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The introduction of tau imaging agents such as  18 F-THK523 offers new hope for the  in vivo  assessment of tau deposition in tauopathies such as Alzheimer’s disease (AD), where preliminary  18 F-THK523-PET studies have demonstrated significantly higher cortical retention of  18 F-THK523 in AD compared to age-matched healthy individuals. In addition to AD, tau imaging with PET may also be of value in assessing non-AD tauopathies, such as corticobasal degeneration (CBD), progressive supranuclear palsy (PSP) and Pick’s disease (PiD).    Methods  To further investigate the ability of THK523 to recognize tau lesions, we undertook immunohistochemical and fluorescence studies in serial brain sections taken from individuals with AD ( n  = 3), CBD ( n  = 2), PSP ( n  = 1), PiD ( n  = 2) and Parkinson’s disease (PD;  n  = 2). In addition to the neuropathological analysis, one PSP patient had undergone a  18 F-THK523 PET scan 5 months before death.    Results  Although THK523 labelled tau-containing lesions such as neurofibrillary tangles and neuropil threads in the hippocampus and frontal regions of AD brains, it failed to label tau-containing lesions in non-AD tauopathies. Furthermore, though THK523 faintly labelled dense-cored amyloid-β plaques in the AD frontal cortex, it failed to label α-synuclein-containing Lewy bodies in PD brain sections.    Conclusion  The results of this study suggest that  18 F-THK523 selectively binds to paired helical filament tau in AD brains but does not bind to tau lesions in non-AD tauopathies, or to α-synuclein in PD brains.

Assessing THK523 selectivity for tau deposits in Alzheimer’s disease and non–Alzheimer’s disease tauopathies