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Pathogenesis of Diseases of the Central Nervous System 2.0

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 18387

Special Issue Editors


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Guest Editor
Department of Physiology, Faculty of Health Sciences (Ceuta), University of Granada, 51001 Ceuta, Spain
Interests: molecular neurobiology; brain pathology; diabetic; Alzheimer’s disease
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Cell Biology, Faculty of Biology, University of Seville, 41012 Seville, Spain
Interests: cell biology; molecular neurobiology; nutrition

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue “Pathogenesis of Diseases of the Central Nervous System”.

Physiology disbalance and pathogenesis of the central nervous system play important roles in quality of life and aging. In this sense, determining the pathways followed by the different pathologies of central nervous system diseases is crucial to prevent and treat them. This Special Issue is focused on the pathogenesis of diseases of the central nervous system, and includes original works on aspects related to the molecular mechanisms of physical and chemical insults, neuronal excitotoxicity, neuronal dysfunction, Alzheimer’s disease, dementia, Parkinson's disease, amyotrophic lateral sclerosis, ischemia, nephropathy, brain atrophies, acute injuries, neurogenesis, and central nervous system treatments, among others. This Special Issue will publish original research articles as well as mini and full reviews, including perspectives in the field on the current understanding of molecular mechanisms involved in the pathogenesis of diseases of the central nervous system. Manuscripts on molecular mechanisms, ideas for new therapies or techniques for diagnosis, and treatment of diseases of the central nervous system are welcome.

Dr. Juan José Ramos-Rodríguez
Prof. Dr. Beatriz Bermudez
Guest Editors

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Related Special Issue

Published Papers (5 papers)

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Research

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14 pages, 1770 KiB  
Communication
Trimethylamine N-Oxide as a Mediator Linking Peripheral to Central Inflammation: An In Vitro Study
by Manuel H. Janeiro, Maite Solas, Josune Orbe, Jose A. Rodríguez, Leyre Sanchez de Muniain, Paula Escalada, Ping K. Yip and Maria J. Ramirez
Int. J. Mol. Sci. 2023, 24(24), 17557; https://doi.org/10.3390/ijms242417557 - 16 Dec 2023
Cited by 4 | Viewed by 1627
Abstract
In this study, the plausible role of trimethylamine N-oxide (TMAO), a microbiota metabolite, was investigated as a link between peripheral inflammation and the inflammation of the central nervous system using different cell lines. TMAO treatment favored the differentiation of adipocytes from preadipocytes (3T3-L1 [...] Read more.
In this study, the plausible role of trimethylamine N-oxide (TMAO), a microbiota metabolite, was investigated as a link between peripheral inflammation and the inflammation of the central nervous system using different cell lines. TMAO treatment favored the differentiation of adipocytes from preadipocytes (3T3-L1 cell line). In macrophages (RAW 264.7 cell line), which infiltrate adipose tissue in obesity, TMAO increased the expression of pro-inflammatory cytokines. The treatment with 200 μM of TMAO seemed to disrupt the blood–brain barrier as it induced a significant decrease in the expression of occludin in hCMECs. TMAO also increased the expression of pro-inflammatory cytokines in primary neuronal cultures, induced a pro-inflammatory state in primary microglial cultures, and promoted phagocytosis. Data obtained from this project suggest that microbial dysbiosis and increased TMAO secretion could be a key link between peripheral and central inflammation. Thus, TMAO-decreasing compounds may be a promising therapeutic strategy for neurodegenerative diseases. Full article
(This article belongs to the Special Issue Pathogenesis of Diseases of the Central Nervous System 2.0)
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Review

