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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
2023 Impact Factor: 2.7
2023 SCImago Journal Rankings: 0.832
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
Grants

 

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.relation.projectEffect of hypoxia on the differentiation of human embryonic stem cells into cardiomyocytes-
dc.identifier.scopusauthoridNg, KM=25122990200en_HK
dc.identifier.scopusauthoridLau, CF=25122803900en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.issnl0006-8993-

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