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. 2019 Jun 6;19(7):45. doi: 10.1007/s11910-019-0962-7

Table 3.

Highlight of recent clinical human PET study

Subjects Major findings References
9 MCI patients (prodromal AD) -[11C]PBB3 preferentially bind to tau deposits with a close spatial relationship to Aβ [46]
-[11C]THK5351 presented the distribution of tau pathology in AD better and was more closely related to downstream disease markers
3 AD patients and 3 HCs [11C]PBB3 tracer distribution was consistent with the spreading of tau pathology with AD progression [12]
2 AD patients, 4 FTD patients (frontotemporal dementia) and 2 HCs -[18F]AV-1451 is more sensitive and specific to Alzheimer’s disease type tau and shows lower off-target binding [48]
[18F]THK5351 may better present non-specific neurodegeneration
69 healthy controls (PIB negative) Explained [18F]AV-1451 variability in healthy controls across the lifespan. [31]
6 AD patients, 3 PSP patients, 2 CBS patients and 4 HCs Described the kinetics of [18F]AV-1451, the optimal scanning time and the reference region for SUVR calculation. [49]
3 subjects carrying the MAPT R406W mutation [18F]AV-1451 PET can be used to accurately quantify in vivo the regional distribution of hyperphosphorylated tau protein. [50]
20 EOAD patients, 21 LOAD patients, 3 prodromal EOAD 13 prodromal LOAD and 30 HCs Described the difference in [18F]AV-1451 tracer retention in early- and late-onset Alzheimer’s disease. [51]
39 AD patients, 14 prodromal AD and 30 HCs Elucidated the relationship of [18F]AV-1451 tracer retention to tau in cerebrospinal fluid. [52•]
11 PSP patients and 11 HCs Characterised the tracer uptake of [18F]AV-1451 in progressive supranuclear palsy. [53•]
[54]
One 71-year-old male subject
31 AD patients, 11 PSP patients, 8 CBS patients and 17 HCs Characterised the tracer uptake of [18F]AV-1451 in corticobasal syndrome. [55•]
17 AD patients and 95 HCs Regional thresholds of [18F]AV-1451 have the potential to be used in clinical trials for the enrolment of individuals with tau abnormalities. [35]
59 cognitively unimpaired with normal amyloid (CUA-) -Rate measurements based on granular Braak–like topographic staging or voxel-wise approaches may not provide significantly more information than simple meta-ROI rate measurements. [34••]
37 cognitively unimpaired with abnormal amyloid (CUA+)
30 cognitively impaired with amnestic phenotype and abnormal amyloid (CIA+) -Tau PET SUVR measures should be an efficient outcome measure in disease-modifying clinical trials.