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Latest Multifactorial Developments on Neuropsychiatric Disorders and Manifestations

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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: 31 August 2024 | Viewed by 4335

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Special Issue Editor

Dr. Alin Ciobica

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Guest Editor

Department of Biology, Faculty of Biology, Alexandru Ioan Cuza University of Iasi, B dul Carol I, No. 11, 700506 Iasi, Romania
Interests: neuropsychiatry; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recently, related neuropsychiatric disorders such as depression and dementia have emerged and cause a huge disease burden. Over the past few decades, the understanding of neuropsychiatric disorders in the population has advanced to a new level. Many molecular mechanisms have been identified and progress has been made in developing prevention and treatment strategies. Considering that, lately, almost all the unidirectional theories referring to neuropsychiatric disorders/manifestations are basically dismissed and that there is an increased awareness of the multifactorial approach of this matter, this Special Issue focuses on understanding the multifactorial basics of these central disorders. This mainly refers but is not limited to: Alzheimer’s disease, Parkinson’s disease, schizophrenia, autism, anxiety, depression, traumatic brain injury, etc.

Dr. Alin Ciobica
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

multifactorial approach
biomarkers
oxidative stress
inflammation
Alzheimer’s disease
Parkinson’s disease
schizophrenia
autism
anxiety
depression
traumatic brain injury

Published Papers (4 papers)

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Research

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10 pages, 2005 KiB

Open AccessArticle

Hippocampal Upregulation of Complement Component C3 in Response to Lipopolysaccharide Stimuli in a Model of Fragile-X Syndrome

by Danielle Santana-Coelho and Joaquin N. Lugo

Curr. Issues Mol. Biol. 2023, 45(11), 9306-9315; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45110582 - 18 Nov 2023

Cited by 1 | Viewed by 747

Abstract

The complement system is part of the innate immune system and has been shown to be altered in autism spectrum disorder (ASD). Fragile-X syndrome (FXS) is the main genetic cause of ASD and studies suggest a dysregulation in the immune system in patients with the disorder. To assess if an animal model of FXS presents with altered complement signaling, we treated male Fmr1 knockout (KO) mice with lipopolysaccharide (LPS) and collected the hippocampus 24 h later. Assessment of the expression of the complement genes C1q, C3, and C4 identified the upregulation of C3 in both wild-type (WT) and knockout mice. Levels of C3 also increased in both genotypes. Analysis of the correlation between the expression of C3 and the cytokines IL-6, IL-1β, and TNF-α identified a different relationship between the expression of the genes in Fmr1 KO when compared to WT mice. Our findings did not support our initial hypotheses that the lack of the FMR1 gene would alter complement system signaling, and that the induction of the complement system in response to LPS in Fmr1 KO mice differed from wild-type conspecifics. Full article

(This article belongs to the Special Issue Latest Multifactorial Developments on Neuropsychiatric Disorders and Manifestations)

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17 pages, 6485 KiB

Open AccessArticle

Mitochondrial Dysfunction in Dopaminergic Neurons Derived from Patients with LRRK2- and SNCA-Associated Genetic Forms of Parkinson’s Disease

by Anna S. Vetchinova, Marina R. Kapkaeva, Mikhail V. Ivanov, Kristina A. Kutukova, Natalia M. Mudzhiri, Lydia E. Frumkina, Anatoly V. Brydun, Vladimir S. Sukhorukov and Sergey N. Illarioshkin

Curr. Issues Mol. Biol. 2023, 45(10), 8395-8411; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45100529 - 17 Oct 2023

Viewed by 1414

Abstract

Parkinson’s disease (PD) is the second most common neurodegenerative disease. Some cases of PD may be caused by genetic factors, among which mutations in the LRRK2 and SNCA genes play an important role. To develop effective neuroprotective strategies for PD, it is important to diagnose the disease at the earliest stages of the neurodegenerative process. Therefore, the detection of diagnostic and prognostic markers of Parkinson’s disease (PD) is an urgent medical need. Advances in induced pluripotent stem cell (iPSC) culture technology provide new opportunities for the search for new biomarkers of PD and its modeling in vitro. In our work, we used a new technology for multiplex profiling of gene expression using barcoding on the Nanostring platform to assess the activity of mitochondrial genes on iPSC-derived cultures of dopaminergic neurons obtained from patients with LRRK2- and SNCA-associated genetic forms PD and a healthy donor. Electron microscopy revealed ultrastructural changes in mitochondria in both LRRK2 and SNCA mutant cells, whereas mitochondria in cells from a healthy donor were normal. In a culture with the SNCA gene mutation, the ratio of the area occupied by mitochondria to the total area of the cytoplasm was significantly lower than in the control and in the line with the LRRK2 gene mutation. Transcriptome analysis of 105 mitochondria proteome genes using the Nanostring platform revealed differences between the diseased and normal cells in the activity of genes involved in respiratory complex function, the tricarboxylic acid cycle, ATP production, mitochondria–endoplasmic reticulum interaction, mitophagy, regulation of calcium concentration, and mitochondrial DNA replication. Full article

