Abstract

Obesity represents a growing global health crisis, characterized by excessive adiposity and associated with 
multiple metabolic, cardiovascular, and neuropsychiatric comorbidities. Recent evidence indicates that obesity is 
strongly linked to neuroinflammation, mediated through peripheral and central immune mechanisms. Excess 
adipose tissue contributes to chronic low-grade systemic inflammation, with elevated pro-inflammatory cytokines 
such as IL-6, TNF-α, and IL-1β crossing the blood–brain barrier and activating microglia and astrocytes in the 
central nervous system (CNS). These neuroinflammatory processes impact cognitive function, mood regulation, 
and the hypothalamic control of energy homeostasis, potentially accelerating neurodegenerative disorders and 
psychiatric conditions. Lifestyle interventions, including dietary modification and physical activity, as well as 
pharmacological strategies targeting inflammation, show promise in mitigating obesity-related 
neuroinflammation. Nevertheless, current research is limited by cross-sectional designs, incomplete mechanistic 
understanding, and insufficient translation from animal models to human populations. Future studies integrating 
multi-omics approaches, longitudinal designs, and precision medicine strategies are needed to clarify the causal 
pathways linking obesity and neuroinflammation, improve early interventions, and reduce the burden of obesity
related neuropsychiatric and cognitive disorders.