Previously, abnormally low levels of CSF t-tau were reported in progressive supranuclear palsy using in-house ELISAs targeting the same N-terminal epitopes as our in-house NTA and NTB t-tau assays for Simoa.3 Our results support the present understanding that tau deposition and metabolism in primary tauopathies differ from that in Alzheimer’s disease, and other forms of tau with better biomarker potential should still be explored to address these disorders. This evidence concerns the gene MAPT and Alzheimer disease.