Studies found that the proBDNF/p75NTR/sortilin complex stimulated neuronal apoptosis, amyloid deposition, depression, and learning and memory dysfunction in neurodegenerative disease models (Sun et al., 2012; Chen et al., 2016) and that proBDNF levels increased in the brain of patients with Alzheimer’s disease (Chen et al., 2017). The gene discussed is BDNF; the disease is early-onset autosomal dominant Alzheimer disease.