0058 Brain Viscoelastic Properties Predict Distinct Domains of Sleep Quality

Abstract Introduction Sleep quality arises from neural systems interactions that regulate arousal, emotional processing, and sleep–wake stability. Emerging work suggests mechanical properties of brain tissue—reflecting microstructural integrity and network organisation—may shape the efficiency and resilience of these regulatory processes. Magnetic Resonance Elastography (MRE) offers a non-invasive means of quantifying viscoelastic properties, yet its relevance to sleep remains largely unexplored. We hypothesised biomechanical characteristics of sleep-relevant neural systems would correspond to specific domains of sleep quality captured by the Pittsburgh Sleep Quality Index (PSQI). Methods We examined 43 healthy older adults (mean age = 59 ± 3 years; 77% female). High-resolution MRE quantified global brain and white matter shear stiffness and damping ratio, as well as regional viscoelastic properties across sleep-related structures, including the medial prefrontal cortex (mPFC), amygdala, hippocampus, putamen, thalamus, caudal and rostral components of the anterior cingulate cortex (ACC), and insula. Subjective sleep characteristics were assessed with the PSQI global score and its component scores. Robust regression models evaluated associations between MRE metrics and PSQI components while adjusting for age, sex, and family history of dementia. Results Higher global PSQI scores were associated with lower mPFC stiffness (β= –19, p=0.038). Component-level analyses revealed distinct biomechanical signatures. Poorer subjective sleep quality corresponded to increased stiffness in the caudal ACC (β=618, p=.022). Longer sleep latency was linked to widespread increases in stiffness across the whole brain (β = 149, p = 0.010), white matter (β=162, p=.004), amygdala (β=445, p=.025), hippocampus (β=308, p=.018), putamen (β=278, p=.015), insula (β=201, p=.041), and mPFC (β=154, p=.028). Greater reliance on sleep medication was associated with lower rostral ACC stiffness (β=–226, p=.007). Conclusion This study is the first to demonstrate that region-specific viscoelastic signatures within the brain map onto distinct dimensions of sleep quality. Increased stiffness in caudal ACC, hippocampus, and related limbic structures may reflect heightened emotional or mnemonic load affecting sleep initiation, whereas reduced rostral ACC stiffness may signal diminished regulatory integrity tied to medication use. Together, results highlight a distributed biomechanical network supporting sleep regulation and demonstrate that MRE-derived tissue properties provide a promising biomarker framework for understanding vulnerability to poor sleep quality and informing targeted interventions. Support (if any)