Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/1645
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dc.contributor.authorSrinivasan, Venkataramanujanes
dc.contributor.authorPandi Perumal, Seithikurippu R.es
dc.contributor.authorKaur, Charanjites
dc.contributor.authorBrown, Gregory M.es
dc.contributor.authorCardinali, Daniel Pedroes
dc.date.accessioned2019-05-02T14:01:15Z-
dc.date.available2019-05-02T14:01:15Z-
dc.date.issued2011-
dc.identifier.citationSrinivasan, V., et al. Melatonin and its agonist ramelteon in Alzheimer's disease : possible therapeutic value [en línea]. International Journal of Alzheimer's Disease, 2011. doi:10.4061/2011/741974. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/1645es
dc.identifier.issn2090-8024 (Print)-
dc.identifier.issn2090-0252 (Online)-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/1645-
dc.description.abstractAbstract: Alzheimer’s disease (AD) is an age-associated neurodegenerative disease characterized by the progressive loss of cognitive function, loss of memory and insomnia, and abnormal behavioral signs and symptoms. Among the various theories that have been put forth to explain the pathophysiology of AD, the oxidative stress induced by amyloid β-protein (Aβ) deposition has received great attention. Studies undertaken on postmortem brain samples of AD patients have consistently shown extensive lipid, protein, and DNA oxidation. Presence of abnormal tau protein, mitochondrial dysfunction, and protein hyperphosphorylation all have been demonstrated in neural tissues of AD patients. Moreover, AD patients exhibit severe sleep/wake disturbances and insomnia and these are associated with more rapid cognitive decline and memory impairment. On this basis, the successful management of AD patients requires an ideal drug that besides antagonizing Aβ-induced neurotoxicity could also correct the disturbed sleep-wake rhythm and improve sleep quality. Melatonin is an effective chronobiotic agent and has significant neuroprotective properties preventing Aβ-induced neurotoxic effects in a number of animal experimental models. Since melatonin levels in AD patients are greatly reduced, melatonin replacement has the potential value to be used as a therapeutic agent for treating AD, particularly at the early phases of the disease and especially in those in whom the relevant melatonin receptors are intact. As sleep deprivation has been shown to produce oxidative damage, impaired mitochondrial function, neurodegenerative inflammation, and altered proteosomal processing with abnormal activation of enzymes, treatment of sleep disturbances may be a priority for arresting the progression of AD. In this context the newly introduced melatonin agonist ramelteon can be of much therapeutic value because of its highly selective action on melatonin MT1/MT2 receptors in promoting sleep.es
dc.formatapplication/pdfes
dc.languageenges
dc.language.isoenges
dc.publisherHindawies
dc.rightsAcceso Abiertoes
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0/es
dc.sourceInternational Journal of Alzheimer's Disease, 2011es
dc.subjectMELATONINAes
dc.subjectRAMELTEONes
dc.subjectENFERMEDAD DE ALZHEIMERes
dc.subjectAGONISTASes
dc.subjectTERAPIAes
dc.titleMelatonin and its agonist ramelteon in Alzheimer's disease : possible therapeutic valuees
dc.typeArtículoes
dc.identifier.doi10.4061/2011/741974-
uca.pathFacultad de Ciencias Médicas|Departamento de Docencia e Investigaciónes
uca.disciplinaMEDICINAes
uca.filename/home/data-uca-generic/folder_generic/IIBiomedicas/melatonin-agonist-ramelteon-alzheimer-disease/metadata.xmles
uca.issnrd1es
uca.affiliationFil: Srinivasan, Venkataramanujan. Sri Sathya Sai Medical Educational and Research Foundation; Indiaes
uca.affiliationFil: Srinivasan, Venkataramanujan. Universidad de Karpagam. Facultad de Medicina; Departamento de Fisiología; Indiaes
uca.affiliationFil: Pandi Perumal, Seithikurippu R. Somnogen Inc; Canadáes
uca.affiliationFil: Kaur, Charanjit. Universidad Nacional de Singapur. Facultad de Medicina Yong Loo. Departamento de Anatomía; Singapures
uca.affiliationFil: Brown, Gregory M. Universidad de Toronto. Facultad de Medicina. Departamento de Psiquiatría Centro de Adicciones y Salud Mental; Canadáes
uca.affiliationFil: Cardinali, Daniel Pedro. Pontificia Universidad de Buenos Aires. Facultad de Medicina. Departamento de Fisiología; Argentinaes
uca.versionpublishedVersiones
item.languageiso639-1en-
item.grantfulltextopen-
item.fulltextWith Fulltext-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.orcid0000-0002-0813-9088-
crisitem.author.parentorgFacultad de Ciencias Médicas-
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