Exploring the contagion routes of digital emotion on health topics: A multidimensional configuration analysis pre-post rumor refutation.

Alzheimer's disease (AD) is the most common cause of dementia and represents a major public health challenge worldwide., Despite extensive research, AD remains a highly heterogeneous neurodegenerative disorder, characterized by substantial inter‐individual variability in clinical presentation, rate of cognitive decline, and underlying biological processes., Although amyloid beta (Aβ) and tau pathology are central features of AD, these canonical hallmarks alone do not fully explain the marked differences observed across individuals, suggesting the involvement of additional mechanisms beyond classical neuropathological models., , Accumulating evidence indicates that environmental and systemic factors (e.g., cardiometabolic dysfunction and inflammation) play an important role in modulating the risk and progression of AD. In the context of the exposome, defined as the totality of environmental, lifestyle, and internal biological exposures accumulated over the life course, factors such as lifestyle behaviors, cardiometabolic dysfunction, chronic inflammation, and immune perturbations have been implicated in neurodegenerative processes. These influences often reflect long‐term exposures, leading to cumulative effects that may not be captured by genetic risk alone. Understanding how the exposome becomes biologically embedded and translated into molecular changes relevant to AD remains a critical challenge. Epigenetic mechanisms, particularly DNA methylation, provide a potential interface through which exposome‐related influences can be recorded as stable molecular signatures. DNA methylation patterns are dynamic and responsive to both intrinsic and extrinsic factors, making them well suited to reflect cumulative biological stress and aging‐related processes., In this context, DNA methylation‐based biological clocks have emerged as robust tools for estimating biological ages, which may diverge substantially from chronological age., Accelerated epigenetic aging has been associated with increased morbidity, mortality, and age‐related diseases, highlighting its relevance as an integrative marker of biological aging., Recent studies have reported associations between DNA methylation‐based epigenetic age acceleration and AD pathologies, risk factors, and cognitive decline., , However, the molecular pathways linking epigenetic aging to AD pathophysiology remain incompletely understood, particularly because epigenetic aging may reflect the long‐term imprint of exposome‐related influences. In particular, it is unclear whether epigenetic age acceleration is accompanied by coordinated shifts in downstream molecular systems that are directly relevant to neurodegeneration.