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Article: Role of melatonin in Alzheimer’s disease: From preclinical studies to novel melatonin-based therapies

TitleRole of melatonin in Alzheimer’s disease: From preclinical studies to novel melatonin-based therapies
Authors
Issue Date2022
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yfrne
Citation
Frontiers in Neuroendocrinology, 2022, v. 65, p. 100986 How to Cite?
AbstractMelatonin and novel melatonin-based therapies such as melatonin-containing hybrid molecules, melatonin analogues, and melatonin derivatives have been investigated as potential therapeutics against Alzheimer’s disease (AD) pathogenesis. In this review, we examine the developmental trends of melatonin therapies for AD from 1997 to 2021. We then highlight the neuroprotective mechanisms of melatonin therapy derived from preclinical studies. These mechanisms include the alleviation of amyloid-related burden, neurofibrillary tangle accumulation, oxidative stress, neuroinflammation, apoptosis, mitochondrial dysfunction, and impaired neuroplasticity and neurotransmission. We further illustrate the beneficial effects of melatonin on behavior in animal models of AD. Next, we discuss the clinical effects of melatonin on sleep, cognition, behavior, psychiatric symptoms, electroencephalography findings, and molecular biomarkers in patients with mild cognitive impairment and AD. We then explore the effectiveness of novel melatonin-based therapies. Lastly, we discuss the limitations of current melatonin therapies for AD and suggest two emerging research themes for future study.
Persistent Identifierhttp://hdl.handle.net/10722/310091
ISSN
2023 Impact Factor: 6.5
2023 SCImago Journal Rankings: 2.078
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorROY, J-
dc.contributor.authorWong, KY-
dc.contributor.authorAquili, L-
dc.contributor.authorUDDIN, MS-
dc.contributor.authorHeng, BC-
dc.contributor.authorTipoe, GL-
dc.contributor.authorWong, KH-
dc.contributor.authorFung, ML-
dc.contributor.authorLim, LW-
dc.date.accessioned2022-01-24T02:23:42Z-
dc.date.available2022-01-24T02:23:42Z-
dc.date.issued2022-
dc.identifier.citationFrontiers in Neuroendocrinology, 2022, v. 65, p. 100986-
dc.identifier.issn0091-3022-
dc.identifier.urihttp://hdl.handle.net/10722/310091-
dc.description.abstractMelatonin and novel melatonin-based therapies such as melatonin-containing hybrid molecules, melatonin analogues, and melatonin derivatives have been investigated as potential therapeutics against Alzheimer’s disease (AD) pathogenesis. In this review, we examine the developmental trends of melatonin therapies for AD from 1997 to 2021. We then highlight the neuroprotective mechanisms of melatonin therapy derived from preclinical studies. These mechanisms include the alleviation of amyloid-related burden, neurofibrillary tangle accumulation, oxidative stress, neuroinflammation, apoptosis, mitochondrial dysfunction, and impaired neuroplasticity and neurotransmission. We further illustrate the beneficial effects of melatonin on behavior in animal models of AD. Next, we discuss the clinical effects of melatonin on sleep, cognition, behavior, psychiatric symptoms, electroencephalography findings, and molecular biomarkers in patients with mild cognitive impairment and AD. We then explore the effectiveness of novel melatonin-based therapies. Lastly, we discuss the limitations of current melatonin therapies for AD and suggest two emerging research themes for future study.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yfrne-
dc.relation.ispartofFrontiers in Neuroendocrinology-
dc.titleRole of melatonin in Alzheimer’s disease: From preclinical studies to novel melatonin-based therapies-
dc.typeArticle-
dc.identifier.emailTipoe, GL: tgeorge@hku.hk-
dc.identifier.emailFung, ML: fungml@hku.hk-
dc.identifier.emailLim, LW: limlw@hku.hk-
dc.identifier.authorityTipoe, GL=rp00371-
dc.identifier.authorityFung, ML=rp00433-
dc.identifier.authorityLim, LW=rp02088-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.yfrne.2022.100986-
dc.identifier.pmid35167824-
dc.identifier.hkuros331522-
dc.identifier.volume65-
dc.identifier.spage100986-
dc.identifier.epage100986-
dc.identifier.isiWOS:000806107100004-
dc.publisher.placeUnited States-

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