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13 pages, 931 KiB  
Review
Interaction between Oligodendrocytes and Interneurons in Brain Development and Related Neuropsychiatric Disorders
by Yingqi Liu, Jie Yuan, Yuhao Dong, Sufang Jiang, Ming Zhang and Xianghui Zhao
Int. J. Mol. Sci. 2024, 25(7), 3620; https://doi.org/10.3390/ijms25073620 - 23 Mar 2024
Cited by 2 | Viewed by 1865
Abstract
A variety of neurological and psychiatric disorders have recently been shown to be highly associated with the abnormal development and function of oligodendrocytes (OLs) and interneurons. OLs are the myelin-forming cells in the central nervous system (CNS), while interneurons are important neural types [...] Read more.
A variety of neurological and psychiatric disorders have recently been shown to be highly associated with the abnormal development and function of oligodendrocytes (OLs) and interneurons. OLs are the myelin-forming cells in the central nervous system (CNS), while interneurons are important neural types gating the function of excitatory neurons. These two types of cells are of great significance for the establishment and function of neural circuits, and they share similar developmental origins and transcriptional architectures, and interact with each other in multiple ways during development. In this review, we compare the similarities and differences in these two cell types, providing an important reference and further revealing the pathogenesis of related brain disorders. Full article
(This article belongs to the Special Issue Pathogenesis of Diseases of the Central Nervous System 2.0)
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13 pages, 3113 KiB  
Review
Distinctive Patterns of 5-Methylcytosine and 5-Hydroxymethylcytosine in Schizophrenia
by Jiaxiang Xie, Yang Wang, Changcheng Ye, Xiao-Jiang Li and Li Lin
Int. J. Mol. Sci. 2024, 25(1), 636; https://doi.org/10.3390/ijms25010636 - 4 Jan 2024
Viewed by 1757
Abstract
Schizophrenia is a highly heritable neuropsychiatric disorder characterized by cognitive and social dysfunction. Genetic, epigenetic, and environmental factors are together implicated in the pathogenesis and development of schizophrenia. DNA methylation, 5-methycytosine (5mC) and 5-hydroxylcytosine (5hmC) have been recognized as key epigenetic elements in [...] Read more.
Schizophrenia is a highly heritable neuropsychiatric disorder characterized by cognitive and social dysfunction. Genetic, epigenetic, and environmental factors are together implicated in the pathogenesis and development of schizophrenia. DNA methylation, 5-methycytosine (5mC) and 5-hydroxylcytosine (5hmC) have been recognized as key epigenetic elements in neurodevelopment, ageing, and neurodegenerative diseases. Recently, distinctive 5mC and 5hmC pattern and expression changes of related genes have been discovered in schizophrenia. Antipsychotic drugs that affect 5mC status can alleviate symptoms in patients with schizophrenia, suggesting a critical role for DNA methylation in the pathogenesis of schizophrenia. Further exploring the signatures of 5mC and 5hmC in schizophrenia and developing precision-targeted epigenetic drugs based on this will provide new insights into the diagnosis and treatment of schizophrenia. Full article
(This article belongs to the Special Issue Pathogenesis of Diseases of the Central Nervous System 2.0)
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34 pages, 2020 KiB  
Review
Frontotemporal Dementia, Where Do We Stand? A Narrative Review
by Annibale Antonioni, Emanuela Maria Raho, Piervito Lopriore, Antonia Pia Pace, Raffaela Rita Latino, Martina Assogna, Michelangelo Mancuso, Daniela Gragnaniello, Enrico Granieri, Maura Pugliatti, Francesco Di Lorenzo and Giacomo Koch
Int. J. Mol. Sci. 2023, 24(14), 11732; https://doi.org/10.3390/ijms241411732 - 21 Jul 2023
Cited by 27 | Viewed by 10848
Abstract
Frontotemporal dementia (FTD) is a neurodegenerative disease of growing interest, since it accounts for up to 10% of middle-age-onset dementias and entails a social, economic, and emotional burden for the patients and caregivers. It is characterised by a (at least initially) selective degeneration [...] Read more.
Frontotemporal dementia (FTD) is a neurodegenerative disease of growing interest, since it accounts for up to 10% of middle-age-onset dementias and entails a social, economic, and emotional burden for the patients and caregivers. It is characterised by a (at least initially) selective degeneration of the frontal and/or temporal lobe, generally leading to behavioural alterations, speech disorders, and psychiatric symptoms. Despite the recent advances, given its extreme heterogeneity, an overview that can bring together all the data currently available is still lacking. Here, we aim to provide a state of the art on the pathogenesis of this disease, starting with established findings and integrating them with more recent ones. In particular, advances in the genetics field will be examined, assessing them in relation to both the clinical manifestations and histopathological findings, as well as considering the link with other diseases, such as amyotrophic lateral sclerosis (ALS). Furthermore, the current diagnostic criteria will be explored, including neuroimaging methods, nuclear medicine investigations, and biomarkers on biological fluids. Of note, the promising information provided by neurophysiological investigations, i.e., electroencephalography and non-invasive brain stimulation techniques, concerning the alterations in brain networks and neurotransmitter systems will be reviewed. Finally, current and experimental therapies will be considered. Full article
(This article belongs to the Special Issue Pathogenesis of Diseases of the Central Nervous System 2.0)
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Other

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6 pages, 2223 KiB  
Case Report
Atypical Intraparenchymal Meningioma with YAP1-MAML2 Fusion in a Young Adult Male: A Case Report and Mini Literature Review
by Alisa Nobee, Mei Xu, Anjali Seth and Yuan Rong
Int. J. Mol. Sci. 2023, 24(16), 12814; https://doi.org/10.3390/ijms241612814 - 15 Aug 2023
Cited by 4 | Viewed by 1577
Abstract
Oncogenic Yes-associated protein (YAP) 1 fusions have been recently identified in several cases of meningioma mostly involving pediatric patients. The meningiomas harboring YAP1-MAML2, which is the most frequent fusion subtype, exhibit activated YAP1 signaling and share similarities with NF2 (neurofibromatosis type 2 gene) [...] Read more.
Oncogenic Yes-associated protein (YAP) 1 fusions have been recently identified in several cases of meningioma mostly involving pediatric patients. The meningiomas harboring YAP1-MAML2, which is the most frequent fusion subtype, exhibit activated YAP1 signaling and share similarities with NF2 (neurofibromatosis type 2 gene) mutant meningiomas. We reported a rare case of atypical intraparenchymal meningioma with YAP1-MAML2 fusion in a 20-year-old male. The patient presented with an episode of seizure without a medical history. MRI revealed a lesion in the right temporal lobe without extra-axial involvement. The radiological and morphological findings, however, were indistinctive from other intracranial diseases, e.g., vascular malformation and glioma. Immunohistochemical results confirmed the presence of abundant meningothelial cells in the tumor and indicated brain invasion, supporting the diagnosis of atypical intraparenchymal meningioma. Targeted RNA fusion analysis further identified a YAP1-MAML2 rearrangement in the tumor. Non-dural-based intraparenchymal meningiomas are uncommon, and the careful selection of specific tumor markers is crucial for an accurate diagnosis. Additionally, the detection of the fusion gene provides valuable insights into the oncogenic mechanism of meningioma. Full article
(This article belongs to the Special Issue Pathogenesis of Diseases of the Central Nervous System 2.0)
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