BACKGROUND: Most syndromes of accelerated aging are caused by mutations 
affecting the integrity of the genetic material. Among them, the most studied is 
Werner's syndrome, "adult progeria", caused by a recessive autosomal mutation 
with a frequency of 1 in 10 million, which affects a helicase involved in DNA 
repair. In Werner syndrome, there is a loss of heterochromatin, though the 
stability of heterochromatin is also affected in "normal" aging. The 
Hutchinson-Gilford Progeria Syndrome (HGPS), "child progeria", has an even lower 
frequency. In most cases, it is caused by a point mutation of a gene coding a 
protein in the nuclear envelope, lamin A.
OBJECTIVES: HGPS may provide valuable insights into the aging process. The 
symptoms of this condition do not entirely overlap with those of "normal" aging.
METHOD: A critical analysis of the accelerated aging syndromes may explain what 
aging is, and also why some tissues and organs age at accelerated rates as 
compared to other tissues.
RESULTS: In this article, we will discuss the implications of HGPS and other 
accelerated aging syndromes in the light of the biochemical hypothesis of aging 
we advanced. According to this hypothesis, some reactions are less stimulated 
and diminish in time, affecting not only specific biochemical functions, but 
cellular energy, and therefore its capacity for synthesis.
CONCLUSION: Besides, a new vision on aging, possible therapeutic strategies for 
these conditions and others, with similar mechanisms, are also presented.