Table 4.

Main findings from other second-generation tau PET studies.

Paper	Tracer	Clinical population	Findings
Ossenkoppele (2021)	[18F]RO-948	673 HC, 443 MCI, 315 CE	[18F]AV-1451 and [18F]RO-948 were able to detect AD-tau, even in preclinical and prodromal stages of AD
Smith (2020)	[18F]RO-948	18 AD, 3 amyloid-beta-positive amnestic MCI, 4 HC	Tracer retention higher in entorhinal cortex but lower in basal ganglia, thalamus, and choroid plexus; SUVR plateaus by the end of scanning interval, indicating less concern for time-dependent biases
Leuzy (2020)	[18F]RO-948	100 CE, 26 PD/PD (with dementia), 6 MSA, 16 PSP, 25 DLB, 7 svPPA, 12 bvFTD, 257 HC, 154 MCI	Elevated tracer binding mostly observed in beta-amyloid-positive cases; provides evidence for [18F]RO-948 specificity for AD-tau
Honer (2018)	[18F]RO-948	In vitro	Tracer binding consistent with Braak staging in AD
Baker (2021)	[18F]JNJ-067	4 HC, 5 MCI, 5 AD, 3 PSP	Significant tracer binding in AD-specific regions only; unlikely that this tracer will be useful in AP research
Gogola (2021)	[18F]MK-6240	5 probable AD, 1 MCI-amnestic, 9 no subjective cognitive complaint	Tracer binding in medial temporal lobe and neocortex consistent with AD pathology; off-target binding observed to similar degrees as [18F]AV-1451
Salinas (2019)	[18F]MK-6240	12 AD, 3 HC	Rapid tracer uptake in AD patients compared to HC; no evidence of off-target binding; high test–retest reliability
Hostetler (2016)	[18F]MK-6240	In vitro	Binding pattern consistent with phosphorylated tau distribution in AD brain slices; favourable tracer kinetics demonstrated
Lindberg (2021)	[18F]CBD-2115	In vitro	High tracer binding affinity in 4R-tau in transgenic mice; human tissue homogenates also showed high tracer specificity for 4R-tau; tracer clearance was rapid, which may serve as an issue with uptake in the future