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State-of-the-Art Molecular Neurobiology in Poland

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: 31 December 2024 | Viewed by 12518

Special Issue Editor


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Guest Editor
Department of Brain Biochemistry, Maj Institute of Pharmacology of the Polish Academy of Sciences, Smętna 12, 31-343 Krakow, Poland
Interests: neuroscience; neuropharmacology; stress-related disorders; depression; psychotropic drugs; GPCR signaling; noradrenergic system; neuroplasticity, neuroimmune interaction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to provide a comprehensive overview of recent advances in molecular neurobiology in Poland by inviting contributions from Poland research institutes/laboratories that consolidate our understanding of this area. Topics include, but are not limited to, the following:

  • Neurobiology
  • Neurochemistry
  • Neuropathology
  • Neurophysiology
  • Neuropharmacology
  • Neurogenetics
  • Neurodegeneration
  • Aging Neuroscience
  • Neurogenesis
  • Neuroplasticity
  • Signalling pathways and networks
  • Systems biology
  • Stress-related processes

Prof. Dr. Irena Nalepa
Guest Editor

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Keywords

  • neurobiology

  • neurochemistry
  • neuropathology
  • neurophysiology
  • neuropharmacology
  • neurogenetics
  • neurodegeneration
  • aging neuroscience
  • neurogenesis
  • neuroplasticity
  • signalling pathways
  • signalling networks
  • systems biology
  • stress-related processes

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Published Papers (5 papers)

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Research

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15 pages, 1129 KiB  
Article
Longitudinal Changes in BDNF and MMP-9 Protein Plasma Levels in Children after Cochlear Implantation
by Monika Matusiak, Dominika Oziębło, Monika Ołdak, Emilia Rejmak, Leszek Kaczmarek and Henryk Skarżyński
Int. J. Mol. Sci. 2023, 24(4), 3714; https://doi.org/10.3390/ijms24043714 - 13 Feb 2023
Cited by 1 | Viewed by 1722
Abstract
Congenitally deaf children who undergo cochlear implantation before 1 year of age develop their auditory skills faster than children who are implanted later. In this longitudinal study, a cohort of 59 implanted children were divided into two subgroups according to their ages at [...] Read more.
Congenitally deaf children who undergo cochlear implantation before 1 year of age develop their auditory skills faster than children who are implanted later. In this longitudinal study, a cohort of 59 implanted children were divided into two subgroups according to their ages at implantation—below or above 1 year old—and the plasma levels of matrix metalloproteinase-9 (MMP-9), brain-derived neurotrophic factor (BDNF), and pro-BDNF were measured at 0, 8, and 18 months after cochlear implant activation, while auditory development was simultaneously evaluated using the LittlEARs Questionnaire (LEAQ). A control group consisted of 49 age-matched healthy children. We identified statistically higher BDNF levels at 0 months and at the 18-month follow-ups in the younger subgroup compared to the older one and lower LEAQ scores at 0 months in the younger subgroup. Between the subgroups, there were significant differences in the changes in BDNF levels from 0 to 8 months and in LEAQ scores from 0 to 18 months. The MMP-9 levels significantly decreased from 0 to 18 months and from 0 to 8 months in both subgroups and from 8 to 18 months only in the older one. For all measured protein concentrations, significant differences were identified between the older study subgroup and the age-matched control group. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Poland)
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13 pages, 3482 KiB  
Article
Changes in T-Cell Subpopulations and Cytokine Levels in Patients with Treatment-Resistant Depression—A Preliminary Study
by Łukasz Piotr Szałach, Wiesław Jerzy Cubała and Katarzyna Aleksandra Lisowska
Int. J. Mol. Sci. 2023, 24(1), 479; https://doi.org/10.3390/ijms24010479 - 28 Dec 2022
Cited by 4 | Viewed by 2407
Abstract
Although there is some evidence for the involvement of cytokines and T cells in the pathophysiology of treatment-resistant depression (TRD), the nature of this relationship is not entirely clear. Therefore, we compared T-cell subpopulations and serum cytokine levels in TRD patients to find [...] Read more.
Although there is some evidence for the involvement of cytokines and T cells in the pathophysiology of treatment-resistant depression (TRD), the nature of this relationship is not entirely clear. Therefore, we compared T-cell subpopulations and serum cytokine levels in TRD patients to find relationships between their immunological profiles, clinical presentation, and episode severity. Blood samples from TRD patients (n = 20) and healthy people (n = 13) were collected and analyzed by flow cytometry. We analyzed the percentages of helper and cytotoxic T cells according to the expression of selected activation markers, including CD28, CD69, CD25, CD95, and HLA-DR. The serum levels of inflammatory cytokines IL12p70, TNF-α, IL-10, IL-6, IL-1β, and IL-8 were also determined. TRD patients had a lower percentage of CD3+CD4+CD25+ and CD3+CD8+CD95+ cells than healthy people. They also had lower serum levels of IL-12p70 and TNF-α, whereas IL-8 levels were significantly higher. Receiver operating characteristic (ROC) analysis demonstrated that serum IL-8 values above 19.55 pg/mL were associated with a 10.26 likelihood ratio of developing TRD. No connections were found between the MADRS score and immunological parameters. These results show that TRD patients have reduced percentages of T cells expressing activation antigens (CD25 and CD95) and higher serum concentrations of proinflammatory and chemotactic IL-8. These changes may indicate reduced activity of the immune system and the important role of IL-8 in maintaining chronic inflammation in the course of depression. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Poland)
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21 pages, 11944 KiB  
Article
GABAergic and Glutamatergic Phenotypes of Neurons Expressing Calcium-Binding Proteins in the Preoptic Area of the Guinea Pig
by Krystyna Bogus-Nowakowska, Anna Robak, Daniel Kalinowski, Anna Kozłowska and Maciej Równiak
Int. J. Mol. Sci. 2022, 23(14), 7963; https://doi.org/10.3390/ijms23147963 - 19 Jul 2022
Cited by 2 | Viewed by 2319
Abstract
The mammalian preoptic area (POA) has large populations of calbindin (CB), calretinin (CR) and parvalbumin (PV) neurons, but phenotypes of these cells are unknown. Therefore, the question is whether neurons expressing CB, CR, and/or PV are GABAergic or glutamatergic. Double-immunofluorescence staining followed by [...] Read more.
The mammalian preoptic area (POA) has large populations of calbindin (CB), calretinin (CR) and parvalbumin (PV) neurons, but phenotypes of these cells are unknown. Therefore, the question is whether neurons expressing CB, CR, and/or PV are GABAergic or glutamatergic. Double-immunofluorescence staining followed by epifluorescence and confocal microscopy was used to determine the coexpression patterns of CB, CR and PV expressing neurons with vesicular GABA transporters (VGAT) as specific markers of GABAergic neurons and vesicular glutamate transporters (VGLUT 2) as specific markers of glutamatergic neurons. The guinea pig was adopted as, like humans, it has a reproductive cycle with a true luteal phase and a long gestation period. The results demonstrated that in the guinea pig POA of both sexes, ~80% of CB+ and ~90% of CR+ neurons coexpress VGAT; however, one-fifth of CB+ neurons and one-third of CR+ cells coexpress VGLUT. About two-thirds of PV+ neurons express VGAT, and similar proportion of them coexpress VGLUT. Thus, many CB+, CR+ and PV+ neurons may be exclusively GABAergic (VGAT-expressing cells) or glutamatergic (VGLUT-expressing cells); however, at least a small fraction of CR+ cells and at least one-third of PV+ cells are likely neurons with a dual GABA/glutamate phenotype that may coexpress both transporters. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Poland)
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Review

