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Metabolism and Molecular Pathology Related Features in Neurological Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 4374

Special Issue Editor


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Guest Editor
Department of Biochemistry and Molecular Biomedicine, University of Barcelona, Diagonal 643, Prevosti Building, 08028 Barcelona, Spain
Interests: neuroprotection; neurodegeneration; Alzheimer's disease; Parkinson's disease; G protein coupled receptors (GPCR); microglia; hormesis; antioxidant; neuroimmunology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue provides a focused exploration of the biochemical hallmarks underlying metabolic dysregulation in neurological disorders. Researchers have delved deeper into the intricate molecular mechanisms that link metabolism to the pathology of neurological diseases such as Alzheimer's, Parkinson's and amyotrophic lateral sclerosis. From this perspective, research is uncovering key molecular events such as alteration of mitochondrial metabolism, oxidative stress, protein aggregation and neuroinflammation. By unraveling the molecular complexities of metabolic alterations, this Special Issue aims to provide insights into the pathogenesis of neurological disorders while striving to identify potential molecular targets for therapeutic intervention. The field is ripe for innovative molecular-based approaches to diagnosis and treatment. Through a rigorous examination of molecular pathways, this Special Issue will advance our understanding of the molecular foundations of neurological diseases, providing a basis to guide future translational research.

Prof. Dr. Rafael Franco
Guest Editor

Manuscript Submission Information

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Keywords

  • metabolic dysregulation
  • neurological disorders
  • Alzheimer's disease
  • Parkinson's disease
  • neuroinflammation

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Published Papers (3 papers)

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Research

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18 pages, 4458 KiB  
Article
Genetics and Traumatic Brain Injury: Findings from an Exome-Based Study of a 50-Patient Case Series
by Alesya S. Gracheva, Darya A. Kashatnikova, Ivan V. Redkin, Vladislav E. Zakharchenko, Artem N. Kuzovlev and Lyubov E. Salnikova
Curr. Issues Mol. Biol. 2024, 46(9), 10351-10368; https://doi.org/10.3390/cimb46090616 - 17 Sep 2024
Viewed by 878
Abstract
Traumatic brain injury (TBI) is the leading cause of global mortality and morbidity. Because TBI is accident-related, the role of genetics in predisposing to TBI has been largely unexplored. However, the likelihood of injury may not be entirely random and may be associated [...] Read more.
Traumatic brain injury (TBI) is the leading cause of global mortality and morbidity. Because TBI is accident-related, the role of genetics in predisposing to TBI has been largely unexplored. However, the likelihood of injury may not be entirely random and may be associated with certain physical and mental characteristics. In this study, we analyzed the exomes of 50 patients undergoing rehabilitation after TBI. Patients were divided into three groups according to rehabilitation outcome: improvement, no change, and deterioration/death. We focused on rare, potentially functional missense and high-impact variants in genes intolerant to these variants. The concordant results from the three independent groups of patients allowed for the suggestion of the existence of a genetic predisposition to TBI, associated with rare functional variations in intolerant genes, with a prevalent dominant mode of inheritance and neurological manifestations in the genetic phenotypes according to the OMIM database. Forty-four of the 50 patients had one or more rare, potentially deleterious variants in one or more neurological genes. Comparison of these results with those of a 50-sampled matched non-TBI cohort revealed significant differences: P = 2.6 × 10−3, OR = 4.89 (1.77–13.47). There were no differences in the distribution of the genes of interest between the TBI patient groups. Our exploratory study provides new insights into the impact of genetics on TBI risk and is the first to address potential genetic susceptibility to TBI. Full article
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13 pages, 6416 KiB  
Article
Evaluation of the Therapeutical Effect of Matricaria Chamomilla Extract vs. Galantamine on Animal Model Memory and Behavior Using 18F-FDG PET/MRI
by Roxana Iacob, Matei Palimariciuc, Tudor Florea, Cosmin Vasilica Pricope, Cristina Mariana Uritu, Bogdan Ionel Tamba, Teodor Marian Ionescu, Cati Raluca Stolniceanu, Wael Jalloul, Romeo Petru Dobrin, Lucian Hritcu, Oana Cioanca, Monica Hancianu, Alexandru Gratian Naum and Cipriana Stefanescu
Curr. Issues Mol. Biol. 2024, 46(5), 4506-4518; https://doi.org/10.3390/cimb46050273 - 9 May 2024
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Abstract
The memory-enhancing activity of Matricaria chamomilla hydroalcoholic extract (MCE) is already being investigated by behavioral and biochemical assays in scopolamine-induced amnesia rat models, while the effects of scopolamine (Sco) on cerebral glucose metabolism are examined as well. Nevertheless, the study of the metabolic [...] Read more.
The memory-enhancing activity of Matricaria chamomilla hydroalcoholic extract (MCE) is already being investigated by behavioral and biochemical assays in scopolamine-induced amnesia rat models, while the effects of scopolamine (Sco) on cerebral glucose metabolism are examined as well. Nevertheless, the study of the metabolic profile determined by an enriched MCE has not been performed before. The present experiments compared metabolic quantification in characteristic cerebral regions and behavioral characteristics for normal, only diseased, diseased, and MCE- vs. Galantamine (Gal)-treated Wistar rats. A memory deficit was induced by four weeks of daily intraperitoneal Sco injection. Starting on the eighth day, the treatment was intraperitoneally administered 30 min after Sco injection for a period of three weeks. The memory assessment comprised three maze tests. Glucose metabolism was quantified after the 18F-FDG PET examination. The right amygdala, piriform, and entorhinal cortex showed the highest differential radiopharmaceutical uptake of the 50 regions analyzed. Rats treated with MCE show metabolic similarity with normal rats, while the Gal-treated group shows features closer to the diseased group. Behavioral assessments evidenced a less anxious status and a better locomotor activity manifested by the MCE-treated group compared to the Gal-treated group. These findings prove evident metabolic ameliorative qualities of MCE over Gal classic treatment, suggesting that the extract could be a potent neuropharmacological agent against amnesia. Full article
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Review

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16 pages, 672 KiB  
Review
Muscarinic Receptors and Alzheimer’s Disease: New Perspectives and Mechanisms
by Martina Monaco, Hanna Trebesova and Massimo Grilli
Curr. Issues Mol. Biol. 2024, 46(7), 6820-6835; https://doi.org/10.3390/cimb46070407 - 2 Jul 2024
Viewed by 2102
Abstract
Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative diseases on a global scale. Historically, this pathology has been linked to cholinergic transmission, and despite the scarcity of effective therapies, numerous alternative processes and targets have been proposed as potential avenues for [...] Read more.
Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative diseases on a global scale. Historically, this pathology has been linked to cholinergic transmission, and despite the scarcity of effective therapies, numerous alternative processes and targets have been proposed as potential avenues for comprehending this complex illness. Nevertheless, the fundamental pathophysiological mechanisms underpinning AD remain largely enigmatic, with a growing body of evidence advocating for the significance of muscarinic receptors in modulating the brain’s capacity to adapt and generate new memories. This review summarizes the current state of the art in the field of muscarinic receptors’ involvement in AD. A specific key factor was the relationship between comorbidity and the emergence of new mechanisms. Full article
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