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Latest Multifactorial Developments on Neuropsychiatric Disorders and Manifestations
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Latest Multifactorial Developments on Neuropsychiatric Disorders and Manifestations

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: closed (31 August 2024) | Viewed by 8519

Special Issue Editor

Dr. Alin Ciobica

E-Mail Website
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

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Keywords

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

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Published Papers (5 papers)

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Research

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10 pages, 2005 KiB  
Article
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://doi.org/10.3390/cimb45110582 - 18 Nov 2023
Cited by 1 | Viewed by 1140
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 [...] Read more.
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  
Article
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://doi.org/10.3390/cimb45100529 - 17 Oct 2023
Cited by 1 | Viewed by 2061
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 [...] Read more.
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  
Article
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://doi.org/10.3390/cimb45100527 - 16 Oct 2023
Viewed by 1442
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, [...] Read more.
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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Review

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17 pages, 1328 KiB  
Review
Structural Variations of Prions and Prion-like Proteins Associated with Neurodegeneration
by Carter Sky Christensen, Sean Wang, Wenshu Li, Danyang Yu and Henry James Li
Curr. Issues Mol. Biol. 2024, 46(7), 6423-6439; https://doi.org/10.3390/cimb46070384 - 26 Jun 2024
Cited by 1 | Viewed by 1804
Abstract
Neurodegeneration is becoming one of the leading causes of death worldwide as the population expands and grows older. There is a growing desire to understand the mechanisms behind prion proteins as well as the prion-like proteins that make up neurodegenerative diseases (NDs), including [...] Read more.
Neurodegeneration is becoming one of the leading causes of death worldwide as the population expands and grows older. There is a growing desire to understand the mechanisms behind prion proteins as well as the prion-like proteins that make up neurodegenerative diseases (NDs), including Alzheimer’s disease (AD) and Parkinson’s disease (PD). Both amyloid-β (Aβ) and hyperphosphorylated tau (p-tau) proteins behave in ways similar to those of the infectious form of the prion protein, PrPSc, such as aggregating, seeding, and replicating under not yet fully understood mechanisms, thus the designation of prion-like. This review aims to highlight the shared mechanisms between prion-like proteins and prion proteins in the structural variations associated with aggregation and disease development. These mechanisms largely focus on the dysregulation of protein homeostasis, self-replication, and protein aggregation, and this knowledge could contribute to diagnoses and treatments for the given NDs. Full article
(This article belongs to the Special Issue Latest Multifactorial Developments on Neuropsychiatric Disorders and Manifestations)
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Other

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9 pages, 1846 KiB  
Brief 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://doi.org/10.3390/cimb45120619 - 9 Dec 2023
Cited by 1 | Viewed by 1222
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 [...] Read more.
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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