Something the article failed to mention was that her telomeres were still progressing like they would in a normal person.
As seen in Fig. 6, the subject's PBMC telomere length at 13 years of age was significantly shorter than that of an age-matched female control as well as male and female controls of younger ages. While variability in average telomere length exists between individuals, the low subject values are probably not due to errors in measurement since the coefficients of variation were sufficiently low to assume adequate precision. Although the subject's telomeres were nearly half the length of a healthy, age-matched female control, this comparison in and of itself does not prove that her cellular age is advanced beyond that of the normal girl. However, an important observation relevant to this difference is that there occurs a precipitous loss of telomere length during early life after which a plateau period is reached (Frenck et al., 1998). As a result, telomere length in newborns is longer on average than that in adolescents so that comparison of the subject's telomeres with newborn controls would be expected to provide more reliable estimate of her cellular age range. For example, significant shortening would be expected if her cellular age proceeded as usual despite her severe developmental delay whereas longer telomeres would suggest that her cellular aging was delayed consistent with that of her somatic development. However, this was not the case. Subject's telomeres were considerably shorter than those of both infant controls as well as the age-matched control suggesting that her cellular age was advanced beyond infancy. Since the rate of telomeric shortening is substantially greater in infants than in adults (Zeichner et al., 1999), subject's prolonged infancy may have caused her to have shorter telomeres than age-matched controls. In addition, accelerated telomeric shortening has been reported in developmentally abnormal conditions including progeroid syndromes (Kruk et al., 1995). These circumstances may have resulted in her cellular age being appropriate for or perhaps even greater than her chronological age. Consistent with other reports showing a lack of telomerase (telomere terminal transferase) expression in human dermal fibroblasts from children (Oâ(TM)Donnell et al., 2008), subject's fibroblasts were telomerase negative. This fact suggests that possible enhancement of telomeric erosion did not stimulate compensatory increases in enzyme activity.
Pulled from:
Richard F. Walker, Lawrence C. Pakula, Maxine J. Sutcliffe, Patricia A. Kruk, Jesper Graakjaer, Jerry W. Shay, A case study of 'disorganized development' and its possible relevance to genetic determinants of aging, Mechanisms of Ageing and Development, Volume 130, Issue 5, May 2009, Pages 350-356, ISSN 0047-6374, DOI: 10.1016/j.mad.2009.02.003.
