonance imaging to determine the burden of amyloid plaque, we found that oral administration of CoQ10 can efficiently reduce the burden of the plaques in this mouse model. These data demonstrate that in addition to reducing intracellular deposition of Aβ, CoQ10 can also reduce plaque pathology. Our study further supports the use of CoQ10 as a therapeutic candidate for AD. © 2009 Humana Press.
Persistent Identifierhttp://hdl.handle.net/10722/155562
ISSN
2015 Impact Factor: 2.352
2015 SCImago Journal Rankings: 0.988
ISI Accession Number ID
Funding AgencyGrant Number
Rejuvenis, Hong Kong Jockey Club Charities Trust
Funding Information:

This study was supported by a grant from Rejuvenis, Hong Kong Jockey Club Charities Trust.

References

 

DC FieldValueLanguage
dc.contributor.authorYang, Xen_US
dc.contributor.authorDai, Gen_US
dc.contributor.authorLi, Gen_US
dc.contributor.authorYang, ESen_US
dc.date.accessioned2012-08-08T08:34:06Z-
dc.date.available2012-08-08T08:34:06Z-
dc.date.issued2010en_US
dc.identifier.citationJournal Of Molecular Neuroscience, 2010, v. 41 n. 1, p. 110-113en_US
dc.identifier.issn0895-8696en_US
dc.identifier.urihttp://hdl.handle.net/10722/155562-
dc.description.abstractWe previously reported that coenzyme Q10 (CoQ10) could reduce intracellular deposition in an aged transgenic mouse model. Here, we further tested the effect of CoQ10 on amyloid plaque in an amyloid precursor protein/presenilin 1 transgenic mouse model of Alzheimer's disease (AD). By using immunohistochemistry and magnetic resonance imaging to determine the burden of amyloid plaque, we found that oral administration of CoQ10 can efficiently reduce the burden of the plaques in this mouse model. These data demonstrate that in addition to reducing intracellular deposition of Aβ, CoQ10 can also reduce plaque pathology. Our study further supports the use of CoQ10 as a therapeutic candidate for AD. © 2009 Humana Press.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Molecular Neuroscienceen_US
dc.subject.meshAlzheimer Disease - Drug Therapy - Pathologyen_US
dc.subject.meshAmyloid Beta-Peptides - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCerebral Cortex - Drug Effects - Pathologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshHippocampus - Drug Effects - Pathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMagnetic Resonance Imagingen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshNeuroprotective Agents - Pharmacology - Therapeutic Useen_US
dc.subject.meshPlaque, Amyloid - Drug Effects - Pathologyen_US
dc.subject.meshPresenilin-1 - Metabolismen_US
dc.subject.meshUbiquinone - Analogs & Derivatives - Pharmacology - Therapeutic Useen_US
dc.subject.meshVitamins - Pharmacology - Therapeutic Useen_US
dc.titleCoenzyme Q10 reduces β-amyloid plaque in an APP/PS1 transgenic mouse model of Alzheimer's diseaseen_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/s12031-009-9297-1en_US
dc.identifier.pmid19834824-
dc.identifier.scopuseid_2-s2.0-77950189527en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77950189527&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume41en_US
dc.identifier.issue1en_US
dc.identifier.spage110en_US
dc.identifier.epage113en_US
dc.identifier.isiWOS:000275905400015-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYang, X=23007172600en_US
dc.identifier.scopusauthoridDai, G=8579465500en_US
dc.identifier.scopusauthoridLi, G=35767974200en_US
dc.identifier.scopusauthoridYang, ES=7202021229en_US
dc.identifier.citeulike5999828-

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