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Detailed neuropathologic studies suggest that the misfolded protein tau is the most common form of proteinopathy resulting in neurodegeneration, including Alzheimer disease (AD), primary age-related tauopathy, and approximately half of frontotemporal lobar degeneration (FTLD-tau). However, the nature of phosphorylated tau inclusions varies across neurodegenerative disorders, including a 4-repeat isoform (4R) in progressive supranuclear palsy and corticobasal degeneration, a 3-repeat isoform (3R) in Pick disease, and a combination of 3R:4Rtau in AD.1 As we enter an era of tau-targeted therapeutic trials, it is critical to identify robust biomarkers that can provide in vivo and specific measurements of tau isoforms to provide screening tools for the identification of aging individuals with tau and to provide endpoints to measure whether there is a response to disease-modifying treatments. However, the heterogeneity of tau isoforms across disorders presents many challenges for pursuing successful tau therapeutic strategies.
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- © 2018 American Academy of Neurology
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