Oxidative Stress and Mitochondrial Dysfunction in Down’s Syndrome: Relevance to Aging and Dementia

Genome-wide gene deregulation and oxidative stress appear to be critical factors determining the high variability of phenotypes in Down’s syndrome (DS). Even though individuals with trisomy 21 exhibit a higher survival rate compared to other aneuploidies, most of them die in utero or early during po...

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Main Authors: Pinar E. Coskun, Jorge Busciglio
Format: Article
Language:English
Published: Hindawi Limited 2012-01-01
Series:Current Gerontology and Geriatrics Research
Online Access:http://dx.doi.org/10.1155/2012/383170
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spelling doaj-aa817b9c60624e45be4c7a9b64753ac92020-11-24T22:51:09ZengHindawi LimitedCurrent Gerontology and Geriatrics Research1687-70631687-70712012-01-01201210.1155/2012/383170383170Oxidative Stress and Mitochondrial Dysfunction in Down’s Syndrome: Relevance to Aging and DementiaPinar E. Coskun0Jorge Busciglio1Department of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders (iMIND), University of California, Irvine, CA 92697, USADepartment of Neurobiology and Behavior, Institute for Memory Impairments and Neurological Disorders (iMIND), University of California, Irvine, CA 92697, USAGenome-wide gene deregulation and oxidative stress appear to be critical factors determining the high variability of phenotypes in Down’s syndrome (DS). Even though individuals with trisomy 21 exhibit a higher survival rate compared to other aneuploidies, most of them die in utero or early during postnatal life. While the survivors are currently predicted to live past 60 years, they suffer higher incidence of age-related conditions including Alzheimer’s disease (AD). This paper is centered on the mechanisms by which mitochondrial factors and oxidative stress may orchestrate an adaptive response directed to maintain basic cellular functions and survival in DS. In this context, the timing of therapeutic interventions should be carefully considered for the successful treatment of chronic disorders in the DS population.http://dx.doi.org/10.1155/2012/383170
collection DOAJ
language English
format Article
sources DOAJ
author Pinar E. Coskun
Jorge Busciglio
spellingShingle Pinar E. Coskun
Jorge Busciglio
Oxidative Stress and Mitochondrial Dysfunction in Down’s Syndrome: Relevance to Aging and Dementia
Current Gerontology and Geriatrics Research
author_facet Pinar E. Coskun
Jorge Busciglio
author_sort Pinar E. Coskun
title Oxidative Stress and Mitochondrial Dysfunction in Down’s Syndrome: Relevance to Aging and Dementia
title_short Oxidative Stress and Mitochondrial Dysfunction in Down’s Syndrome: Relevance to Aging and Dementia
title_full Oxidative Stress and Mitochondrial Dysfunction in Down’s Syndrome: Relevance to Aging and Dementia
title_fullStr Oxidative Stress and Mitochondrial Dysfunction in Down’s Syndrome: Relevance to Aging and Dementia
title_full_unstemmed Oxidative Stress and Mitochondrial Dysfunction in Down’s Syndrome: Relevance to Aging and Dementia
title_sort oxidative stress and mitochondrial dysfunction in down’s syndrome: relevance to aging and dementia
publisher Hindawi Limited
series Current Gerontology and Geriatrics Research
issn 1687-7063
1687-7071
publishDate 2012-01-01
description Genome-wide gene deregulation and oxidative stress appear to be critical factors determining the high variability of phenotypes in Down’s syndrome (DS). Even though individuals with trisomy 21 exhibit a higher survival rate compared to other aneuploidies, most of them die in utero or early during postnatal life. While the survivors are currently predicted to live past 60 years, they suffer higher incidence of age-related conditions including Alzheimer’s disease (AD). This paper is centered on the mechanisms by which mitochondrial factors and oxidative stress may orchestrate an adaptive response directed to maintain basic cellular functions and survival in DS. In this context, the timing of therapeutic interventions should be carefully considered for the successful treatment of chronic disorders in the DS population.
url http://dx.doi.org/10.1155/2012/383170
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