medRxiv : the preprint server for health sciences · 2025
Structural Similarity Networks Reveal Brain Vulnerability in Dementia.
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Montagnese Marcella, Ebneabbasi Amir, García-San-Martín Natalia, Pecci-Terroba Clara, Romero-García Rafael, Morgan Sarah E, Cole James H, Seidlitz Jakob, Rittman Timothy, Bethlehem Richard A I
Аннотация
INTRODUCTION: Alzheimer's disease (AD) is characterised by inter-individual heterogeneity in brain degeneration, limiting diagnostic and prognostic precision. We present a novel framework integrating Morphometric Inverse Divergence (MIND) networks with hierarchical Bayesian large-scale population modelling to identify individual-level neuroanatomical deviations.
METHODS: MIND networks quantify similarity between brain regions using multivariate MRI features. A normative model of regional MIND values trained on UK Biobank (N=35,133) was applied to the National Alzheimer's Coordinating Center cohort (N=3,567). We examined brain deviations across clinical stages, APOE genotypes, mortality risk, and neuropathological burden.
RESULTS: Negative deviations (reduced MIND) stratified disease stages (p<0.01) and showed functional network enrichment in AD. Greater negative deviations characterised APOE ε4 homozygotes and correlated with postmortem neuropathological severity (p=0.032). Neurobiological decoding revealed associations with neurotransmitter receptor distributions and cortical organisation properties.
DISCUSSION: This population neuroimaging modelling enables individualised brain mapping with direct utility for diagnosis, prognosis, and understanding of biological mechanisms.
METHODS: MIND networks quantify similarity between brain regions using multivariate MRI features. A normative model of regional MIND values trained on UK Biobank (N=35,133) was applied to the National Alzheimer's Coordinating Center cohort (N=3,567). We examined brain deviations across clinical stages, APOE genotypes, mortality risk, and neuropathological burden.
RESULTS: Negative deviations (reduced MIND) stratified disease stages (p<0.01) and showed functional network enrichment in AD. Greater negative deviations characterised APOE ε4 homozygotes and correlated with postmortem neuropathological severity (p=0.032). Neurobiological decoding revealed associations with neurotransmitter receptor distributions and cortical organisation properties.
DISCUSSION: This population neuroimaging modelling enables individualised brain mapping with direct utility for diagnosis, prognosis, and understanding of biological mechanisms.