She presented in a manner typical for type 3 Alzheimer's disease, with a non-amnestic onset (although her memory was affected later in the course), multiple stresses, onset at a young age (50 years of age), in association with hormonal reduction, ApoE ε4-negative genotype, hypozincemia, hypothalamic-pituitary-adrenal axis (HPA) abnormality, and negative family history. This evidence concerns the gene APOE and early-onset autosomal dominant Alzheimer disease.