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Article: Melatonin reduces hippocampal β-amyloid generation in rats exposed to chronic intermittent hypoxia

TitleMelatonin reduces hippocampal β-amyloid generation in rats exposed to chronic intermittent hypoxia
Authors
Keywordsβ-amyloid
β-amyloid precursor protein
Alzheimer's disease
Beta-site APP cleavage enzyme
Chronic intermittent hypoxia
Melatonin
Issue Date2010
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainres
Citation
Brain Research, 2010, v. 1354, p. 163-171 How to Cite?
AbstractThe deposition of neurotoxic β-amyloid plaques plays a central role in the pathogenesis of Alzheimer's disease. At the molecular level, the generation of β-amyloid peptides involves the site-specific cleavage of the precursor protein by β-site APP cleavage enzyme (BACE) and presenilin. Although acute or chronic sustained hypoxia appears to increase the generation of β-amyloid peptides via the HIF-1α dependent upregulation of BACE, the effect of chronic intermittent hypoxia (CIH) on the generation of β-amyloid peptides remains uncertain. In this study, we have evaluated such contention in the rat hippocampus, and we found that short-term CIH exposure (3 days) caused significant increases in the generation of β-amyloid peptides, and the expressions of BACE, presenilin and HIF-1α protein levels, in the hippocampus of CIH rats. Moreover, the CIH-induced hippocampal β-amyloid peptide generation could be abolished by a daily pharmacological administration of melatonin (10 mg/kg), which reduced the BACE but not presenilin expression. Also, there were no significant differences in the hippocampal HIF-1α protein levels between the melatonin- and vehicle-treated CIH groups. Our study not only provided the first evidence that short-term CIH exposure could induce the β-amyloid peptide generation in the hippocampus, but also pointed out the therapeutic value of melatonin in reducing β-amyloid peptide generation in patients suffering from chronic obstructive sleep apnea syndrome. © 2010 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/139667
ISSN
2015 Impact Factor: 2.561
2015 SCImago Journal Rankings: 1.351
ISI Accession Number ID
Funding AgencyGrant Number
HKU200707176046
Funding Information:

We are grateful for the technical assistance of Mr. Y.M. Lo. This work was supported by grants from the HKU Small Project Funding (200707176046 to K.M.Ng).

References

 

DC FieldValueLanguage
dc.contributor.authorNg, KMen_HK
dc.contributor.authorLau, CFen_HK
dc.contributor.authorFung, MLen_HK
dc.date.accessioned2011-09-23T05:53:13Z-
dc.date.available2011-09-23T05:53:13Z-
dc.date.issued2010en_HK
dc.identifier.citationBrain Research, 2010, v. 1354, p. 163-171en_HK
dc.identifier.issn0006-8993en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139667-
dc.description.abstractThe deposition of neurotoxic β-amyloid plaques plays a central role in the pathogenesis of Alzheimer's disease. At the molecular level, the generation of β-amyloid peptides involves the site-specific cleavage of the precursor protein by β-site APP cleavage enzyme (BACE) and presenilin. Although acute or chronic sustained hypoxia appears to increase the generation of β-amyloid peptides via the HIF-1α dependent upregulation of BACE, the effect of chronic intermittent hypoxia (CIH) on the generation of β-amyloid peptides remains uncertain. In this study, we have evaluated such contention in the rat hippocampus, and we found that short-term CIH exposure (3 days) caused significant increases in the generation of β-amyloid peptides, and the expressions of BACE, presenilin and HIF-1α protein levels, in the hippocampus of CIH rats. Moreover, the CIH-induced hippocampal β-amyloid peptide generation could be abolished by a daily pharmacological administration of melatonin (10 mg/kg), which reduced the BACE but not presenilin expression. Also, there were no significant differences in the hippocampal HIF-1α protein levels between the melatonin- and vehicle-treated CIH groups. Our study not only provided the first evidence that short-term CIH exposure could induce the β-amyloid peptide generation in the hippocampus, but also pointed out the therapeutic value of melatonin in reducing β-amyloid peptide generation in patients suffering from chronic obstructive sleep apnea syndrome. © 2010 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainresen_HK
dc.relation.ispartofBrain Researchen_HK
dc.subjectβ-amyloiden_HK
dc.subjectβ-amyloid precursor proteinen_HK
dc.subjectAlzheimer's diseaseen_HK
dc.subjectBeta-site APP cleavage enzymeen_HK
dc.subjectChronic intermittent hypoxiaen_HK
dc.subjectMelatoninen_HK
dc.subject.meshAmyloid beta-Peptides - metabolism-
dc.subject.meshAnoxia - drug therapy - metabolism - pathology-
dc.subject.meshHippocampus - drug effects - metabolism - pathology-
dc.subject.meshMelatonin - pharmacology - therapeutic use-
dc.subject.meshAspartic acid endopeptidases-
dc.titleMelatonin reduces hippocampal β-amyloid generation in rats exposed to chronic intermittent hypoxiaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-8993&volume=1354&spage=163&epage=171&date=2010&atitle=Melatonin+reduces+hippocampal+beta-amyloid+generation+in+rats+exposed+to+chronic+intermittent+hypoxiaen_US
dc.identifier.emailNg, KM: skykmng@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.authorityNg, KM=rp01670en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.brainres.2010.07.044en_HK
dc.identifier.pmid20654588-
dc.identifier.scopuseid_2-s2.0-77956417605en_HK
dc.identifier.hkuros195740en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77956417605&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1354en_HK
dc.identifier.issue1-
dc.identifier.spage163en_HK
dc.identifier.epage171en_HK
dc.identifier.isiWOS:000282162400017-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridNg, KM=25122990200en_HK
dc.identifier.scopusauthoridLau, CF=25122803900en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK

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