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Article: Regulation of Melatonin and Neurotransmission in Alzheimer's Disease

TitleRegulation of Melatonin and Neurotransmission in Alzheimer's Disease
Authors
Keywordsmelatonin
neurotransmission
Alzheimer’s disease
Issue Date2021
PublisherMolecular Diversity Preservation International. The Journal's web site is located at http://www.mdpi.org/ijms
Citation
International Journal of Molecular Sciences, 2021, v. 22 n. 13, p. article no. 6841 How to Cite?
AbstractAlzheimer’s disease is a neurodegenerative disorder associated with age, and is characterized by pathological markers such as amyloid-beta plaques and neurofibrillary tangles. Symptoms of AD include cognitive impairments, anxiety and depression. It has also been shown that individuals with AD have impaired neurotransmission, which may result from the accumulation of amyloid plaques and neurofibrillary tangles. Preclinical studies showed that melatonin, a monoaminergic neurotransmitter released from the pineal gland, is able to ameliorate AD pathologies and restore cognitive impairments. Theoretically, inhibition of the pathological progression of AD by melatonin treatment should also restore the impaired neurotransmission. This review aims to explore the impact of AD on neurotransmission, and whether and how melatonin can enhance neurotransmission via improving AD pathology.
Persistent Identifierhttp://hdl.handle.net/10722/300875
ISSN
2011 Impact Factor: 2.598
2020 SCImago Journal Rankings: 1.455
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorROY, J-
dc.contributor.authorTSUI, KC-
dc.contributor.authorNg, J-
dc.contributor.authorFung, ML-
dc.contributor.authorLim, LW-
dc.date.accessioned2021-07-06T03:11:24Z-
dc.date.available2021-07-06T03:11:24Z-
dc.date.issued2021-
dc.identifier.citationInternational Journal of Molecular Sciences, 2021, v. 22 n. 13, p. article no. 6841-
dc.identifier.issn1661-6596-
dc.identifier.urihttp://hdl.handle.net/10722/300875-
dc.description.abstractAlzheimer’s disease is a neurodegenerative disorder associated with age, and is characterized by pathological markers such as amyloid-beta plaques and neurofibrillary tangles. Symptoms of AD include cognitive impairments, anxiety and depression. It has also been shown that individuals with AD have impaired neurotransmission, which may result from the accumulation of amyloid plaques and neurofibrillary tangles. Preclinical studies showed that melatonin, a monoaminergic neurotransmitter released from the pineal gland, is able to ameliorate AD pathologies and restore cognitive impairments. Theoretically, inhibition of the pathological progression of AD by melatonin treatment should also restore the impaired neurotransmission. This review aims to explore the impact of AD on neurotransmission, and whether and how melatonin can enhance neurotransmission via improving AD pathology.-
dc.languageeng-
dc.publisherMolecular Diversity Preservation International. The Journal's web site is located at http://www.mdpi.org/ijms-
dc.relation.ispartofInternational Journal of Molecular Sciences-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectmelatonin-
dc.subjectneurotransmission-
dc.subjectAlzheimer’s disease-
dc.titleRegulation of Melatonin and Neurotransmission in Alzheimer's Disease-
dc.typeArticle-
dc.identifier.emailFung, ML: fungml@hku.hk-
dc.identifier.emailLim, LW: limlw@hku.hk-
dc.identifier.authorityFung, ML=rp00433-
dc.identifier.authorityLim, LW=rp02088-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3390/ijms22136841-
dc.identifier.pmid34202125-
dc.identifier.pmcidPMC8268832-
dc.identifier.scopuseid_2-s2.0-85108421866-
dc.identifier.hkuros323221-
dc.identifier.volume22-
dc.identifier.issue13-
dc.identifier.spagearticle no. 6841-
dc.identifier.epagearticle no. 6841-
dc.identifier.isiWOS:000671067600001-
dc.publisher.placeSwitzerland-

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