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In typical (memory-predominant) AD, the spatial progression of tau pathology mirrors the functional connections from temporal lobe epicentres. However, given the limited spatial heterogeneity of tau in typical AD, atypical (non-amnestic-predominant) AD variants with distinct tau patterns provide a key opportunity to investigate the universality of connectivity as a scaffold for tau progression.<\/jats:p>\n                  <jats:p>In this large-scale, multicentre study across 14 international sites, we included cross-sectional tau-PET data from 320 individuals with atypical AD (n = 139 posterior cortical atrophy\/PCA-AD; n = 103 logopenic variant primary progressive aphasia\/lvPPA-AD; n = 35 behavioural variant AD\/bvAD; n = 43 corticobasal syndrome\/CBS-AD), with a subset of individuals (n = 78) having longitudinal tau-PET data. Additionally, as an independent sample, we included regional post-mortem tau stainings from 93 atypical AD patients from two sites (n = 19 PCA-AD, n = 32 lvPPA-AD, n = 23 bvAD, n = 19 CBS-AD). Gaussian mixture modelling was used to harmonize different tau-PET tracers by transforming tau-PET standardized uptake value ratios to tau positivity probabilities (a uniform scale ranging from 0% to 100%). Using linear regression, we assessed whether brain regions with stronger resting-state functional MRI-based functional connectivity, derived from healthy elderly controls in the Alzheimer\u2019s Disease Neuroimaging Initiative (ADNI), showed greater covariance in cross-sectional and longitudinal tau-PET and post-mortem tau pathology. Furthermore, we examined whether functional connectivity of tau-PET epicentres (i.e. the top 5% of regions with the highest baseline tau load) and tau-PET accumulation epicentres (i.e. the top 5% of regions with the highest tau accumulation rates) was associated with cross-sectional and longitudinal tau patterns.<\/jats:p>\n                  <jats:p>Our findings show that tau-PET epicentres aligned with clinical variants, e.g. a visual network predominant pattern in PCA-AD (\u2018visual AD\u2019) and left-hemispheric temporal predominance, particularly within the language network, in lvPPA-AD (\u2018language AD\u2019). Moreover, more strongly functionally connected regions showed correlated concurrent tau-PET levels (confirmed with post-mortem data) and tau-PET accumulation rates. The functional connectivity profile of tau-PET epicentres and accumulation epicentres corresponded to tau-PET progression patterns, with higher tau-PET levels and accumulation rates in functionally close regions, and lower tau-PET levels and accumulation rates in functionally distant regions.<\/jats:p>\n                  <jats:p>Our data are consistent with the hypothesis that tau propagation occurs along functional connections originating from local epicentres, across all AD clinical variants. Since tau proteinopathy is a major driver of neurodegeneration and cognitive decline, this finding may advance personalized medicine and participant-specific end points in clinical trials.<\/jats:p>","DOI":"10.1093\/brain\/awaf279","type":"journal-article","created":{"date-parts":[[2025,8,8]],"date-time":"2025-08-08T12:06:53Z","timestamp":1754654813000},"page":"3893-3912","source":"Crossref","is-referenced-by-count":11,"title":["Connectivity as a universal predictor of tau progression in atypical Alzheimer\u2019s disease"],"prefix":"10.1093","volume":"148","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9011-1120","authenticated-orcid":false,"given":"Hannah","family":"de Bruin","sequence":"first","affiliation":[{"name":"Alzheimer Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC Location VUmc , Amsterdam 1081 HV ,","place":["The Netherlands"]},{"name":"Amsterdam Neuroscience, Neurodegeneration , Amsterdam 1081 HV ,","place":["The 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