Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.3
5.5
Journals
Biomolecules
Special Issues
Recent Advances in Neuropharmacology and Brain Physiology
share announcement

Recent Advances in Neuropharmacology and Brain Physiology

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 8302

Special Issue Editor

Prof. Alexander V. Kulikov

E-Mail Website
Guest Editor
Head of Department of Genetic Models of Neurological Disorders, Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, Novosibirsk 630090, Russia
Interests: serotonin, STEP, behavior, neurogenomics, behavioral genetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The main aim of this Special Issue is to highlight recent promising ideas regarding molecular mechanisms of mental disorders, as well as new molecular targets for new classes of psychotropic drugs. Original articles and reviews on the following emerging areas are welcome:

- Molecular aspects of the brain and intestinal microbiotic interaction;
- Relationship of microbiota imbalance with the risk of psychopathologies;
- Treatment of some psychopathologies with prebiotics;
- Molecular mechanisms linking psychopathologies with obesity and general metabolism disorders;
- Molecules of intracellular signal transduction (for example STEP) as potential targets for new psychotropic drugs;
- Neurotrophins in the therapy of neurological and mental disorders;
- Glutamate receptors as potential targets for new antidepressant drugs;
- Molecular mechanism by which some mutations increase the risk of psychopathologies and resistance to psychotropic drugs treatment;
- Pharmacological chaperones in the correction of hereditary mental disorders caused by biomolecule misfolding.

Prof. Alexander V. Kulikov
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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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

  • psychiatric disorders 
  • molecular mechanism of neuropathologies 
  • brain and microbiota interaction 
  • pharmacological chaperones 
  • STEP 
  • neurotrophins

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

15 pages, 2100 KiB  
Article
Effects of the Combination of the C1473G Mutation in the Tph2 Gene and Lethal Yellow Mutations in the Raly-Agouti Locus on Behavior, Brain 5-HT and Melanocortin Systems in Mice
by Polyna D. Komleva, Ghofran Alhalabi, Arseniy E. Izyurov, Nikita V. Khotskin and Alexander V. Kulikov
Biomolecules 2023, 13(6), 963; https://doi.org/10.3390/biom13060963 - 08 Jun 2023
Cited by 1 | Viewed by 921
Abstract
Tryptophan hydroxylase 2 (TPH2) is the key and rate-limited enzyme of serotonin (5-HT) synthesis in the brain. The C1473G mutation in the Tph2 gene results in a two-fold decrease in enzyme activity in the mouse brain. The lethal yellow (AY) [...] Read more.
Tryptophan hydroxylase 2 (TPH2) is the key and rate-limited enzyme of serotonin (5-HT) synthesis in the brain. The C1473G mutation in the Tph2 gene results in a two-fold decrease in enzyme activity in the mouse brain. The lethal yellow (AY) mutation in the Raly-Agouti locus results in the overexpression of the Agouti gene in the brain and causes obesity and depressive-like behavior in mice. Herein, the possible influences of these mutations and their combination on body mass, behavior, brain 5-HT and melanocortin systems in mice of the B6-1473CC/aa. B6-1473CC/AYa, B6-1473GG/aa are investigated. B6-1473GG/AYa genotypes were studied. The 1473G and AY alleles increase the activity of TPH2 and the expression of the Agouti gene, respectively, but they do not alter 5-HT and 5-HIAA levels or the expression of the genes Tph2, Maoa, Slc6a4, Htr1a, Htr2a, Mc3r and Mc4r in the brain. The 1473G allele attenuates weight gain and depressive-like immobility in the forced swim test, while the AY allele increases body weight gain and depressive-like immobility. The combination of these alleles results in hind limb dystonia in the B6-1473GG/AYa mice. This is the first evidence for the interaction between the C1473G and AY mutations. Full article
(This article belongs to the Special Issue Recent Advances in Neuropharmacology and Brain Physiology)
►▼ Show Figures

Figure 1

14 pages, 835 KiB  
Article
Relationship between Brain-Derived Neurotrophic Factor and Cognitive Decline in Patients with Mild Cognitive Impairment and Dementia
by Matea Nikolac Perkovic, Fran Borovecki, Igor Filipcic, Barbara Vuic, Tina Milos, Gordana Nedic Erjavec, Marcela Konjevod, Lucija Tudor, Ninoslav Mimica, Suzana Uzun, Oliver Kozumplik, Dubravka Svob Strac and Nela Pivac
Biomolecules 2023, 13(3), 570; https://doi.org/10.3390/biom13030570 - 21 Mar 2023
Cited by 6 | Viewed by 1915
Abstract
In the last decade, increasing evidence has emerged linking alterations in the brain-derived neurotrophic factor (BDNF) expression with the development of Alzheimer’s disease (AD). Because of the important role of BDNF in cognition and its association with AD pathogenesis, the aim of this [...] Read more.
In the last decade, increasing evidence has emerged linking alterations in the brain-derived neurotrophic factor (BDNF) expression with the development of Alzheimer’s disease (AD). Because of the important role of BDNF in cognition and its association with AD pathogenesis, the aim of this study was to evaluate the potential difference in plasma BDNF concentrations between subjects with mild cognitive impairment (MCI; N = 209) and AD patients (N = 295) and to determine the possible association between BDNF plasma levels and the degree of cognitive decline in these individuals. The results showed a significantly higher (p < 0.001) concentration of plasma BDNF in subjects with AD (1.16; 0.13–21.34) compared with individuals with MCI (0.68; 0.02–19.14). The results of the present study additionally indicated a negative correlation between cognitive functions and BDNF plasma concentrations, suggesting higher BDNF levels in subjects with more pronounced cognitive decline. The correlation analysis revealed a significant negative correlation between BDNF plasma levels and both Mini-Mental State Examination (p < 0.001) and Clock Drawing test (p < 0.001) scores. In conclusion, the results of our study point towards elevated plasma BDNF levels in AD patients compared with MCI subjects, which may be due to the body’s attempt to counteract the early and middle stages of neurodegeneration. Full article
(This article belongs to the Special Issue Recent Advances in Neuropharmacology and Brain Physiology)
►▼ Show Figures

