Evaluation of a visual interpretation method for tau‐PET with ¹⁸ F‐flortaucipir

Abstract

Introduction Positron emission tomography targeting tau (tau‐PET) is a promising diagnostic tool for the identification of Alzheimer's disease (AD). Currently available data rely on quantitative measures, and a visual interpretation method, critical for clinical translation, is needed. Methods We developed a visual interpretation method for 18F‐flortaucipir tau‐PET and tested it on 274 individuals (cognitively normal controls, patients with mild cognitive impairment [MCI], AD dementia, and non‐AD diagnoses). Two readers interpreted 18F‐flortaucipir PET using two complementary indices: a global visual score and a visual distribution pattern. Results Global visual scores were reliable, correlated with global cortical 18F‐flortaucipir standardized uptake value ratio (SUVR) and were associated with clinical diagnosis and amyloid status. The AD‐like 18F‐flortaucipir pattern had good sensitivity and specificity to identify amyloid‐positive patients with AD dementia or MCI. Discussion This 18F‐flortaucipir visual rating scheme is associated with SUVR quantification, clinical diagnosis, and amyloid status, and constitutes a promising approach to tau measurement in clinical settings.

Diagnostic value of amyloid-PET and tau-PET: a head-to-head comparison

“…Indeed, while in clinical practice the amyloid-PET result is usually dichotomized based on established cut-offs, there are no clinically validated positivity cut-offs for tau-PET, the result of which can then be described on the basis of its topography. In the present study, significant tracer deposition in brain areas corresponding to Braak stages IV-VI was classified as tau positive in accordance with current knowledge on the cognitive impact of tau pathology [25] and on the detectability of tau pathology with 18F-Flortaucipir [26], and consistently with a recent study [27]. According to a different classification method, a positive tau-PET interpretation is consistent with Braak stages V-VI [23].…”

“…Raters had access to PET reports. To binarize the tau-PET result in data analyses, Braak stages 0-III were considered as tau negative, and Braak stages IV-VI as tau positive, in accordance with current knowledge on the cognitive impact of tau pathology [25] and on the detectability of tau pathology with 18F-Flortaucipir [26], and consistently with a recent study [27].…”

Tau Biomarkers in Dementia: Positron Emission Tomography Radiopharmaceuticals in Tauopathy Assessment and Future Perspective

“…Moreover, Sonni et al elaborated four [ 18 F]Flortaucipir distribution patterns, constituting a promising approach to Tau measurement in clinical practice. Pattern I (negative scan): absence of [ 18 F]Flortaucipir signal in any brain area; Pattern II (mild temporal binding only): mild to moderate increase of [ 18 F]Flortaucipir signal, limited to the medial temporal cortex and fusiform gyrus, probably consistent with early Braak stage Tau pathology in older individuals with or without cognitive decline [ 11 , 27 , 30 ]; Pattern III (AD-like binding): [ 18 F]Flortaucipir distribution not localized only in the medial temporal/fusiform area (extension to lateral temporal, parietal or frontal cortices) consistent with the neuropathological distribution of Tau in advanced Braak stage [ 11 , 27 , 30 ]; Pattern IV (non-AD-like): atypical [ 18 F]FTP signal distribution, not following the expected Braak distribution of Tau tangles (for example, predominant white matter or subcortical binding consistent with non-AD syndromes) [ 107 ]. …”

“…In a recent paper, Sonni et al developed a visual interpretation method for [ 18 F]Flortaucipir Tau-PET and tested it on 274 individuals (including controls, MCI, AD, non-AD) [ 107 ]. A global visual score was described (0 = no binding; 1 = mild binding; 2 = intense binding) in seven cortical regions.…”

“…Pattern IV (non-AD-like): atypical [ 18 F]FTP signal distribution, not following the expected Braak distribution of Tau tangles (for example, predominant white matter or subcortical binding consistent with non-AD syndromes) [ 107 ].…”