However, the BIN1-mediated increase in the intraneuronal pool of Aβ1–42 only weakly translated into higher extraneuronal levels of Aβ1–42, i.e., a core feature of AD, and several histochemical brain autopsy and cell culture studies suggested that alterations in BIN1 expression were associated with stronger tau pathology rather than Aβ15,16. The gene discussed is BIN1; the disease is Alzheimer disease.