Obesity-Induced Brain Neuroinflammatory and Mitochondrial Changes

TL;DR

This review explains how obesity causes brain inflammation and mitochondrial issues, which may lead to cognitive decline and neurodegenerative problems.

Contribution

The paper reviews how obesity and high-fat diets affect brain neuroinflammation and mitochondrial function, linking metabolic issues to cognitive decline.

Findings

Obesity causes chronic low-grade inflammation in adipose tissue, which may contribute to brain disorders.

Mitochondrial dysfunction in the brain is linked to obesity-related inflammation and oxidative stress.

Neuronal damage and cognitive decline may result from impaired mitochondrial activity due to obesity.

Abstract

Obesity is defined as abnormal and excessive fat accumulation, and it is a risk factor for developing metabolic and neurodegenerative diseases and cognitive deficits. Obesity is caused by an imbalance in energy homeostasis resulting from increased caloric intake associated with a sedentary lifestyle. However, the entire physiopathology linking obesity with neurodegeneration and cognitive decline has not yet been elucidated. During the progression of obesity, adipose tissue undergoes immune, metabolic, and functional changes that induce chronic low-grade inflammation. It has been proposed that inflammatory processes may participate in both the peripheral disorders and brain disorders associated with obesity, including the development of cognitive deficits. In addition, mitochondrial dysfunction is related to inflammation and oxidative stress, causing cellular oxidative damage. Preclinical and clinical studies of obesity and metabolic disorders have demonstrated mitochondrial brain dysfunction. Since neuronal cells have a high energy demand and mitochondria play an important role in maintaining a constant energy supply, impairments in mitochondrial activity lead to neuronal damage and dysfunction and, consequently, to neurotoxicity. In this review, we highlight the effect of obesity and high-fat diet consumption on brain neuroinflammation and mitochondrial changes as a link between metabolic dysfunction and cognitive decline.

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