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Nutrients and Gut Microbiota-Derived Nutrients in Brain Homeostasis: From Basic Mechanisms to Diseases and Identification of Possible Therapeutic Targets

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

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 11257

Special Issue Editor


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Guest Editor
1. Department of Biology and Biotechnology "Charles Darwin", Sapienza University of Rome, Rome, Italy
2. Research Center for Nanotechnology for Engineering of Sapienza (CNIS), Sapienza University of Rome, Rome, Italy
Interests: nutrients; nutrition; neurogenesis; neurodegeneration; aging; nutraceuticals; rare diseases; brain homeostasis; microbione; gut–brain axis
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Special Issue Information

Dear Colleagues,

Although the role of nutrients in brain homeostasis is well-known, the fine regulatory mechanisms and possible consequences due to alterations in nutrients-related pathways following metabolic defects (e.g., inborn errors) or nutrient deficiency remain to be further investigated. Expanding our knowledge in this field could not only contribute to better characterizing nutrient–metabolism regulatory pathways but also to identifying therapeutic targets. For instance, the description of some regulatory mechanisms such as insulin-IGF, AMPK/mTOR, and transcription factors (CREB and Sirt-1) in the brain opened up a new point of view on neural stem cell fate decision, neurodegeneration, and brain aging linked to the metabolic status of cells and the availability of specific nutrients (both macro- and micronutrients). In addition, the involvement of nutrients has been reported in high-order cognitive functions. Moreover, a strong relationship between gut microbiota and brain homeostasis has emerged in recent years. Indeed, microbiota-derived metabolites are nutrients including short-chain fatty acids, B vitamins, and vitamin K, and changes in microbiota balance (due to nutrition and alterations in the gastroenteric tract, such as the resection of a part of it, inflammatory bowel disease, infections, etc.) lead to modifications in the gut–brain axis, thus affecting brain homeostasis.

Altogether, several pieces of evidence and findings support the pivotal role of nutrients in the maintenance of brain homeostasis; however, the underlying cellular and molecular mechanisms have not been fully described.

For the Special Issue “Nutrients and Gut Microbiota-Derived Nutrients in Brain Homeostasis: From Basic Mechanisms to Diseases and Identification of Possible Therapeutic Targets”, we welcome your contributions in the form of original research and review articles on molecular and cellular aspects regarding nutrients (micro- and macronutrients and gut microbiota-derived nutrients) and nutrients-related pathways, including inborn error defects, and their role in physiological and pathophysiological metabolic processes related to the brain.

Dr. Marco Fidaleo
Guest Editor

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Keywords

  • nutrients
  • nutrition
  • neurogenesis
  • neurodegeneration
  • aging
  • nutraceuticals
  • rare diseases
  • brain homeostasis
  • microbiome
  • gut–brain axis
 

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Published Papers (1 paper)

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Review

29 pages, 2631 KiB  
Review
Vitamin B12 Deficiency and the Nervous System: Beyond Metabolic Decompensation—Comparing Biological Models and Gaining New Insights into Molecular and Cellular Mechanisms
by Aimee Rachel Mathew, Giacomo Di Matteo, Piergiorgio La Rosa, Saviana Antonella Barbati, Luisa Mannina, Sandra Moreno, Ada Maria Tata, Virve Cavallucci and Marco Fidaleo
Int. J. Mol. Sci. 2024, 25(1), 590; https://doi.org/10.3390/ijms25010590 - 2 Jan 2024
Cited by 12 | Viewed by 10649
Abstract
Vitamin B12 (VitB12) is a micronutrient and acts as a cofactor for fundamental biochemical reactions: the synthesis of succinyl-CoA from methylmalonyl-CoA and biotin, and the synthesis of methionine from folic acid and homocysteine. VitB12 deficiency can determine a wide range of diseases, including [...] Read more.
Vitamin B12 (VitB12) is a micronutrient and acts as a cofactor for fundamental biochemical reactions: the synthesis of succinyl-CoA from methylmalonyl-CoA and biotin, and the synthesis of methionine from folic acid and homocysteine. VitB12 deficiency can determine a wide range of diseases, including nervous system impairments. Although clinical evidence shows a direct role of VitB12 in neuronal homeostasis, the molecular mechanisms are yet to be characterized in depth. Earlier investigations focused on exploring the biochemical shifts resulting from a deficiency in the function of VitB12 as a coenzyme, while more recent studies propose a broader mechanism, encompassing changes at the molecular/cellular levels. Here, we explore existing study models employed to investigate the role of VitB12 in the nervous system, including the challenges inherent in replicating deficiency/supplementation in experimental settings. Moreover, we discuss the potential biochemical alterations and ensuing mechanisms that might be modified at the molecular/cellular level (such as epigenetic modifications or changes in lysosomal activity). We also address the role of VitB12 deficiency in initiating processes that contribute to nervous system deterioration, including ROS accumulation, inflammation, and demyelination. Consequently, a complex biological landscape emerges, requiring further investigative efforts to grasp the intricacies involved and identify potential therapeutic targets. Full article
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