Aging, particularly in the brain, involves impairments in multiple cellular and molecular functions, many of which are regulated at the nucleus. Chromatin structure plays a critical role in the regulation of gene expression and the maintenance of genomic stability. During differentiation, chromosomes acquire their unique topology depending on the cell type that should be kept for a lifetime, but this may deteriorate as we age. However, the effects of aging on the chromatin 3D structure of neurons remain largely unknown. By combining chromosome conformation capture (Hi-C) and microscopy techniques, we investigated cortical neurons of young and aged mice and discovered neuronal nuclear expansion during aging, leading to increased distances between chromosomes. This expansion alters the topology of compartments, topologically associating domains (TADs) and chromatin loops. While larger TADs tend to dissociate, smaller TADs and loops exhibit strengthened interactions to maintain the cohesiveness of chromatin in aged neurons. We attribute these alterations to changes in the physical forces of an expanding nucleus, filling a growing nuclear area, affecting downstream gene expression and chromatin topology. While our research proposes that an augmented chromosomal area may underlie these changes, the induction of such enlargement experimentally within the brain remains challenging. Nevertheless, the observed correlation between nuclear enlargement and Lamin-B disruption together with the broadening of TAD regions, indicative of a less compact chromatin structure, paradoxically with a reduction in chromosomal contacts. These findings prompt a nuanced exploration of the intricate interplay between chromatin architecture, nuclear dynamics, and genomic organization during the aging process.