Accelerated aging disease

An accelerated aging disease is a genetic disorder in which various tissues, organs or systems of the human body age prematurely. Because the accelerated aging diseases display different aspects of aging, but never every aspect, they are often called segmental progerias by biogerontologists.

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Some of the diseases usually described as representing "accelerated aging" include:

Bloom syndrome
Cockayne's syndrome
Down syndrome
Progeria (Hutchinson-Gilford Progeria syndrome)
Werner syndrome
Xeroderma pigmentosum

The most common feature of such diseases is defective DNA repair.

Debate concerning "accelerated aging"

Some biogerontologists question that such a thing as "accelerated aging" actually exists, at least partly on the grounds that all of the so-called accelerated aging diseases are segmental progerias. Many disease conditions such as diabetes, high blood pressure, etc. are associated with increased mortality. Without reliable biomarkers of ageing it is hard to justify the claim that a disease condition represents more than accelerated mortality^[1].

Against this position other biogerontologists argue that premature aging phenotypes are identifiable symptoms associated with mechanisms of molecular damage. The fact that these phenotypes are widely recognized justifies classification of the relevant diseases as "accelerated aging"^[2]. Such conditions, it is argued, are readily distinguishable from genetic diseases associated with increased mortality, but not associated with an aging phenotype, such as cystic fibrosis and sickle cell anemia. It is further argued that segmental aging phenotype is a natural part of aging insofar as genetic variation leads to some people being more disposed than others to aging-associated diseases such as cancer and Alzheimer's disease^[3].

References

^ Miller RA (2004). "'Accelerated aging': a primrose path to insight?". AGING CELL 3 (2): 47-51. PMID 15038817.
^ Hasty P, Vijg J (2004). "Accelerating aging by mouse reverse genetics: a rational approach to understanding longevity". AGING CELL 3 (2): 55-65. PMID 15038819.
^ Hasty P, Vijg J (2004). "Rebuttal to Miller: 'Accelerated aging': a primrose path to insight?'". AGING CELL 3 (2): 67-69. PMID 15038820.