Brain‐derived tau to measure treatment effect in Alzheimer's disease and frontotemporal dementia

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Abstract INTRODUCTION Brain‐derived tau (BD‐tau) measures tau specifically from brain‐derived sources and can differentiate Alzheimer's disease (AD) from other diseases. This study investigated BD‐tau as a potential biomarker of treatment effect. METHODS BD‐tau and phosphorylated tau‐217 (p‐tau217) levels were measured after treatment with an anti‐tau drug in AD and behavioral variant frontotemporal dementia (bvFTD) clinical trials, and the association with total tau (t‐tau), p‐tau181 , and amyloid beta 42 (Aβ42) was examined. RESULTS Cerebrospinal fluid (CSF) BD‐tau decreased after treatment in the AD cohort; however, no change was seen in bvFTD or p‐tau217 in either cohort. CSF t‐tau and p‐tau181 correlated with BD‐tau in AD ( r = 0.9113 and 0.7746, p < 0.0001) and bvFTD ( r = 1.0 and r = 0.79, p < 0.05). CSF BD‐tau did not correlate with serum or plasma BD‐tau in bvFTD. DISCUSSION CSF BD‐tau shows potential as a biomarker of treatment effect in AD but not bvFTD. Further research is needed to investigate this effect in blood‐based samples and in other neurodegenerative diseases. Trial registration : ACTRN12611001200976, ACTRN12617001218381. Highlights Cerebrospinal fluid (CSF) brain‐derived tau (BD‐tau) levels decreased with sodium selenate treatment in patients with Alzheimer's disease (AD). CSF BD‐tau levels did not change with sodium selenate treatment in bvFTD. Baseline CSF BD‐tau correlated with CSF total tau (t‐tau) and phosphorylated tau‐181 (p‐tau181) in AD and behavioral variant frontotemporal dementia (bvFTD). Baseline serum and plasma BD‐tau levels did not correlate with CSF BD‐tau in bvFTD. CSF p‐tau217 did not change with sodium selenate treatment in AD or bvFTD.

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