Chronic exposure of neuronal cultures to tau26–44 fragment resulted in many features characteristic of presymptomatic stages of AD pathology such as neuritic dystrophy, breakdown of microtubules, loss of mitochondria and impairment of oxidative phosphorylation, indicating that the extracellularly secreted N-terminal truncated tau fragments may largely contribute to the development of AD pathology (Atlante et al., 2008; Florenzano et al., 2017). The gene discussed is MAPT; the disease is Alzheimer disease.