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Melatonin in Alzheimer’s Disease: A Latent Endogenous Regulator of Neurogenesis to Mitigate Alzheimer’s Neuropathology

dc.contributor.authorHossain M.F.
dc.contributor.authorUddin M.S.
dc.contributor.authorUddin G.M.S.
dc.contributor.authorSumsuzzman D.M.
dc.contributor.authorIslam M.S.
dc.contributor.authorBarreto G.E.
dc.contributor.authorMathew B.
dc.contributor.authorAshraf G.M.
dc.date.accessioned2020-09-02T22:20:32Z
dc.date.available2020-09-02T22:20:32Z
dc.date.issued2019
dc.identifier10.1007/s12035-019-01660-3
dc.identifier.citation56, 12, 8255-8276
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4912
dc.descriptionMelatonin, a pineal gland synthesized neurohormone is known as a multifunctioning pleiotropic agent which has a wide range of neuroprotective role in manifold age-related neurodegenerative disorders especially Alzheimer’s diseases (AD). AD is a devastating neurodegenerative disorder and common form of dementia which is defined by abnormal and excessive accumulation of several toxic peptides including amyloid β (Aβ) plaques and neurofibrillary tangles (NFTs). The Alzheimer’s dementia relates to atrophic changes in the brain resulting in loss of memory, cognitive dysfunction, and impairments of the synapses. Aging, circadian disruption, Aβ accumulation, and tau hyperphosphorylation are the utmost risk factor regarding AD pathology. To date, there is no exact treatment against AD progression. In this regard, melatonin plays a crucial role for the inhibition of circadian disruption by controlling clock genes and also attenuates Aβ accumulation and tau hyperphosphorylation by regulating glycogen synthase kinase-3 (GSK3) and cyclin-dependent kinase-5 (CDK5) signaling pathway. In this review, we highlight the possible mechanism of AD etiology and how melatonin influences neurogenesis by attenuating circadian disruption, Aβ formation, as well as tau hyperphosphorylation. Furthermore, we also find out and summarize the neuroprotective roles of melatonin by the blockage of Aβ production, Aβ oligomerization and fibrillation, tau hyperphosphorylation, synaptic dysfunction, oxidative stress, and neuronal death during AD progression. © 2019, Springer Science+Business Media, LLC, part of Springer Nature.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subjectAlzheimer’s disease
dc.subjectAmyloid β
dc.subjectCircadian rhythm
dc.subjectMelatonin
dc.subjectNeurofibrillary tangles
dc.subjectamyloid beta protein
dc.subjectcyclin dependent kinase 5
dc.subjectglycogen synthase kinase 3
dc.subjectmelatonin
dc.subjecttau protein
dc.subjecttranscription factor CLOCK
dc.subjectmelatonin
dc.subjectAlzheimer disease
dc.subjectcholinergic system
dc.subjectcircadian rhythm
dc.subjectclock gene
dc.subjectdisease exacerbation
dc.subjectenzyme regulation
dc.subjectgene expression regulation
dc.subjecthormone action
dc.subjecthuman
dc.subjectnerve cell necrosis
dc.subjectnervous system development
dc.subjectnervous system inflammation
dc.subjectneuropathology
dc.subjectneuroprotection
dc.subjectnonhuman
dc.subjectoligomerization
dc.subjectoxidative stress
dc.subjectprotein phosphorylation
dc.subjectprotein synthesis
dc.subjectReview
dc.subjectsignal transduction
dc.subjectsynapse
dc.subjectAlzheimer disease
dc.subjectanimal
dc.subjectbiosynthesis
dc.subjectbrain
dc.subjectdrug effect
dc.subjectmolecularly targeted therapy
dc.subjectpathology
dc.subjectpathophysiology
dc.subjectAlzheimer Disease
dc.subjectAnimals
dc.subjectBrain
dc.subjectCircadian Rhythm
dc.subjectHumans
dc.subjectMelatonin
dc.subjectMolecular Targeted Therapy
dc.subjectNeurogenesis
dc.titleMelatonin in Alzheimer’s Disease: A Latent Endogenous Regulator of Neurogenesis to Mitigate Alzheimer’s Neuropathology
dc.typeReview


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