Metadata Supervised MRI Representations for Modelling and Controlling Acquisition Variability

Magnetic resonance imaging exhibits substantial acquisition variability, where identical anatomy can appear markedly different across scanners and imaging protocols. Consequently, learned representations entangle biological structure with acquisition-dependent appearance, limiting interpretability, generalisation, and clinical deployment. We show that these sources of variation can be separated by jointly modelling MRI images and DICOM metadata. Using large-scale clinical brain MRI data, we learn representations that separate anatomical structure from contrast-dependent appearance. Resulting contrast representations organise heterogeneous acquisitions, support sequence understanding, and detect image--metadata inconsistencies, whereas anatomical representations suppress acquisition-specific variation while preserving biologically relevant information. Building on these disentangled representations, we introduce a unified anatomy-preserving harmonisation model for cross-modality and cross-site adaptation, conditioned on image or acquisition metadata. Our findings suggest that acquisition variability is a structured component of the imaging process that can be modelled, audited, and controlled, providing a foundation for acquisition-aware representation learning in large-scale medical imaging.

Dynamic causal discovery in Alzheimer's disease through latent pseudotime modelling

The application of causal discovery to diseases like Alzheimer's (AD) is limited by the static graph assumptions of most methods; such models cannot account for an evolving pathophysiology, modulated by a latent disease pseudotime. We propose to apply an existing latent variable model to real-world AD data, inferring a pseudotime that orders patients along a data-driven disease trajectory independent of chronological age, then learning how causal relationships evolve. Pseudotime outperformed age in predicting diagnosis (AUC 0.82 vs 0.59). Incorporating minimal, disease-agnostic background knowledge substantially improved graph accuracy and orientation. Our framework reveals dynamic interactions between novel (NfL, GFAP) and established AD markers, enabling practical causal discovery despite violated assumptions.