Cellular senescence and premature aging in Down Syndrome

Down syndrome (DS) is a genetic disorder caused by an extra copy of chromosome 21, resulting in cognitive impairment, physical abnormalities, and an increased risk of age-related co-morbidities. Individuals with DS exhibit accelerated aging, which has been attributed to several cellular mechanisms,...

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Veröffentlicht in:Mechanisms of ageing and development 2023-06, Vol.212, p.111824-111824, Article 111824
Hauptverfasser: Peng, Lianli, Baradar, Alireza A., Aguado, Julio, Wolvetang, Ernst
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Sprache:eng
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Zusammenfassung:Down syndrome (DS) is a genetic disorder caused by an extra copy of chromosome 21, resulting in cognitive impairment, physical abnormalities, and an increased risk of age-related co-morbidities. Individuals with DS exhibit accelerated aging, which has been attributed to several cellular mechanisms, including cellular senescence, a state of irreversible cell cycle arrest that is associated with aging and age-related diseases. Emerging evidence suggests that cellular senescence may play a key role in the pathogenesis of DS and the development of age-related disorders in this population. Importantly, cellular senescence may be a potential therapeutic target in alleviating age-related DS pathology. Here, we discuss the importance of focusing on cellular senescence to understand accelerated aging in DS. We review the current state of knowledge regarding cellular senescence and other hallmarks of aging in DS, including its putative contribution to cognitive impairment, multi-organ dysfunction, and premature aging phenotypes. •Down Syndrome patients undergo accelerated aging phenotypes.•Emerging evidence identifies cellular senescence as a central pillar of aging in Down Syndrome pathology.•Senolytic drugs may represent putative therapies to treat Down Syndrome patients.
ISSN:0047-6374
1872-6216
DOI:10.1016/j.mad.2023.111824