The human brain has dedicated mechanisms for processing other people’s movements. Previous research has revealed how these mechanisms contribute to perceiving the movements of individuals but has left open how we perceive groups of people moving together. Across three experiments, we test whether movement perception depends on the spatiotemporal relationships among the movements of multiple agents. In Experiment 1, we combine EEG frequency tagging with apparent human motion and show that posture and movement perception can be dissociated at harmonically related frequencies of stimulus presentation. We then show that movement but not posture processing is enhanced when observing multiple agents move in synchrony. Movement processing was strongest for fluently moving synchronous groups (Experiment 2) and was perturbed by inversion (Experiment 3). Our findings suggest that processing group movement relies on binding body postures into movements and individual movements into groups. Enhanced perceptual processing of movement synchrony may form the basis for higher order social phenomena such as group alignment and its social consequences.

Purpose: [¹⁸F]MK-6240, a second-generation tau PET tracer, is increasingly used for the detection and the quantification of in vivo cerebral tauopathy in Alzheimer’s disease (AD). Given that neurological symptoms are better explained by the topography rather than by the nature of brain lesions, our study aimed to evaluate whether cognitive impairment would be more closely associated with the spatial extent than with the intensity of tau-PET signal, as measured by the standard uptake value ratio (SUVr). Methods: [¹⁸F]MK6240 tau-PET data from 82 participants in the AD spectrum were quantified in three different brain regions (Braak ≤ 2, Braak ≤ 4, and Braak ≤ 6) using SUVr and the extent of tauopathy (EOT, percentage of voxels with SUVr ≥ 1.3). PET data were first compared between diagnostic categories, and ROC curves were computed to evaluate sensitivity and specificity. PET data were then correlated to cognitive performances and cerebrospinal fluid (CSF) tau values. Results: The EOT in the Braak ≤ 2 region provided the highest diagnostic accuracies, distinguishing between amyloid-negative and positive clinically unimpaired individuals (threshold = 9%, sensitivity = 79%, specificity = 82%) as well as between prodromal AD and preclinical AD (threshold = 38%, sensitivity = 81%, specificity = 93%). The EOT better correlated with cognition than SUVr (∆R² + 0.08–0.09) with the best correlation observed for EOT in the Braak ≤ 4 region (R² = 0.64). Cognitive performances were more closely associated with PET metrics than with CSF values. Conclusions: Quantifying [¹⁸F]MK-6240 tau PET in terms of EOT rather than SUVr significantly increases the correlation with cognitive performances. Quantification in the mesiotemporal lobe is the most useful to diagnose preclinical AD or prodromal AD.

INTRODUCTION: Magnetic resonance imaging (MRI) segmentation algorithms make it possible to study detailed medial temporal lobe (MTL) substructures as hippocampal subfields and amygdala subnuclei, offering opportunities to develop biomarkers for preclinical Alzheimer's disease (AD).METHODS: We identified the MTL substructures significantly associated with tau‐positron emission tomography (PET) signal in 581 non‐demented individuals from the Alzheimer's Disease Neuroimaging Initiative (ADNI‐3). We confirmed our results in our UCLouvain cohort including 110 non‐demented individuals by comparing volumes between individuals with different visual Braak's stages and clinical diagnosis.RESULTS: Four amygdala subnuclei (cortical, central, medial, and accessory basal) were associated with tau in amyloid beta‐positive (Aβ+) clinically normal (CN) individuals, while the global amygdala and hippocampal volumes were not. Using UCLouvain data, we observed that both Braak I‐II and Aβ+ CN individuals had smaller volumes in these subnuclei, while no significant difference was observed in the global structure volumes or other subfields.CONCLUSION: Measuring specific amygdala subnuclei, early atrophy may serve as a marker of temporal tauopathy in preclinical AD, identifying individuals at risk of progression.Highlights: Amygdala atrophy is not homogeneous in preclinical Alzheimer's disease (AD). Tau pathology is associated with atrophy of specific amygdala subnuclei, specifically, the central, medial, cortical, and accessory basal subnuclei. Hippocampal and amygdala volume is not associated with tau in preclinical AD. Hippocampus and CA1‐3 volume is reduced in preclinical AD, regardless of tau.

