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Abstract
<p class="first" id="d2297309e69">Pathological accumulated misfolded tau underlies
various neurodegenerative diseases
and associated clinical syndromes. To diagnose those diseases reliable before death
or even at early stages, many different tau-specific radiotracers have been developed
in the last decade to be used with positron-emission-tomography. In contrast to amyloid-β
imaging, different isoforms of tau exist further complicating radiotracer development.
First-generation radiotracers like [11C]PBB3, [18F]AV1451 and [18F]THK5351 have been
extensively investigated in vitro and in vivo. In Alzheimer's disease (AD), high specific
binding could be detected, and evidence of clinical applicability recently led to
clinical approval of [18F]flortaucipir ([18F]AV1451) by the FDA. Nevertheless, absent
or minor binding to non-AD tau isoforms and high off-target binding to non-tau brain
structures limit the diagnostic applicability especially in non-AD tauopathies demanding
further tracer development. In vitro assays and autoradiography results of next-generation
radiotracers [18F]MK-6240, [18F]RO-948, [18F]PM-PBB3, [18F]GTP-1 and [18F]PI-2620
clearly indicate less off-target binding and high specific binding to tau neurofibrils.
First in human studies have been conducted with promising results for all tracers
in AD patients, and also some positive experience in non-AD tauopathies. Overall,
larger scaled autoradiography and human studies are needed to further evaluate the
most promising candidates and support future clinical approval.
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