TL;DR
GSMAP-based spatial enrichment provides a hypothesis-generating framework for understanding vascular, meningeal, and myelin-related pathways linking hypertension to increased brain age gap.
It is revealed that the genetically predisposed higher risk of diabetic maculopathy was associated with increased salience network connectivity, shedding light on the neural drivers of diabetic pathologies.
The results support a prioritized genomic map with substantial instrument- and model-specific uncertainty, and disease-to-clock signals were richer than clock-to-disease signals, GrimAA shared polygenic architecture with osteoarthritis, and selected loci showed strong shared-variant evidence.
Lower lymphocyte percentage and higher NMR-derived glucose had direct relationships with dementia in the joint constituent-biomarker network, supporting examination of composite exposures alongside their constituent biomarkers.
This study identifies three genetic pathways linking biological aging to vascular disease, offering new molecular targets for its prevention and treatment.
These findings provide a hypothesis-generating reframing of the traditional comorbidity model, suggesting that divergent molecular programs may converge on shared pathways and offer a preliminary foundation for exploring therapeutic strategies at the mood–metabolism interface.
These findings identify shared genetic loci between T2D and neurodegenerative dementia, revealing systemic metabolic-neurodegenerative trade-offs and highlighting key genes that underpin the comorbidity, providing a framework for improved understanding of age-related multi-morbidity.
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