Background: There is good evidence that elevated amyloid-β (Aβ) positron emission tomography (PET) signal is associated with cognitive decline in clinically normal (CN) individuals. However, it is less well established whether there is an association between the Aβ burden and decline in daily living activities in this population. Moreover, Aβ-PET Centiloids (CL) thresholds that can optimally predict functional decline have not yet been established. Methods: Cross-sectional and longitudinal analyses over a mean three-year timeframe were performed on the European amyloid-PET imaging AMYPAD-PNHS dataset that phenotypes 1260 individuals, including 1032 CN individuals and 228 participants with questionable functional impairment. Amyloid-PET was assessed continuously on the Centiloid (CL) scale and using Aβ groups (CL < 12 = Aβ-, 12 ≤ CL ≤ 50 = Aβ-intermediate/Aβ± , CL > 50 = Aβ+). Functional abilities were longitudinally assessed using the Clinical Dementia Rating (Global-CDR, CDR-SOB) and the Amsterdam Instrumental Activities of Daily Living Questionnaire (A-IADL-Q). The Global-CDR was available for the 1260 participants at baseline, while baseline CDR-SOB and A-IADL-Q scores and longitudinal functional data were available for different subsamples that had similar characteristics to those of the entire sample. Results: Participants included 765 Aβ- (61%, Mdn_age = 66.0, IQR_age = 61.0–71.0; 59% women), 301 Aβ± (24%; Mdn_age = 69.0, IQR_age = 64.0–75.0; 53% women) and 194 Aβ+ individuals (15%, Mdn_age = 73.0, IQR_age = 68.0–78.0; 53% women). Cross-sectionally, CL values were associated with CDR outcomes. Longitudinally, baseline CL values predicted prospective changes in the CDR-SOB (b_CL*Time = 0.001/CL/year, 95% CI [0.0005,0.0024], p = .003) and A-IADL-Q (b_CL*Time = -0.010/CL/year, 95% CI [-0.016,-0.004], p = .002) scores in initially CN participants. Increased clinical progression (Global-CDR > 0) was mainly observed in Aβ+ CN individuals (HR_{Aβ+ vs Aβ-} = 2.55, 95% CI [1.16,5.60], p = .020). Optimal thresholds for predicting decline were found at 41 CL using the CDR-SOB (b_{Aβ+ vs Aβ-} = 0.137/year, 95% CI [0.069,0.206], p < .001) and 28 CL using the A-IADL-Q (b_{Aβ+ vs Aβ-} = -0.693/year, 95% CI [-1.179,-0.208], p = .005). Conclusions: Amyloid-PET quantification supports the identification of CN individuals at risk of functional decline. Trial registration: The AMYPAD PNHS is registered at www.clinicaltrialsregister.eu with the EudraCT Number: 2018-002277-22.

Introduction: Second‐generation tau‐PET tracers like [¹⁸F]MK‐6240 are increasingly used both for diagnosing and quantifying Alzheimer's Disease (AD) tauopathy. However, while [¹⁸F]MK‐6240 tau‐PET has demonstrated excellent sensitivity for AD tauopathy, data assessing its specificity and binding in non‐AD tauopathies are still scarce.Methods: Participants were assigned to exclusive categorical diagnoses based on their amyloid (Aβ) and cognitive status. We quantified mesiotemporal (MTL) and neocortical [¹⁸F]MK‐6240 tau‐PET signal in 28 Aβ− cognitively impaired (CI) patients presenting various non‐AD neurodegenerative disorders. Tau‐PET quantifications were compared with Aβ− cognitively unimpaired (CU) subjects (n = 51) and Aβ+ CI patients (n = 77).Results: Among the 28 Aβ− impaired subjects, only five presented significant and isolated mesiotemporal signal, most of them being suspected of primary age‐related tauopathy (PART). Only two Aβ− impaired patients (7%) presented positive neocortical signal, both being diagnosed with fronto‐temporal degeneration (FTD). The Tau‐PET results of all the remaining Aβ− patients were comparable to the CU population, including eight other FTD patients. Importantly, 4R‐only tauopathies (CBD and PSP) and sv‐PPA were negative.Conclusion: [¹⁸F]MK‐6240 tau‐PET has a special affinity for tauopathies involving 3R/4R paired helical filaments: AD, PART (Aβ− subjects with MTL‐restricted tau‐PET signal) and some forms of FTD while most primary tauopathies do not exhibit significant cortical signal. Positive neocortical scans are therefore highly specific for AD tauopathy. Based on those and previous results, we propose a diagnostic flowchart for MCI subjects suspected of AD or another tauopathy which may significantly reduce the need for amyloid PET or CSF measurement.

Objectives:Relatively few studies have investigated relationships between performance on clinical memory measures and indexes of underlying neuropathology related to Alzheimer’s disease (AD). This study investigated predictive relationships between Free and Cued Selective Reminding Test (FCSRT) cue efficiency (CE) and free-recall (FR) measures and brain amyloid levels, hippocampal volume (HV), and regional cortical thickness.Methods:Thirty-one older controls without memory complaints and 60 patients presenting memory complaints underwent the FCSRT, amyloid imaging using [F¹⁸]-flutemetamol positron emission tomography, and surface-based morphometry (SBM) using brain magnetic resonance imaging. Three groups were considered: patients with high (Aβ+P) and low (Aβ− P) amyloid load and controls with low amyloid load (Aβ− C).Results:Aβ+P showed lower CE than both Aβ− groups, but the Aβ− groups did not differ significantly. In contrast, FR discriminated all groups. SBM analyses revealed that CE indexes were correlated with the cortical thickness of a wider set of left-lateralized temporal and parietal regions than FR. Regression analyses demonstrated that amyloid load and left HV independently predicted FCSRT scores. Moreover, CE indexes were predicted by the cortical thickness of some regions involved in early AD, such as the entorhinal cortex.Conclusions:Compared to FR measures, CE indexes appear to be more specific for differentiating persons on the basis of amyloid load. Both CE and FR performance were predicted independently by brain amyloid load and reduced left HV. However, CE performance was also predicted by the cortical thickness of regions known to be atrophic early in AD. (JINS, 2016,22, 991–1004)