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Metabolic Modulation of Inflammasome and Reactive Gliosis in Central Nervous System

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A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 6535

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Special Issue Information

Dear Colleagues,

Neuroinflammation of the central nervous system (CNS) is a primer of normal brain aging and many neurological disorders, including neurodegenerative disease and chronic pain states. It is well known that activation of glial cells, paralleled by energetic failure and ROS production, is a key part of the inflammatory process, boosting maladaptive synaptic changes and also cell death; however, metabolic control of inflammasome through glucose and lipid metabolism in CNS is essential for maintaining homeostasis and neural function in health and disease. To sustain neuronal function, activated glial cells undergo metabolic reprogramming (from glucose to the lipidic metabolism) that activates Toll-like receptor-4 (TLR4), caspases, NLPR1-3, sustaining neuroinflammation and leading to cell death. Therefore, it is conceivable that the overall metabolic state influences brain function and represents a new putative target for preserving long-term brain wellness and preventing neurodegenerative disorders.

Dr. Giovanni Cirillo
Guest Editor

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Keywords

lipid rafts
glucidic metabolism
neuroinflammation
reactive gliosis
maladaptive plasticity

Published Papers (2 papers)

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Research

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22 pages, 4547 KiB

Open AccessArticle

Cognitive Performance during the Development of Diabetes in the Zucker Diabetic Fatty Rat

by Marcia Spoelder, Yami Bright, Martine C. Morrison, Veerle van Kempen, Lilian de Groodt, Malvina Begalli, Nikita Schuijt, Eva Kruiger, Ronald Bulthuis, Gabriele Gross, Robert Kleemann, Janna A. van Diepen and Judith R. Homberg

Cells 2023, 12(20), 2463; https://doi.org/10.3390/cells12202463 - 16 Oct 2023

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Abstract

Increased insulin levels may support the development of neural circuits involved in cognition, while chronic mild inflammation may also result in cognitive impairment. This study aimed to gain more insight into whether cognition is already impacted during adolescence in a genetic rat model for obesity and type 2 diabetes. Visual discrimination learning throughout adolescence and the level of motivation during early adulthood were investigated in Zucker Diabetic Fatty (ZDF) obese and ZDF lean rats using operant touchscreens. Blood glucose, insulin, and lipids were longitudinally analyzed. Histological analyses were performed in the liver, white adipose tissues, and the prefrontal cortex. Prior to the experiments with the genetic ZDF research model, all experimental assays were performed in two groups of outbred Long Evans rats to investigate the effect of different feeding circumstances. Adolescent ZDF obese rats outperformed ZDF lean rats on visual discrimination performance. During the longitudinal cognitive testing period, insulin levels sharply increased over weeks in ZDF obese rats and were significantly enhanced from 6 weeks of age onwards. Early signs of liver steatosis and enlarged adipocytes in white adipose tissue were observed in early adult ZDF obese rats. Histological analyses in early adulthood showed no group differences in the number of prefrontal cortex neurons and microglia, nor PSD95 and SIRT1 mRNA expression levels. Together, our data show that adolescent ZDF obese rats even display enhanced cognition despite their early diabetic profile. Full article

(This article belongs to the Special Issue Metabolic Modulation of Inflammasome and Reactive Gliosis in Central Nervous System)

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Review

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24 pages, 3670 KiB

Open AccessReview

Vagus Nerve Stimulation: A Personalized Therapeutic Approach for Crohn’s and Other Inflammatory Bowel Diseases

by Giovanni Cirillo, Flor Negrete-Diaz, Daniela Yucuma, Assunta Virtuoso, Sohaib Ali Korai, Ciro De Luca, Eugenijus Kaniusas, Michele Papa and Fivos Panetsos

Cells 2022, 11(24), 4103; https://doi.org/10.3390/cells11244103 - 17 Dec 2022

Cited by 11 | Viewed by 4929

Abstract

Inflammatory bowel diseases, including Crohn’s disease and ulcerative colitis, are incurable autoimmune diseases characterized by chronic inflammation of the gastrointestinal tract. There is increasing evidence that inappropriate interaction between the enteric nervous system and central nervous system and/or low activity of the vagus nerve, which connects the enteric and central nervous systems, could play a crucial role in their pathogenesis. Therefore, it has been suggested that appropriate neuroprosthetic stimulation of the vagus nerve could lead to the modulation of the inflammation of the gastrointestinal tract and consequent long-term control of these autoimmune diseases. In the present paper, we provide a comprehensive overview of (1) the cellular and molecular bases of the immune system, (2) the way central and enteric nervous systems interact and contribute to the immune responses, (3) the pathogenesis of the inflammatory bowel disease, and (4) the therapeutic use of vagus nerve stimulation, and in particular, the transcutaneous stimulation of the auricular branch of the vagus nerve. Then, we expose the working hypotheses for the modulation of the molecular processes that are responsible for intestinal inflammation in autoimmune diseases and the way we could develop personalized neuroprosthetic therapeutic devices and procedures in favor of the patients. Full article

(This article belongs to the Special Issue Metabolic Modulation of Inflammasome and Reactive Gliosis in Central Nervous System)

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