Aging is a physiological process that is in part genetically determined. Some of the signs and symptoms of aging also occur prematurely in Mendelian disorders. Such disorders are excellent sources of information of underlying mechanisms for these components of aging, and studying these may allow detection of pathways that have not yet considered in detail in physiological aging.

Here I define the clinical characteristics that constitute aging and propose that at least 40% of aging signs and symptoms should be present before an entity should be tagged as progeroid. A literature search using these characteristics yields 17 entities that fulfill this definition: Hutchinson-Gilford progeria, mandibulo-acral dysplasia, Nestor-Guillermo progeria, Werner syndrome, Cockayne syndrome, cutis laxa progeroid, Penttinen progeroid syndrome, Mandibular underdevelopment, Deafness, Progeroid features, Lipodystrophy, Fontaine progeroid syndrome, SHORT syndrome, Wiedemann-Rautenstrauch syndrome, Mulvihill-Smith syndrome, dyskeratosis congenita, Marfan syndrome lipodystrophy type, Warburg-Cinotti syndrome, Lessel syndrome and Bloom syndrome. The presenting and main characteristics of these entities are indicated briefly. Their pathophysiology is not complete pathophysiology is reviewed but only the pathophysiology of the premature aging characteristics of this series of entities is compared to the known mechanisms (“Hallmarks”) of physiological aging as summarized in the review paper by Lopez-Otin and colleagues. Although many causative genes have not been studied fully for all known aging mechanisms the comparison demonstrates that additional mechanisms must play a role to explain the aging characteristic in some of the progeroid entities of the progeroid entities, and possibly also in physiological aging.

衰老是部分遗传决定的生理过程。在孟德尔疾病中，一些衰老的体征和症状也会过早出现。这些疾病是衰老这些方面的潜在机制的极好的信息来源，对这些疾病的研究可能允许检测尚未在生理学衰老中详细考虑的途径。

在这里，我定义了构成衰老的临床特征，并提出在将一个实体标记为类胚之前，应至少存在40％的衰老迹象和症状。使用这些特征进行的文献检索产生了满足以下定义的17个实体：Hutchinson-Gilford早衰，下颌骨-不典型增生，Nestor-Guillermo早衰，Werner综合征，Cockayne综合征，角质层松弛早老体，Penttinen早老综合症，下颌骨发育不足，耳聋，前突特征，脂肪代谢障碍，枫丹白露综合征，SHORT综合征，Wiedemann-Rautenstrauch综合征，Mulvihill-Smith综合征，先天性角化不全，Marfan综合征脂肪营养不良类型，Warburg-Cinotti综合征，Lessel综合征和Bloom综合征。简要说明了这些实体的外观和主要特征。他们的病理生理学还不完整，仅对这一系列实体的过早衰老特征的病理生理学与生理学衰老的已知机制（“霍尔马克”）进行了比较，如Lopez-Otin及其同事在综述文件中所总结。尽管尚未针对所有已知的衰老机制对许多致病基因进行充分研究，但比较表明，其他机制必须在解释早衰实体的某些早衰实体中以及可能在生理衰老中发挥衰老特性的作用。