Reverse geroscience: how does exposure to early diseases accelerate the age-related decline in health?
Reverse geroscience: how does exposure to early diseases accelerate the age-related decline in health?
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DOI：
10.1111/nyas.13297
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发表时间：
2016-01-01
期刊：
影响因子：
--
通讯作者：
Sierra, Felipe
中科院分区：
文献类型：
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作者：
Kohanski, Ronald A.;Deeks, Steven G.;Sierra, Felipe
衰老是慢性疾病发展和功能丧失的主要危险因素。老年科学提供了衰老生物学、疾病生物学和衰弱生理学之间的联系，这三个领域在过去几十年中取得了巨大进展。虽然以前的重点是衰老在疾病和残疾易感性中的作用，但这种关系的另一面，即疾病对衰老的影响，在分子/细胞水平上的探索较少。事实上，流行病学中众所周知，童年或成年早期接触慢性疾病和/或治疗对加速衰老表型的作用，但其生物学基础却知之甚少。最近由美国国立卫生研究院老年科学兴趣小组和纽约科学院联合举办的一次峰会探讨了这些关系，以三种慢性疾病为例：癌症、艾滋病毒/艾滋病和糖尿病。流行病学文献清楚地表明，早期接触任何这些疾病和/或其治疗都会导致衰老表型加速出现，包括功能丧失和加速出现与早期事件没有明显关系的衰老相关疾病的临床症状。峰会的讨论重点是这些疾病与最近定义的衰老的分子和细胞支柱之间的分子和细胞关系。会议得出的两个主要结论包括希望完善衰老的操作定义，并同时开发衰老的生物标志物，以便从实足年龄转向生理年龄。讨论还开启了关于通过包括延缓年龄的方式以及针对相关疾病的标准护理来改善受慢性病影响的患者晚年结局的可能性的对话。
Aging is the major risk factor for both the development of chronic diseases and loss of functional capacity. Geroscience provides links among the biology of aging, the biology of disease, and the physiology of frailty, three fields where enormous progress has been made in the last few decades. While, previously, the focus was on the role of aging in susceptibility to disease and disability, the other side of this relationship, which is the contribution of disease to aging, has been less explored at the molecular/cellular level. Indeed, the role of childhood or early adulthood exposure to chronic disease and/or treatment on accelerating aging phenotypes is well known in epidemiology, but the biological basis is poorly understood. A recent summit co-organized by the National Institutes of Health GeroScience Interest Group and the New York Academy of Sciences explored these relationships, using three chronic diseases as examples: cancer, HIV/AIDS, and diabetes. The epidemiological literature clearly indicates that early exposure to any of these diseases and/or their treatments results in an acceleration of the appearance of aging phenotypes, including loss of functional capacity and accelerated appearance of clinical symptoms of aging-related diseases not obviously related to the earlier event. The discussions at the summit focused on the molecular and cellular relationships between each of these diseases and the recently defined molecular and cellular pillars of aging. Two major conclusions from the meeting include the desire to refine an operational definition of aging and to concomitantly develop biomarkers of aging, in order to move from chronological to physiological age. The discussion also opened a dialogue on the possibility of improving late-life outcomes in patients affected by chronic disease by including age-delaying modalities along with the standard care for the disease in question.