Previous work targeting different N-terminal epitopes of tau in CSF have shown that these fragments are increased in Alzheimer’s disease at the mild cognitive impairment (MCI) and dementia stages.17–19 In addition, p-tau assays targeting N-terminal fragments phosphorylated at threonine-181 (N-p-tau181) and threonine-217 (N-p-tau217) have shown earlier abnormal levels in CSF in comparison to mid-region p-tau181 across the Alzheimer’s disease continuum.20,21. The gene discussed is MAPT; the disease is dementia.