Ultra-Processed Foods, MASLD, and Cognitive Aging: A Processing-Centered Gut–Liver–Brain Axis Perspective

Background/Objectives: Ultra-processed foods (UPFs) are increasingly recognized as dietary exposures associated with cardiometabolic, hepatic, and neurocognitive outcomes. However, UPFs are often treated mainly as nutrient-poor foods, whereas their processing-related features may perturb gut–liver–brain communication. This review examines whether metabolic dysfunction-associated steatotic liver disease (MASLD) can be conceptualized as a hepatic metabolic amplifier linking UPF exposure to cognitive aging. Methods: We conducted a structured narrative search of PubMed/MEDLINE, Web of Science Core Collection, and Scopus from January 2010 to 11 May 2026 across four evidence modules: UPFs and MASLD/NAFLD; UPFs and cognitive aging or dementia; UPFs and gut–liver–brain mechanisms; and MASLD/NAFLD and cognitive aging. Representative studies were prioritized according to direct relevance to the proposed axis, study design, exposure and outcome validity, mechanistic specificity, and contribution to major evidence gaps. Results: Observational and mechanistic evidence links higher UPF consumption with liver steatosis, MASLD/NAFLD-related outcomes, cognitive decline, cognitive impairment, stroke, and dementia-related outcomes, although causality remains incompletely established and residual confounding is important. Candidate pathways include food-matrix disruption, rapid eating, displacement of microbial substrates, selected additives and processing-derived compounds, intestinal barrier dysfunction, metabolic endotoxemia, bile acid signaling, hepatic lipotoxicity, systemic inflammation, vascular dysfunction, and neuroimmune activation. Many pathways overlap with general cardiometabolic dysfunction; the processing-centered contribution lies in positioning industrial formulation as an upstream exposure and MASLD as a hepatic node that may amplify gut-derived and metabolic signals relevant to brain aging. Conclusions: A processing-centered gut–liver–brain framework integrates UPFs, MASLD, and cognitive aging as linked metabolic-aging phenomena. Future studies should test UPF substitution using liver imaging, microbiome profiling, metabolomics, bile acid and inflammatory biomarkers, neuroimaging, and cognitive assessment.