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Metabolic Syndrome and Its Cross-Talk with Brain Neurodegenerative Diseases: Emerging Role of G-protein Coupled Receptors

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 733

Special Issue Editors

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Guest Editor
Department of Health Sciences, University of Magna Graecia Catanzaro, 88100 Catanzaro, Italy
Interests: immune system; pharmacology; cell signaling; COVID 19
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
1. Galascreen Laboratories, University of Calabria, 87040 Rende, CS, Italy
2. Research Division, Dynamical Business, and Science Society–DBSS International SAS, Bogotá, Colombia
Interests: sport nutrition; miRNA; nutritional biochemistry; nutritional supplementation; nutraceutical; nutrition in pathologies; lipoedema; CMT disease; ketogenic diet; low-carb diet; functional food
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic syndrome (MetS) has become a global health concern that recognizes obesity as major driver and risk factor for the development of T2D and related cardiovascular diseases. Over the past decade, research has demonstrated that obesity and its comorbidities are not only disorders of peripheral tissues, but also involve neurological changes, resulting in neuronal circuits dysregulation, impaired metabolic physiology in the central nervous system and neurodegeneration. The cross-talk between MetS and brain neurodegenerative diseases was initially highlighted by epidemiological studies, whereas animal models have provided insight into complex relationships between these conditions, with the development of insulin resistance being the main determinant. Extensive research is ongoing in an attempt to better clarify the pathobiology of both MetS and related neurodegenerative processes. Within this context several pieces of evidence strongly suggest the involvement of G protein-coupled receptors (GPCRs). These integral membrane proteins sense a diverse spectrum of chemical signals in a highly selective way and mediate a wide array of cellular signaling cascades, resulting in a plethora of homeostatic responses. Drugs targeting GPCRs account for more than a third of all currently accessible commercially available medications, making them an attractive therapeutic option for the treatment of obesity and related metabolic diseases, as well as for developing novel therapeutics for central nervous system degenerative disorders. Guest editing by Dr. Maria Cristina Caroleo, Dr. Erika Cione, and Dr. Roberto Cannataro, with the assistance of Dr. Diana Marisol Abrego Guandique, the Special Issue interests in the expression, signaling, molecule interactions, pathophysiology, and current pharmacological developments in relation to GPCRs, in the context of metabolic syndrome and brain neurodegenerative diseases.

Dr. Maria Cristina Caroleo
Dr. Erika Cione
Dr. Roberto Cannataro
Guest Editors

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  • GPCRs
  • metabolic syndrome
  • T2D
  • neurodegenerative disorders
  • pharmacology

Published Papers (1 paper)

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18 pages, 4042 KiB  
The Expression and Functionality of CB1R-NMDAR Complexes Are Decreased in A Parkinson’s Disease Model
by Irene Reyes-Resina, Jaume Lillo, Iu Raïch, Joan Biel Rebassa and Gemma Navarro
Int. J. Mol. Sci. 2024, 25(5), 3021; https://doi.org/10.3390/ijms25053021 - 05 Mar 2024
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One of the hallmarks of Parkinson’s disease (PD) is the alteration in the expression and function of NMDA receptor (NMDAR) and cannabinoid receptor 1 (CB1R). The presence of CB1R-NMDAR complexes has been described in neuronal primary cultures. The activation [...] Read more.
One of the hallmarks of Parkinson’s disease (PD) is the alteration in the expression and function of NMDA receptor (NMDAR) and cannabinoid receptor 1 (CB1R). The presence of CB1R-NMDAR complexes has been described in neuronal primary cultures. The activation of CB1R in CB1R-NMDAR complexes was suggested to counteract the detrimental NMDAR overactivation in an AD mice model. Thus, we aimed to explore the role of this receptor complex in PD. By using Bioluminescence Resonance Energy Transfer (BRET) assay, it was demonstrated that α-synuclein induces a reorganization of the CB1R-NMDAR complex in transfected HEK-293T cells. Moreover, α-synuclein treatment induced a decrease in the cAMP and MAP kinase (MAPK) signaling of both CB1R and NMDAR not only in transfected cells but also in neuronal primary cultures. Finally, the interaction between CB1R and NMDAR was studied by Proximity Ligation Assay (PLA) in neuronal primary cultures, where it was observed that the expression of CB1R-NMDAR complexes was decreased upon α-synuclein treatment. These results point to a role of CB1R-NMDAR complexes as a new therapeutic target in Parkinson’s disease. Full article
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