• Shorena Janelidze, Erik Stomrud, Ruben Smith, Sebastian Palmqvist, Niklas Mattsson, David C Airey, Nicholas K Proctor, Xiyun Chai, Sergey Shcherbinin, John R Sims, Gallen Triana-Baltzer, Clara Theunis, Randy Slemmon, Marc Mercken, Hartmuth Kolb, Jeffrey L Dage, and Oskar Hansson.
• Clinical Memory Research Unit, Lund University, Sölvegatan 18, Lund, Sweden. shorena.janelidze@med.lu.se.
• Nat Commun. 2020 Apr 3; 11 (1): 1683.

AbstractCerebrospinal fluid (CSF) p-tau181 (tau phosphorylated at threonine 181) is an established biomarker of Alzheimer's disease (AD), reflecting abnormal tau metabolism in the brain. Here we investigate the performance of CSF p-tau217 as a biomarker of AD in comparison to p-tau181. In the Swedish BioFINDER cohort (n = 194), p-tau217 shows stronger correlations with the tau positron emission tomography (PET) tracer [18F]flortaucipir, and more accurately identifies individuals with abnormally increased [18F]flortaucipir retention. Furthermore, longitudinal increases in p-tau217 are higher compared to p-tau181 and better correlate with [18F]flortaucipir uptake. P-tau217 correlates better than p-tau181 with CSF and PET measures of neocortical amyloid-β burden and more accurately distinguishes AD dementia from non-AD neurodegenerative disorders. Higher correlations between p-tau217 and [18F]flortaucipir are corroborated in an independent EXPEDITION3 trial cohort (n = 32). The main results are validated using a different p-tau217 immunoassay. These findings suggest that p-tau217 might be more useful than p-tau181 in the diagnostic work up of AD.

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