(This article belongs to the Special Issue Latest Multifactorial Developments on Neuropsychiatric Disorders and Manifestations)

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13 pages, 1228 KiB

Open AccessArticle

Association of OXTR, AVPR1a, LNPEP, and CD38 Genes’ Expression with the Clinical Presentation of Autism Spectrum Disorder

by Krzysztof Maria Wilczyński, Aleksandra Auguściak-Duma, Aleksandra Stasik, Lena Cichoń, Alicja Kawalec and Małgorzata Janas-Kozik

Curr. Issues Mol. Biol. 2023, 45(10), 8359-8371; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45100527 - 16 Oct 2023

Viewed by 969

Abstract

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder that affects social interactions, communication, and behavior. Although the predominant genetic predisposition to ASD seems beyond doubt, its exact nature remains unclear. In the context of social cognition disorders and the basis of ASD, the oxytocinergic and vasopresynergic systems arouse great interest among researchers. The aim of the present study was to analyze gene expression levels for oxytocin and vasopressin receptors, as well as CD38 protein and oxytocinase, in the context of the clinical picture of autism spectrum disorders. The study included 90 people, of whom 63 were diagnosed with ASD based on anamnesis, mental status testing, and the ADOS-2 protocol. The results obtained in the presented study indicate that the balance between the levels of expression of the CD38 gene and the oxytocinase gene plays a key role in the risk and clinical presentation of ASD. In a hypothetical scenario, an imbalance in the expression of CD38 and LNPEP could potentially lead to alterations in the concentrations of oxytocin and vasopressin. At the same time, the most frequently studied genes—AVPR1a and OXTR—seem to be at best of marginal importance for the risk of ASD. Full article

(This article belongs to the Special Issue Latest Multifactorial Developments on Neuropsychiatric Disorders and Manifestations)

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9 pages, 1846 KiB

Open AccessBrief Report

A Novel Mutation in Sacsin, p.Val1335IIe, May Cause Late-Onset Sacsinopathy Due to Haploinsufficiency

by Danyeong Kim, Nayoung Ryoo, Young Ho Park, Eva Bagyinszky, Seong Soo Alexander An and SangYun Kim

Curr. Issues Mol. Biol. 2023, 45(12), 9917-9925; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45120619 - 09 Dec 2023

Viewed by 730

Abstract

Autosomal recessive spastic ataxia in Charlevoix-Saguenay (ARSACS) is a neurodegenerative disorder caused by mutations in the sacsin molecular chaperone protein (SACS) gene. Since the first report from Quebec in 1978, many pathogenic ARSACS variants with significantly reduced chaperone activities have been reported worldwide in adolescents, with presumably altered protein folding. In this study, a novel SACS mutation (p.Val1335IIe, Heterozygous) was identified in a Korean patient in their 50s with late-onset ARSACS characterized by cerebellar ataxia and spasticity without peripheral neuropathy. The mutation was confirmed via whole exome sequencing and Sanger sequencing and was predicted to likely cause disease using prediction software. RT-PCR and ELISA showed decreased SACS mRNA expression and sacsin protein concentrations in the proband, supporting its implications in diseases with pathogenicity and reduced chaperone function from haploinsufficiency. Our results revealed the pathogenicity of the SACS Val1335IIe mutation in the proband patient’s disease manifestation, even though the symptoms had a limited correlation with the typical ARSACS clinical triad, which could be due to the reduced chaperon function from haploinsufficiency. Furthermore, our study suggests that variants of SACS heterozygosity may have diverse symptoms, with a wide range of disease onsets for late-onset sacsinopathy. Full article

(This article belongs to the Special Issue Latest Multifactorial Developments on Neuropsychiatric Disorders and Manifestations)

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