Dysmetabolism, obesity and inflammation: three prominent actors in the drama of major neuropsychiatric disorders

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Background

A large and convincing body of evidence demonstrates that medical conditions associated with chronic inflammatory and immunological abnormalities may represent risk factors for neuropsychiatric disorders. Indeed obesity, dysmetabolic conditions, including diabetes and metabolic syndrome, autoimmune diseases and malignancies are frequently associated to the development of neurodegenerative and psychiatric illnesses. Therefore the potential contribution of chronic inflammation to the development of such disorders is presently attracting much attention. Indeed elevated biomarkers of inflammation have been associated with the development of neurological and psychiatric diseases. Recent data have demonstrated that inflammatory cytokines can interact with multiple transmitter pathways, neuroendocrine function, synaptic plasticity, and neurocircuits relevant to behavior regulation. Therefore, further understanding of mechanisms linking obesity, dysmetabolism and (neuro)inflammation to neurological and mental alterations may be especially relevant to the treatment and prevention for such debilitating diseases that represent a major public health concern.
This is the case of obesity, as this disorder is associated with an increased and preoccupying risk of neuropsychiatric comorbidities contributing to a significant rise in mortality.
Obesity is characterized by a chronic low-grade inflammatory state that is likely to influence neuropsychiatric status given the well-known and highly documented effects of inflammation on brain activity/function and behavior. This hypothesis is supported by recent findings coming from clinical investigations in obese subjects and from studies conducted in animal models of obesity. These studies converge to show that obesity-related inflammatory processes spread to the brain where they lead to substantial changes in neurocircuitry, neuroendocrine activity, neurotransmitter metabolism and activity, and neurogenesis.
In addition, albeit metabolic abnormalities have been associated with cognitive dysfunctions and brain alterations, only recent evidence has been provided supporting the notion that metabolic dysfunction could lead to specific mental disorders, thus revealing incredible possibility to clarify pathogenetic mechanisms responsible for the frequent comorbidity. Conversely, it has been certainly better understood the pathogenetic pathways linking systemic or brain inflammation to neurodegeneration or to the onset of psychiatric disorders, such as depression and psychosis. However, in this case many aspects remain to be elucidated, including the precise role of neuroglia in relation to the stage and the type of the disease as well as the potential contribution of mast cells in the pathogenesis of other neuropsychiatric disorders, such as autism or autistic spectrum.
In conclusion it is possible to suggest that neurodegenerative diseases and psychiatric disorders are still awaiting for new explanatory paradigms in the attempt to possibly find innovative tools for prevention and treatment. Connecting metabolic disorders, obesity and, (neuro)inflammation to the onset of many neuropsychiatric diseases raises from epidemiological and clinical evidence that confirms the high frequency of such comorbidities. Metabolic changes, inflammation and obesity are closely interrelated, so that one feeds the others in a vicious circle, in which everyone contributes and strengthens the others in inducing the onset of psychiatric and neurodegenerative diseases. In this Research Topic we will focus on all these aspects together and we would like to shed new light on the issue and expand our knowledge, as these strict correlation are commonly treated separately.

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