The main finding of our study is that aging is normally associated with increased H-FABP level but this is not true in DS which display not only the same level in the different ages of life but have also lower level compared to their age-matched healthy subjects. Our study is in agreement with previous observation which described a striking increase in H-FABP value with aging  and, to our knowledge, is also the first comparing circulating H-FABP level in DS and healthy subjects.
The unchanged H-FABP level during aging in DS and the lack of atherosclerosis in these subjects prompted us to consider H-FABP as one potential molecule linking aging and atherosclerosis.
It is well know that aging is associated with reduced cellular proliferative potential, increased propensity to undergo death, elevated DNA damage and, at vascular level, increased expression of pro-inflammatory and leukocyte adhesion molecules and increased uptake of plasma lipoproteins, all key events that ultimately promote atherosclerosis . Although the same mechanisms are present in DS, which also display an accelerated aging process compared to healthy subjects, anyway they resulted protected against atherosclerosis [10, 11]. The mechanisms that may be involved in such protective effect are not well known. Anyway, our observation highlighted that reduced H-FABP level may contribute to this general protection.
Our study have some limitations, including the reduced sample size, the lack of correlation with bioclinical parameters and atherosclerosis-related risk factors. For these reasons, our data may be considered preliminary observations which need further investigation to better understand the relationship between H-FABP, atherosclerosis and coronary artery disease.
In conclusion, reduced H-FABP level during aging in DS may play a protective role against atherosclerosis. This observation highlighted a potential involvement of H-FABP in the relationship between aging and atherosclerosis.