Obesity has been increasingly recognized as a potential modifiable risk factor for cognitive dysfunction and dementia. Accumulating evidence indicates that excess adiposity is associated with impairments in multiple cognitive domains, particularly executive function, attention, processing speed, and, to a lesser extent, memory. The strongest and most consistent associations are observed in midlife obesity, suggesting a life-course effect of prolonged metabolic exposure on brain health. This narrative review synthesizes current epidemiological, neuroimaging, mechanistic, and interventional evidence linking obesity with cognitive outcomes. Structural and functional brain alterations associated with obesity include reduced gray matter volume, white matter integrity disruption, and altered connectivity within key cognitive networks such as frontoparietal and hippocampal circuits. Proposed biological mechanisms include chronic low-grade systemic inflammation, insulin resistance with impaired central glucose metabolism, cerebrovascular dysfunction, oxidative stress, adipokine imbalance, and gut–brain axis alterations. The relationship between obesity and cognition is further modified by age, adiposity distribution, metabolic health status, genetic susceptibility, and lifestyle factors, indicating substantial inter-individual heterogeneity. Emerging interventional evidence suggests that cognitive impairment associated with obesity may be at least partially reversible, particularly following lifestyle modification, multidomain interventions, bariatric surgery, and pharmacological treatments targeting metabolic pathways; however, long-term randomized controlled data remain limited. Overall, obesity should be considered a heterogeneous and potentially modifiable risk factor for cognitive decline, with early metabolic intervention representing a promising strategy for preserving long-term cognitive health.
Trocka et al. (2026) studied this question.