function, projection development, and Ca2+ homeostasis, which in turn impacts functions such as synaptic plasticity and projection (Burke and Barnes, 2006; Fraser et al., 2005; Lu et al., 2004). Interestingly, while only less than 4% of the iN aging genes overlapped with the fibroblast aging genes, 7-fold more overlapped with the postmortem cortex, suggesting the presence of an aging transcriptome signature relevant for the aging brain. Our findings also raise the question of how cellular age is encoded during the fibroblasts-to-neurons transition. A possible explanation, in addition to preserved macromolecular damage, is that only a small number of genes function as master regulators of aging; if perturbed, they impair important downstream processes that eventually unfold as phenotypical aging. RanBP17 emerged as being one of these genes identified in this study.