Figure 1

17 pages, 3849 KiB  
Article
Low-Affinity/High-Selectivity Dopamine Transport Inhibition Sufficient to Rescue Cognitive Functions in the Aging Rat
by Jana Lubec, Ahmed M. Hussein, Predrag Kalaba, Daniel Daba Feyissa, Edgar Arias-Sandoval, Anita Cybulska-Klosowicz, Mekite Bezu, Tamara Stojanovic, Volker Korz, Jovana Malikovic, Nilima Y. Aher, Martin Zehl, Vladimir Dragacevic, Johann Jakob Leban, Claudia Sagheddu, Judith Wackerlig, Marco Pistis, Merce Correa, Thierry Langer, Ernst Urban, Harald Höger and Gert Lubecadd Show full author list remove Hide full author list
Biomolecules 2023, 13(3), 467; https://doi.org/10.3390/biom13030467 - 03 Mar 2023
Cited by 5 | Viewed by 1561
Abstract
The worldwide increase in cognitive decline, both in aging and with psychiatric disorders, warrants a search for pharmacological treatment. Although dopaminergic treatment approaches represent a major step forward, current dopamine transporter (DAT) inhibitors are not sufficiently specific as they also target other transporters [...] Read more.
The worldwide increase in cognitive decline, both in aging and with psychiatric disorders, warrants a search for pharmacological treatment. Although dopaminergic treatment approaches represent a major step forward, current dopamine transporter (DAT) inhibitors are not sufficiently specific as they also target other transporters and receptors, thus showing unwanted side effects. Herein, we describe an enantiomerically pure, highly specific DAT inhibitor, S-CE-123, synthetized in our laboratory. Following binding studies to DAT, NET and SERT, GPCR and kinome screening, pharmacokinetics and a basic neurotoxic screen, S-CE-123 was tested for its potential to enhance and/or rescue cognitive functions in young and in aged rats in the non-invasive reward-motivated paradigm of a hole-board test for spatial learning. In addition, an open field study with young rats was carried out. We demonstrated that S-CE-123 is a low-affinity but highly selective dopamine reuptake inhibitor with good bioavailability. S-CE-123 did not induce hyperlocomotion or anxiogenic or stereotypic behaviour in young rats. Our compound improved the performance of aged but not young rats in a reward-motivated task. The well-described impairment of the dopaminergic system in aging may underlie the age-specific effect. We propose S-CE-123 as a possible candidate for developing a tentative therapeutic strategy for age-related cognitive decline and cognitive dysfunction in psychiatric disorders. Full article
(This article belongs to the Special Issue Recent Advances in Neuropharmacology and Brain Physiology)
►▼ Show Figures

Figure 1

Review

Jump to: Research

33 pages, 3137 KiB  
Review
The Neurobiological Underpinnings of Obsessive-Compulsive Symptoms in Psychosis, Translational Issues for Treatment-Resistant Schizophrenia
by Licia Vellucci, Mariateresa Ciccarelli, Elisabetta Filomena Buonaguro, Michele Fornaro, Giordano D’Urso, Giuseppe De Simone, Felice Iasevoli, Annarita Barone and Andrea de Bartolomeis
Biomolecules 2023, 13(8), 1220; https://doi.org/10.3390/biom13081220 - 05 Aug 2023
Viewed by 3270
Abstract
Almost 25% of schizophrenia patients suffer from obsessive-compulsive symptoms (OCS) considered a transdiagnostic clinical continuum. The presence of symptoms pertaining to both schizophrenia and obsessive-compulsive disorder (OCD) may complicate pharmacological treatment and could contribute to lack or poor response to the therapy. Despite [...] Read more.
Almost 25% of schizophrenia patients suffer from obsessive-compulsive symptoms (OCS) considered a transdiagnostic clinical continuum. The presence of symptoms pertaining to both schizophrenia and obsessive-compulsive disorder (OCD) may complicate pharmacological treatment and could contribute to lack or poor response to the therapy. Despite the clinical relevance, no reviews have been recently published on the possible neurobiological underpinnings of this comorbidity, which is still unclear. An integrative view exploring this topic should take into account the following aspects: (i) the implication for glutamate, dopamine, and serotonin neurotransmission as demonstrated by genetic findings; (ii) the growing neuroimaging evidence of the common brain regions and dysfunctional circuits involved in both diseases; (iii) the pharmacological modulation of dopaminergic, serotoninergic, and glutamatergic systems as current therapeutic strategies in schizophrenia OCS; (iv) the recent discovery of midbrain dopamine neurons and dopamine D1- and D2-like receptors as orchestrating hubs in repetitive and psychotic behaviors; (v) the contribution of N-methyl-D-aspartate receptor subunits to both psychosis and OCD neurobiology. Finally, we discuss the potential role of the postsynaptic density as a structural and functional hub for multiple molecular signaling both in schizophrenia and OCD pathophysiology. Full article
(This article belongs to the Special Issue Recent Advances in Neuropharmacology and Brain Physiology)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop