Progeroid syndromes such as progeria and Werner syndrome have at least the superficial appearance of accelerated aging, but are not in fact accelerated aging. They are caused by specific breakages due to genetic mutation, usually in DNA repair mechanisms, that allow a few types of cellular dysfunction and damage to grow over time much more rapidly than is the case in unaffected individuals. Some of these types of damage are thought to be significant in normal aging, but some are clearly not present to any great degree even in very old individuals. What this should tell us is that aging is exactly an accumulation of molecular damage leading to cellular dysfunction. All forms of damage will produce outcomes that can be compared to aging, some more so than others. Whether or not this is useful in aging research depends very much on the specific details in each case.

Link: https://doi.org/10.12688/f1000research.12110.1