In addition, overexpression of STMN2 in the hippocampus of an Alzheimer’s disease mouse model resulted in decreased amyloid β (Aβ) staining and plaque burden, presumably through STMN2-dependent regulation of the intracellular trafficking and processing of amyloid precursor protein (APP) (Wang et al., 2013). This evidence concerns the gene STMN2 and early-onset autosomal dominant Alzheimer disease.