Oxidative Stress and Mitochondrial Dysfunction in Down's Syndrome: Relevance to Aging and Dementia.
Oxidative Stress and Mitochondrial Dysfunction in Down's Syndrome: Relevance to Aging and Dementia.
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DOI：
10.1155/2012/383170
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发表时间：
2012
影响因子：
--
通讯作者：
Busciglio J
中科院分区：
文献类型：
--
作者：
Coskun PE;Busciglio J
全基因组基因失调和氧化应激似乎是决定唐氏综合征（DS）表型高变异性的关键因素。尽管与其他非整倍体相比，患有21三体的个体表现出更高的存活率，但他们中的大多数在子宫内或产后早期死亡。虽然幸存者目前预计能活到60岁以上，但他们患老年痴呆症（AD）等与年龄有关的疾病的几率更高。本文的核心是线粒体因子和氧化应激可能协调适应性反应的机制，以维持DS的基本细胞功能和生存。在这种情况下，治疗干预的时机应该仔细考虑，以成功治疗退行性痴呆人群中的慢性疾病。
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.