Atrial Fibrillation and Cognitive Decline: A Systematic Review of Pathophysiological Mechanisms, Therapeutic Strategies, and Digital Health Technologies in Neuroprotection

<b>Background</b>: Atrial fibrillation (AF) is consistently associated with cognitive impairment and dementia through mechanisms that extend beyond classical cardioembolic stroke. However, the relative contribution of these pathways and the effectiveness of available therapeutic strategies for preserving cognition remain uncertain, as most data come from observational studies with a substantial risk of bias. <b>Objectives</b>: This review narratively synthesizes contemporary evidence on epidemiology, pathophysiological mechanisms, therapeutic strategies-including anticoagulation, rhythm control, and comprehensive risk-factor management-and the role of digital health technologies in the relationship between AF and cognitive decline. <b>Methods</b>: We performed a narrative, PRISMA-informed scoping review of observational cohorts, mechanistic studies, randomized clinical trials, systematic reviews, and meta-analyses published up to January 2026, identified through structured searches in MEDLINE/PubMed and complementary sources. Studies were selected if they examined (i) associations between AF and cognitive impairment or dementia, (ii) mechanistic pathways linking AF to brain injury, (iii) therapeutic interventions with cognitive or brain imaging outcomes, or (iv) digital health technologies applied to AF management. Heterogeneity in study design and outcome assessment precluded meta-analysis; therefore, we provide a qualitative synthesis, explicitly distinguishing observational evidence from randomized data and discussing key sources of confounding. Risk of bias was evaluated using validated tools: ROBINS-I for non-randomized studies, RoB 2.0 for RCTs, Newcastle-Ottawa Scale for observational cohorts, and AMSTAR-2 for systematic reviews. <b>Results</b>: Large population-based cohorts and meta-analyses indicate that AF is associated with a 1.4-2.2-fold higher risk of cognitive impairment or incident dementia, even after adjustment for shared vascular risk factors and exclusion of patients with prior stroke; nevertheless, residual confounding and selection bias cannot be excluded. Silent cerebral infarcts are detected in roughly one-quarter to two-fifths of AF patients without clinical stroke and are themselves associated with cognitive deficits, suggesting that subclinical embolism represents one important, but not exclusive, pathway. Additional mechanisms include chronic cerebral hypoperfusion, neuroinflammation, small vessel disease, and structural brain atrophy, all of which are incompletely disentangled from comorbidities. Observational data suggest that oral anticoagulation, particularly with direct oral anticoagulants (DOACs), is associated with lower rates of dementia compared with no anticoagulation or warfarin, but randomized trials such as BRAIN-AF and GIRAF have not demonstrated a clear cognitive benefit, underlining the low-to-moderate certainty of this evidence. Rhythm-control interventions, especially catheter ablation, are associated with lower dementia incidence in registry studies, yet strong selection effects and short follow-up limit causal inference. Digital health tools and ABC-pathway mobile applications improve cardiovascular outcomes and adherence, although cognitive endpoints remain largely unexplored. <b>Conclusions</b>: AF should be conceptualized as a neurovascular condition with important implications for brain health, rather than a purely cardiac rhythm disorder confined to stroke prevention. A comprehensive heart-brain management strategy that combines optimal anticoagulation, individualized rhythm control, aggressive vascular risk factor modification, routine cognitive screening in older or high-risk patients, and judicious use of digital health technologies may offer the best opportunity for preserving cognition, although rigorous trials with cognitive endpoints are still needed to establish causality.