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dc.contributor.author
Spinedi, Eduardo Julio
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dc.contributor.author
Cardinali, Daniel Pedro
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dc.date.available
2019-10-21T13:44:08Z
dc.date.issued
2018-10
dc.identifier.citation
Spinedi, Eduardo Julio; Cardinali, Daniel Pedro; Neuroendocrine-metabolic dysfunction and sleep disturbances in neurodegenerative disorders: Focus on Alzheimer's disease and melatonin; Karger; Neuroendocrinology; 108; 4; 10-2018; 354-364
dc.identifier.issn
0028-3835
dc.identifier.uri
http://hdl.handle.net/11336/86560
dc.description.abstract
Alzheimer's disease (AD) is associated with altered eating behavior and metabolic disruption. Amyloid plaques and neurofilament tangles are observed in many hypothalamic nuclei from AD brains. Some of these areas (suprachiasmatic nuclei, lateral hypothalamic area) also play a role in the regulation of the sleep/wake cycle and may explain the comorbidity of eating and sleep disorders observed in AD patients. Inadequate sleep increases the neurodegenerative process, for example, the decrease of slow-wave sleep impairs clearance of β-amyloid peptide (Aβ) and tau protein from cerebral interstitial fluid. Cerebrospinal fluid (CSF) melatonin levels decrease even in preclinical stages (Braak-1 stage) when patients manifest no cognitive impairment, suggesting that reduction of melatonin in CSF may be an early marker (the cause for which is still unknown) of oncoming AD. Melatonin administration augments glymphatic clearance of Aβ and reduces generation and deposition of Aβ in transgenic animal models of AD. It may also set up a new equilibrium among hypothalamic feeding signals. While melatonin trials performed in the clinical phase of AD have failed to show or showed only modest positive effects on cognition, in the preclinical stage of dementia (minimal cognitive impairment) the effect of melatonin is demonstrable with significant improvement of sleep and quality of life. In this review, we discuss the main aspects of hypothalamic alterations in AD, the association between interrupted sleep and neurodegeneration, and the possible therapeutic effect of melatonin on these processes.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Karger
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
AGING
dc.subject
ALZHEIMER'S DISEASE
dc.subject
FEEDING BEHAVIOR
dc.subject
GLYMPHATIC SYSTEM
dc.subject
INFLAMMATION
dc.subject
INSULIN SIGNALING
dc.subject
MELATONIN
dc.subject
SLEEP
dc.subject.classification
Otras Medicina Clínica
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dc.subject.classification
Medicina Clínica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Neuroendocrine-metabolic dysfunction and sleep disturbances in neurodegenerative disorders: Focus on Alzheimer's disease and melatonin
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-10-15T14:49:01Z
dc.journal.volume
108
dc.journal.number
4
dc.journal.pagination
354-364
dc.journal.pais
Suiza
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dc.journal.ciudad
Basel
dc.description.fil
Fil: Spinedi, Eduardo Julio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico La Plata. Centro de Endocrinología Experimental y Aplicada (i); Argentina
dc.description.fil
Fil: Cardinali, Daniel Pedro. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
dc.journal.title
Neuroendocrinology
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1159/000494889
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.karger.com/Article/FullText/494889
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