More importantly, disturbed lipid metabolites and dynamic brain network changes occurred prior to measurable amyloid deposition and tau tangles related to ageing [18], while lipid pathway genetic variants, including APOEε4 genotype and lipoproteins markedly enhanced the disruption of brain network architecture in preclinical AD patients [34, 46] and even in the cognitively normal elderly [47, 48]. The gene discussed is MAPT; the disease is Alzheimer disease.