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Article: Berberine ameliorates β-amyloid pathology, gliosis, and cognitive impairment in an Alzheimer's disease transgenic mouse model
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TitleBerberine ameliorates β-amyloid pathology, gliosis, and cognitive impairment in an Alzheimer's disease transgenic mouse model
 
AuthorsDurairajan, SSK2
Liu, LF2
Lu, JH2
Chen, LL2
Yuan, Q4
Chung, SK1
Huang, L3
Li, XS3
Huang, JD1
Li, M2
 
KeywordsΒ-Amyloid
Alzheimer's Disease
Amyloid Precursor Protein
Berberine
Glycogen Synthase Kinase
Tau Phosphorylation
Tgcrnd8 Mice
 
Issue Date2012
 
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/neuaging
 
CitationNeurobiology Of Aging, 2012, v. 33 n. 12, p 2903-2919 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.neurobiolaging.2012.02.016
 
AbstractThe accumulation of β-amyloid (Aβ) peptide derived from abnormal processing of amyloid precursor protein (APP) is a common pathological hallmark of Alzheimer's disease (AD) brains. In this study, we evaluated the therapeutic effect of berberine (BBR) extracted from Coptis chinensis Franch, a Chinese medicinal herb, on the neuropathology and cognitive impairment in TgCRND8 mice, a well established transgenic mouse model of AD. Two-month-old TgCRND8 mice received a low (25 mg/kg per day) or a high dose of BBR (100 mg/kg per day) by oral gavage until 6 months old. BBR treatment significantly ameliorated learning deficits, long-term spatial memory retention, as well as plaque load compared with vehicle control treatment. In addition, enzyme-linked immunosorbent assay (ELISA) measurement showed that there was a profound reduction in levels of detergent-soluble and -insoluble β-amyloid in brain homogenates of BBR-treated mice. Glycogen synthase kinase (GSK)3, a major kinase involved in APP and tau phosphorylation, was significantly inhibited by BBR treatment. We also found that BBR significantly decreased the levels of C-terminal fragments of APP and the hyperphosphorylation of APP and tau via the Akt/glycogen synthase kinase 3 signaling pathway in N2a mouse neuroblastoma cells stably expressing human Swedish mutant APP695 (N2a-SwedAPP). Our results suggest that BBR provides neuroprotective effects in TgCRND8 mice through regulating APP processing and that further investigation of the BBR for therapeutic use in treating AD is warranted. © 2012 Elsevier Inc. All rights reserved.
 
ISSN0197-4580
2013 Impact Factor: 4.853
2013 SCImago Journal Rankings: 2.479
 
DOIhttp://dx.doi.org/10.1016/j.neurobiolaging.2012.02.016
 
ISI Accession Number IDWOS:000310200000017
 
DC FieldValue
dc.contributor.authorDurairajan, SSK
 
dc.contributor.authorLiu, LF
 
dc.contributor.authorLu, JH
 
dc.contributor.authorChen, LL
 
dc.contributor.authorYuan, Q
 
dc.contributor.authorChung, SK
 
dc.contributor.authorHuang, L
 
dc.contributor.authorLi, XS
 
dc.contributor.authorHuang, JD
 
dc.contributor.authorLi, M
 
dc.date.accessioned2012-06-26T05:58:37Z
 
dc.date.available2012-06-26T05:58:37Z
 
dc.date.issued2012
 
dc.description.abstractThe accumulation of β-amyloid (Aβ) peptide derived from abnormal processing of amyloid precursor protein (APP) is a common pathological hallmark of Alzheimer's disease (AD) brains. In this study, we evaluated the therapeutic effect of berberine (BBR) extracted from Coptis chinensis Franch, a Chinese medicinal herb, on the neuropathology and cognitive impairment in TgCRND8 mice, a well established transgenic mouse model of AD. Two-month-old TgCRND8 mice received a low (25 mg/kg per day) or a high dose of BBR (100 mg/kg per day) by oral gavage until 6 months old. BBR treatment significantly ameliorated learning deficits, long-term spatial memory retention, as well as plaque load compared with vehicle control treatment. In addition, enzyme-linked immunosorbent assay (ELISA) measurement showed that there was a profound reduction in levels of detergent-soluble and -insoluble β-amyloid in brain homogenates of BBR-treated mice. Glycogen synthase kinase (GSK)3, a major kinase involved in APP and tau phosphorylation, was significantly inhibited by BBR treatment. We also found that BBR significantly decreased the levels of C-terminal fragments of APP and the hyperphosphorylation of APP and tau via the Akt/glycogen synthase kinase 3 signaling pathway in N2a mouse neuroblastoma cells stably expressing human Swedish mutant APP695 (N2a-SwedAPP). Our results suggest that BBR provides neuroprotective effects in TgCRND8 mice through regulating APP processing and that further investigation of the BBR for therapeutic use in treating AD is warranted. © 2012 Elsevier Inc. All rights reserved.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationNeurobiology Of Aging, 2012, v. 33 n. 12, p 2903-2919 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.neurobiolaging.2012.02.016
 
dc.identifier.citeulike11522637
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.neurobiolaging.2012.02.016
 
dc.identifier.hkuros199688
 
dc.identifier.isiWOS:000310200000017
 
dc.identifier.issn0197-4580
2013 Impact Factor: 4.853
2013 SCImago Journal Rankings: 2.479
 
dc.identifier.pmid22459600
 
dc.identifier.scopuseid_2-s2.0-84866744899
 
dc.identifier.urihttp://hdl.handle.net/10722/149785
 
dc.languageeng
 
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/neuaging
 
dc.publisher.placeUnited States
 
dc.relation.ispartofNeurobiology of Aging
 
dc.subjectΒ-Amyloid
 
dc.subjectAlzheimer's Disease
 
dc.subjectAmyloid Precursor Protein
 
dc.subjectBerberine
 
dc.subjectGlycogen Synthase Kinase
 
dc.subjectTau Phosphorylation
 
dc.subjectTgcrnd8 Mice
 
dc.titleBerberine ameliorates β-amyloid pathology, gliosis, and cognitive impairment in an Alzheimer's disease transgenic mouse model
 
dc.typeArticle
 
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<contributor.author>Liu, LF</contributor.author>
<contributor.author>Lu, JH</contributor.author>
<contributor.author>Chen, LL</contributor.author>
<contributor.author>Yuan, Q</contributor.author>
<contributor.author>Chung, SK</contributor.author>
<contributor.author>Huang, L</contributor.author>
<contributor.author>Li, XS</contributor.author>
<contributor.author>Huang, JD</contributor.author>
<contributor.author>Li, M</contributor.author>
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<subject>Alzheimer&apos;s Disease</subject>
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<subject>Tau Phosphorylation</subject>
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. Hong Kong Baptist University
  3. Sun Yat-Sen University
  4. Chinese University of Hong Kong