Since Alzheimer’s disease neuropathology is characterized by the accumulation of the two canonical proteins, amyloid-β and tau [14], we used semi-automated quantification to determine the area occupied by pathological inclusions of phosphorylated TDP-43, tau and amyloid-β in post-mortem amygdala of Alzheimer’s disease patients with (CE +) or without (CE−) STMN2 or UNC13A cryptic exons (Fig. 3). This evidence concerns the gene STMN2 and early-onset autosomal dominant Alzheimer disease.