The pathological hallmarks of aberrant genomic expression in the nucleus of AD neurons are the absence of the chromatin-modifier Tau protein [33,34], the instability of heterochromatin blocs constituting the domains associated with lamin (LADs) and the nucleolus (NADs) [28,35], histone modifications, and a dysfunctional nucleus-cytoplasm restructuration, whereby lamin A expression and altered nucleus-cytoplasm transport through the nuclear pore play an essential role [30,36]. This evidence concerns the gene LMNA and Alzheimer disease.