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14 pages, 578 KiB  
Review
Autism Spectrum Disorder Pathogenesis—A Cross-Sectional Literature Review Emphasizing Molecular Aspects
by Agata Horecka-Lewitowicz, Wojciech Lewitowicz, Monika Wawszczak-Kasza, Hyebin Lim and Piotr Lewitowicz
Int. J. Mol. Sci. 2024, 25(20), 11283; https://doi.org/10.3390/ijms252011283 - 20 Oct 2024
Viewed by 1074
Abstract
The etiology of autism spectrum disorder (ASD) has not yet been completely elucidated. Through time, multiple attempts have been made to uncover the causes of ASD. Different theories have been proposed, such as being caused by alterations in the gut–brain axis with an [...] Read more.
The etiology of autism spectrum disorder (ASD) has not yet been completely elucidated. Through time, multiple attempts have been made to uncover the causes of ASD. Different theories have been proposed, such as being caused by alterations in the gut–brain axis with an emphasis on gut dysbiosis, post-vaccine complications, and genetic or even autoimmune causes. In this review, we present data covering the main streams that focus on ASD etiology. Data collection occurred in many countries covering ethnically diverse subjects. Moreover, we aimed to show how the progress in genetic techniques influences the explanation of medical White Papers in the ASD area. There is no single evidence-based pathway that results in symptoms of ASD. Patient management has constantly only been symptomatic, and there is no ASD screening apart from symptom-based diagnosis and parent-mediated interventions. Multigene sequencing or epigenetic alterations hold promise in solving the disjointed molecular puzzle. Further research is needed, especially in the field of biogenetics and metabolomic aspects, because young children constitute the patient group most affected by ASD. In summary, to date, molecular research has confirmed multigene dysfunction as the causative factor of ASD, the multigene model with metabolomic influence would explain the heterogeneity in ASD, and it is proposed that ion channel dysfunction could play a core role in ASD pathogenesis. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Poland)
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15 pages, 1563 KiB  
Review
The Downstaging Concept in Treatment-Resistant Depression: Spotlight on Ketamine
by Alina Wilkowska and Wiesław Jerzy Cubała
Int. J. Mol. Sci. 2022, 23(23), 14605; https://doi.org/10.3390/ijms232314605 - 23 Nov 2022
Cited by 12 | Viewed by 3876
Abstract
Treatment-resistant depression is a pleomorphic phenomenon occurring in 30% of patients with depression. The chance to achieve remission decreases with every subsequent episode. It constitutes a significant part of the global disease burden, causes increased morbidity and mortality, and is associated with poor [...] Read more.
Treatment-resistant depression is a pleomorphic phenomenon occurring in 30% of patients with depression. The chance to achieve remission decreases with every subsequent episode. It constitutes a significant part of the global disease burden, causes increased morbidity and mortality, and is associated with poor quality of life. It involves multiple difficult-to-treat episodes, with increasing resistance over time. The concept of staging captures the process of changes causing increasing treatment resistance and global worsening of functioning in all areas of life. Ketamine is a novel rapid-acting antidepressant with neuroplastic potential. Here, we argue that ketamine use as an add-on treatment of resistant major depressive disorder, based on its unique pharmacological properties, can reverse this process, give hope to patients, and prevent therapeutic nihilism. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Neurobiology in Poland)
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