However, the term RS actually implies three separate phenomena that are not causally related: there is a RS that correlates with the progressive shortening of chromosome telomeres as a function of number of cell divisions, but this phenomenon has only be observed in cells from primates. A second kind of RS known as STASIS may occur prematurely as a response to diverse cellular stressors, this STASIS depends on specific genetic functions and so it can be reverted by mutation or inactivation of such genetic functions. There is a third kind of RS that occurs stochastically and so it increases its probability as a function of time, this seems to occur in all cells both in vitro and in vivo and it is not reversible. A self-stabilizing model for DNA-NM interactions as a function of age, in which a stochastic but time-dependent process leads to a significant increase of DNA-NM interactions, resulting in an integral and highly-stable structural system, has been proposed for explaining a common physical basis for both stochastic RS senescence and the post-mitotic state. We have recently shown that aged hepatocytes and early post-mitotic neurons have similar highly-stable NHOS. The present work 3,4,5-Trimethoxyphenylacetic acid expands such result by showing that continued stabilization of the NHOS occurs in post-mitotic neurons even after the fourth post-natal week when according to microanatomical criteria they formally become TD. The fact that the continued stabilization of the neuronal NHOS as a function of time has no overt impact on gene expression in neurons, suggests that this phenomenon do not depends on functional constraints. The DNA of each chromosome constitutes a continuous double-stranded fibre in which each strand has a rigid helical backbone resulting from the strong phosphodiester bonds between the deoxyribose sugars of thousands of nucleotides along the strand, whereas the weak hydrogen bonds between the nitrogenous bases in the anti-parallel strands can be broken and reestablished quite easily. Thus the torsional stress of the long DNA molecule along its axis might be dissipated by breaking the hydrogen bonds between both strands, yet by looping and supercoiling along its axis DNA can dissipate the stress without compromising its structural integrity. Hence the interactions DNA-NM that result in a large number of structural DNA loops in the interphase nucleus may be a natural answer to a structural stress problem posed by the intrinsic configuration of DNA. This phenomenon is independent of proteins that constitute chromatin and apparently depends on DNA-NM interactions by means of so-called indirect Atropine sulfate readouts. Nevertheless, the local chromatin conformation may have a role in determining the choice of DNA sequences available for interaction with the NM in vivo, since chromatin proteins may compete or hinder such DNANM interaction. A DNA loop pattern in which most genes lie close to the actual MARs attached to the NM is observed in baby and young neurons, similarly to what was reported in hepatocytes of equivalent age, but this is a highly improbable distribution considering that protein-coding genes are rare within the genome and so most potential MARs are not close to any protein-coding gene. Yet in the hepatocytes this anomalous distribution changes in time to one in which most genes are distal to the NM, this correlates with a trend towards shortening and homogenization of the average DNA- loop size as a function of age. In aged neurons most target genes studied also become distal to the NM indicating.