Predicting Change in Brief Treatment for BPD: The Role of Defensive Functioning and Pervasiveness in Relationship Patterns.

Cognitive impairment, which disproportionately affects older adults, is a major public health concern in ageing societies [, ]. Its burden is expected to increase substantially as populations age, imposing considerable clinical, caregiving, and socioeconomic costs [, ]. Although disease-modifying therapies for cognitive decline have recently advanced, their applicability remains limited, highlighting the continued importance of prevention [, ]. Accordingly, identifying modifiable risk factors remains an urgent public health priority for safeguarding cognitive health in ageing societies [, ]. Among lifestyle-related factors, insomnia warrants particular attention because it is prevalent among older adults and can be modified through scalable, evidence-based treatments [, ]. Emerging evidence indicates that insomnia serves as a significant risk factor for the development of various chronic diseases, particularly neurodegenerative diseases [–]. Insomnia may exert its effects early in the neurocognitive disease process through plausible biological pathways, including sleep fragmentation, circadian dysregulation, and downstream neuroimmune alterations, thereby potentially influencing the transition from normal cognition to cognitive impairment [–]. Nonetheless, current research examining the association between insomnia and cognitive impairment faces several critical gaps. First, the evidence linking specific insomnia symptoms to cognitive impairment is inconsistent, making it difficult to draw definitive conclusions about their distinct effects on cognitive health []. Second, the impact of changes in chronic insomnia patterns on the risk of incident cognitive impairment has yet to be sufficiently elucidated []. Although a recent study has examined the association between trajectories of overall insomnia symptom burden and subsequent cognitive decline [], evidence remains limited regarding the distinct information conveyed by changes in individual insomnia symptoms. Third, accumulating evidence suggests that insomnia is associated with immune dysregulation, including alterations in specific immune cell subsets [, –]. In parallel, dysregulation of immune cell subsets has been linked with cognitive impairment and related pathology [–]. Compared with conventional inflammatory markers, immune cell subsets may capture more granular and potentially targetable immunological features that point to specific immune pathways (e.g., immunosenescence [], T-cell exhaustion [], and regulatory imbalance []) and reflect immune remodelling. However, it remains unclear whether specific immune cell subsets mediate the insomnia-cognitive impairment association. Therefore, leveraging longitudinal data on various insomnia symptoms and immune cell subsets from the Health and Retirement Study (HRS), this study aims to: (1) examine the prospective associations between insomnia trajectories and the risk of incident cognitive impairment, and (2) delineate the mediating effects of distinct immune cell subsets in these associations. The findings may help identify potential neuroprotective targets and facilitate the development of preventive strategies to mitigate cognitive impairment.