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dc.contributor.authorBarone E.
dc.contributor.authorArena A.
dc.contributor.authorHead E.
dc.contributor.authorButterfield D.A.
dc.contributor.authorPerluigi M.
dc.date.accessioned2020-09-02T22:12:58Z
dc.date.available2020-09-02T22:12:58Z
dc.date.issued2018
dc.identifier10.1016/j.freeradbiomed.2017.07.009
dc.identifier.citation114, , 84-93
dc.identifier.issn08915849
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3679
dc.descriptionDown Syndrome (DS) is the most common genetic form of intellectual disability that leads in the majority of cases to development of early-onset Alzheimer-like dementia (AD). The neuropathology of DS has several common features with AD including alteration of redox homeostasis, mitochondrial deficits, and inflammation among others. Interestingly, some of the genes encoded by chromosome 21 are responsible of increased oxidative stress (OS) conditions that are further exacerbated by decreased antioxidant defense. Previous studies from our groups showed that accumulation of oxidative damage is an early event in DS neurodegeneration and that oxidative modifications of selected proteins affects the integrity of the protein degradative systems, antioxidant response, neuronal integrity and energy metabolism. In particular, the current review elaborates recent findings demonstrating the accumulation of oxidative damage in DS and we focus attention on specific deregulation of iron metabolism, which affects both the central nervous system and the periphery. Iron dysmetabolism is a well-recognized factor that contributes to neurodegeneration; thus we opine that better understanding how and to what extent the concerted loss of iron dyshomeostasis and increased OS occur in DS could provide novel insights for the development of therapeutic strategies for the treatment of Alzheimer-like dementia. © 2017 Elsevier Inc.
dc.language.isoen
dc.publisherElsevier Inc.
dc.subjectIron
dc.subjectOxidative stress
dc.subjectProtein oxidation
dc.subjectRedox proteomics
dc.subjectTrisomy 21
dc.subject4 hydroxynonenal
dc.subjectamyloid beta protein
dc.subjectamyloid precursor protein
dc.subjectceruloplasmin
dc.subjectcopper zinc superoxide dismutase
dc.subjectheme oxygenase 1
dc.subjectheme oxygenase 2
dc.subjecttransferrin
dc.subjectiron
dc.subjectAlzheimer disease
dc.subjectantioxidant responsive element
dc.subjectcognitive defect
dc.subjectDown syndrome
dc.subjectendosome
dc.subjectenergy metabolism
dc.subjecthuman
dc.subjectiron deficiency anemia
dc.subjectiron homeostasis
dc.subjectiron metabolism
dc.subjectiron transport
dc.subjectlipid peroxidation
dc.subjectmitochondrial respiration
dc.subjectnerve degeneration
dc.subjectneuropathology
dc.subjectnonhuman
dc.subjectoxidation reduction state
dc.subjectoxidative stress
dc.subjectprenatal diagnosis
dc.subjectpriority journal
dc.subjectprotein carbonylation
dc.subjectprotein degradation
dc.subjectprotein expression
dc.subjectproteomics
dc.subjectReview
dc.subjecttrisomy 21
dc.subjectanimal
dc.subjectDown syndrome
dc.subjecthomeostasis
dc.subjectmetabolism
dc.subjectoxidation reduction reaction
dc.subjectoxidative stress
dc.subjectpathophysiology
dc.subjectAnimals
dc.subjectDown Syndrome
dc.subjectHomeostasis
dc.subjectHumans
dc.subjectIron
dc.subjectOxidation-Reduction
dc.subjectOxidative Stress
dc.titleDisturbance of redox homeostasis in Down Syndrome: Role of iron dysmetabolism
dc.typeReview


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