Integrated mental health treatment and employment services for refugees with PTSD: randomised controlled trial.

Obesity is a growing global health concern and a well-established risk factor for metabolic disorders, including type 2 diabetes and cardiovascular disease. Increasing evidence also implicates obesity as a modifiable risk factor for cognitive decline and dementia later in life [, ]. Epidemiological studies link early- and mid-life obesity to increased risk of Alzheimer’s disease and related dementias [, ], yet the biological mechanisms underlying this association remain poorly defined. Age of onset [, ], diet quality [], and sex [] independently influence dementia risk, but how these factors interact to shape brain and cerebrovascular health remains unclear. Obesity-related cognitive impairment is often attributed to metabolic dysregulation, including insulin resistance and impaired glucose homeostasis, which can adversely affect neuronal function and brain energy metabolism [, ]. However, obesity is also associated with cerebrovascular dysfunction, including altered cerebral blood flow, endothelial dysfunction, and disruption of the blood–brain barrier [–]. Because vascular alterations are among the earliest pathological changes observed across dementia subtypes [], cerebrovascular vulnerability may represent a critical link between systemic metabolic dysfunction and cognitive decline. Yet, how diet-induced obesity affects cerebral perfusion and vascular structure across the lifespan remains unclear. Sex is an important but underexplored biological variable in metabolic and neurodegenerative research. Males and females differ in adipose tissue distribution, metabolic regulation, and susceptibility to insulin resistance [–], but many preclinical studies examining obesity-related cognitive decline have focused primarily on males []. Understanding sex-specific vulnerability across the lifespan is therefore essential.