The Obese Brain: Mechanisms of Systemic and Local Inflammation, and Interventions to Reverse the Cognitive Deficit

Salas-Venegas, Verónica; Flores-Torres, Rosa Pamela; Rodríguez-Cortés, Yesica María; Rodríguez-Retana, Diego; Ramírez-Carreto, Ricardo Jair; Concepción-Carrillo, Luis Edgar; Pérez‐Flores, Laura J.; Alarcón-Aguilar, Adriana; López‐Díazguerrero, Norma Edith; Gómez-González, Beatriz; Chavarría, Anahí; Königsberg, Mina

doi:10.3389/fnint.2022.798995

Cited by 33 publications

(25 citation statements)

References 217 publications

(194 reference statements)

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“…Most of these inflammatory mediators (TNF-α, IL-1β, IL-6, MCP1) derive from M1 macrophages in the adipose tissue, which perpetuate mitochondrial dysfunction, oxidative stress, and cellular senescence. The endocrine communication between the brain, skeletal muscle, liver, and adipose tissue ensures that microglia become M1–phenotype, inducing chronic neuronal inflammation, neuronal death, and perturbances in neuronal synapses [ 77 ]. Of recent interest is the relationship between childhood obesity, neuroinflammation and CI.…”

Section: Discussionmentioning

confidence: 99%

NHANES 2011–2014 Reveals Decreased Cognitive Performance in U.S. Older Adults with Metabolic Syndrome Combinations

Díaz-Camargo

Hernández-Lalinde

Sánchez‐Rubio

et al. 2023

IJERPH

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A relationship between metabolic syndrome and cognitive impairment has been evidenced across research; however, conflicting results have been observed. A cross-sectional study was conducted on 3179 adults older than 60 from the 2011–2014 National Health and Nutrition Examination Survey (NHANES) to analyze the relationship between metabolic syndrome and cognitive impairment. In our results, we found that adults with abdominal obesity, high triglycerides, and low HDL cholesterol had 4.39 fewer points in the CERAD immediate recall test than adults without any metabolic syndrome factors [Beta = −4.39, SE = 1.32, 17.75 (1.36) vs. 22.14 (0.76)]. In addition, people with this metabolic syndrome combination exhibited 2.39 fewer points in the CERAD delayed recall test than those without metabolic syndrome criteria [Beta = −2.39, SE = 0.46, 4.32 (0.49) vs. 6.71 (0.30)]. It was also found that persons with high blood pressure, hyperglycemia, and low HDL–cholesterol levels reached 4.11 points less in the animal fluency test than people with no factors [Beta = −4.11, SE = 1.55, 12.67 (2.12) vs. 16.79 (1.35)]. These findings suggest that specific metabolic syndrome combinations are essential predictors of cognitive impairment. In this study, metabolic syndrome combinations that included obesity, fasting hyperglycemia, high triglycerides, and low HDL–cholesterol were among the most frequent criteria observed.

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Section: Discussionmentioning

confidence: 99%

NHANES 2011–2014 Reveals Decreased Cognitive Performance in U.S. Older Adults with Metabolic Syndrome Combinations

Díaz-Camargo

Hernández-Lalinde

Sánchez‐Rubio

et al. 2023

IJERPH

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“…Although the mechanisms underlying the relationship between obesity and cognitive functions need to be further investigated, physiology research has identified a reliable mechanism of action in the activity of the neuro-immune-endocrine systems. Adipose tissue fulfills neuro-immune-endocrine functions, participating in the homeostasis [ 101 ]. In obesity, adipose tissue produces cytokines such as interleukin (specifically IL1ß and IL6), interferon γ (IFNγ), Tumor Necrosis Factor α (TNFα), and Monocyte Chemoattractant Protein 1 (MCP1), which promote chronic inflammation [ 102 , 103 , 104 , 105 , 106 , 107 ].…”

Section: Discussionmentioning

confidence: 99%

Functional Relationship between Inhibitory Control, Cognitive Flexibility, Psychomotor Speed and Obesity

et al. 2022

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In the last decades, it has been proposed that executive functions may be particularly vulnerable to weight-related issues. However, evidence on the matter is mixed, especially when the effects of sociodemographic variables are weighted. Thus, the current study aimed at further examining the relationship between executive functions and obesity. To this aim, we compared treatment-seeking overweight, obese, and morbidly obese patients with normal-weight control participants. We examined general executive functioning (Frontal Assessment Battery–15) and different executive subdomains (e.g., inhibitory control, verbal fluency, and psychomotor speed) in a clinical sample including 208 outpatients with different degrees of BMI (52 overweight, BMI 25–30, M age = 34.38; 76 obese, BMI 30–40, M age = 38.00; 80 morbidly obese, BMI > 40, M age = 36.20). Ninety-six normal-weight subjects served as controls. No difference on executive scores was detected when obese patients were compared with over- or normal-weight subjects. Morbidly obese patients reported lower performance on executive scores than obese, overweight, and normal-weight subjects. Between-group difference emerged also when relevant covariates were taken into account. Our results support the view that morbid obesity is associated with lower executive performance, also considering the critical role exerted by sociodemographic (i.e., sex, age, and education) variables. Our results support the view that executive functioning should be accounted into the management of the obese patient because of non-negligible clinical relevance in diagnostic, therapeutic, and prognostic terms.

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“…The decrease in tight junction protein expression and the disturbed blood–brain barrier are regulated by the NF-κB pathway, which increases the expression of proinflammatory proteins, such as IL-1β, TNFα, and IL-6. The loss of the blood–brain barrier during obesity facilitates proinflammatory cytokines to enter the brain parenchyma, thus allowing them to interact and activate glial cells (microglia and astrocytes) [ 76 ]. Activated microglia secrete more inflammatory cytokines (TNFα, IL-1β, and IL-6), perpetuating the neuroinflammation and leading to neuronal damage.…”

Section: Obesity Induces Cognitive Declinementioning

confidence: 99%

Obesity-Induced Brain Neuroinflammatory and Mitochondrial Changes

Schmitt

Gaspar

2023

Metabolites

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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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The Obese Brain: Mechanisms of Systemic and Local Inflammation, and Interventions to Reverse the Cognitive Deficit

Cited by 33 publications

References 217 publications

NHANES 2011–2014 Reveals Decreased Cognitive Performance in U.S. Older Adults with Metabolic Syndrome Combinations

NHANES 2011–2014 Reveals Decreased Cognitive Performance in U.S. Older Adults with Metabolic Syndrome Combinations

Functional Relationship between Inhibitory Control, Cognitive Flexibility, Psychomotor Speed and Obesity

Obesity-Induced Brain Neuroinflammatory and Mitochondrial Changes

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