This finding is important for two reasons: first, it confirms that the initial inability to detect hyper-phosphorylated tau in the supernatants from stimulated human synaptosomes was likely due to its low levels; second, and most relevant, it demonstrates that hyper-phosphorylated and aggregated tau is released from human Alzheimer’s disease synaptosomes stimulated by treatment with calcium ionophores, such as ionomycin. The gene discussed is MAPT; the disease is Alzheimer disease.