Thus, the goal was to reveal differential changes in brain transcriptomes and lipidomes possibly associated with APOE genotype that favors a delayed neurofibrillary tangle formation and slower amyloid deposition; (2) morphological and histochemical studies have shown that the initiation and progression of AD-related destruction inversely recapitulate primarily the progress of cortical myelination [28]. The gene discussed is APOE; the disease is Alzheimer disease.