Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
2.7
3.2
Journals
Life
Special Issues
Neurological Diseases: From Molecular Mechanisms to Therapy
share announcement

Neurological Diseases: From Molecular Mechanisms to Therapy

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (25 November 2022) | Viewed by 8572

Special Issue Editors

Dr. Maria Shadrina

E-Mail Website
Guest Editor
Institute of Molecular Genetics of National Research Center “Kurchatov Institute”, 123182 Moscow, Russia
Interests: Parkinson’s disease; models; transcriptome study; RNA markers; neurology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Pyotr A. Slominsky

E-Mail Website
Guest Editor
Institute of Molecular Genetics of National Research Centre “Kurchatov Institute”, 2 Kurchatova Sq., 123182 Moscow, Russia
Interests: neurology; inherited disorders; genetics; DNA markers; mutations
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We would like to devote this Special Issue to problems related to the study of neurological diseases; simultaneously, we plan to consider a wide range of problems—from studying the genetic and molecular mechanisms of their pathogenesis to new approaches to therapy. In this case, special attention will be paid to diseases of the central nervous system—both monogenic and complex—, although this does not mean that studies related to the study of other neurological diseases will not be considered. The most important aspect is for Special Issue articles to be of interest to a wide range of scientists and clinicians, considering important aspects of the biology of neurological diseases and providing a significant contribution to their study. This Special Issue of Life should improve our understanding of the pathogenesis of neurological diseases and possible approaches to early diagnosis and treatment.

Dr. Maria Shadrina
Prof. Dr. Pyotr A. Slominsky
Guest Editors

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. Life 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 2600 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

  • neurological diseases
  • genetics
  • molecular mechanisms
  • early diagnostics
  • novel therapeutics

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: Other

12 pages, 321 KiB  
Article
Alzheimer’s Disease Risk Variant rs3865444 in the CD33 Gene: A Possible Role in Susceptibility to Multiple Sclerosis
by Juraj Javor, Mária Bucová, Vladimíra Ďurmanová, Dominika Radošinská, Zuzana Párnická, Daniel Čierny, Egon Kurča, Daniela Čopíková-Cudráková, Karin Gmitterová and Ivana Shawkatová
Life 2022, 12(7), 1094; https://doi.org/10.3390/life12071094 - 21 Jul 2022
Cited by 1 | Viewed by 1685
Abstract
Polymorphisms in genes encoding receptors that modulate the activity of microglia and macrophages are attractive candidates for participation in genetic susceptibility to multiple sclerosis (MS). The aims of the study were to (1) investigate the association between Alzheimer’s disease-linked variant rs3865444:C>A in the [...] Read more.
Polymorphisms in genes encoding receptors that modulate the activity of microglia and macrophages are attractive candidates for participation in genetic susceptibility to multiple sclerosis (MS). The aims of the study were to (1) investigate the association between Alzheimer’s disease-linked variant rs3865444:C>A in the CD33 gene and MS risk, (2) assess the effect of the strongest MS risk allele HLA-DRB1*15:01 on this association, and (3) analyze the correlation of rs3865444 with selected clinical phenotypes, i.e., age of onset and disease severity. CD33 rs3865444 was genotyped in a cohort of 579 patients and 1145 controls and its association with MS risk and clinical phenotypes was analyzed by logistic and linear regression analysis, respectively. Statistical evaluation revealed that rs3865444 reduces the risk of MS in the HLA-DRB1*15:01-positive subpopulation but not in the cohort negative for HLA-DRB1*15:01. A significant antagonistic epistasis between rs3865444 A and HLA-DRB1*15:01 alleles in the context of MS risk was detected by the interaction synergy factor analysis. Comparison of allele and genotype distribution between relapsing-remitting MS, secondary progressive MS, and control groups revealed that rs3865444 C to A substitution may also be associated with a decreased risk of transition of MS to its secondary progressive form, irrespective of the HLA-DRB1*15:01 carrier status. On the other hand, no correlation could be found between rs3865444 and the age of disease onset or MS severity score. Future studies are required to shed more light on the role of CD33 in MS pathogenesis. Full article
(This article belongs to the Special Issue Neurological Diseases: From Molecular Mechanisms to Therapy)
13 pages, 3638 KiB  
Article
Differential Activation of pERK1/2 and c-Fos Following Injury to Different Regions of Primary Sensory Neuron
by Bei Miao, Hongyu Yao, Peng Chen and Xue-Jun Song
Life 2022, 12(5), 752; https://doi.org/10.3390/life12050752 - 19 May 2022
Cited by 2 | Viewed by 2315
Abstract
Nerve injury causes hyperexcitability of the dorsal root ganglion (DRG) and spinal dorsal horn (DH) neurons, which results in neuropathic pain. We have previously demonstrated that partial dorsal rhizotomy (PDR) produced less severe pain-like behavior than chronic constriction injury (CCI) or chronic compression [...] Read more.
Nerve injury causes hyperexcitability of the dorsal root ganglion (DRG) and spinal dorsal horn (DH) neurons, which results in neuropathic pain. We have previously demonstrated that partial dorsal rhizotomy (PDR) produced less severe pain-like behavior than chronic constriction injury (CCI) or chronic compression of DRG (CCD) and did not enhance DRG neuronal excitability. However, the mechanisms underlying such discrepancy remain unclear. This study was designed to compare the activation of phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) in DRG and DH, and c-Fos in DH following treatments of CCI, CCD, and PDR. We confirmed that thermal hyperalgesia produced by PDR was less severe than that produced by CCI or CCD. We showed that pERK1/2 in DRG and DH was greatly activated by CCI or CCD, whereas PDR produced only transient and mild pERK1/2 activation. CCI, CCD, and PDR induced robust c-Fos expression in DH; nevertheless, c-Fos+ neurons following PDR were much fewer than that following CCI or CCD. Blocking retrograde axonal transport by colchicine proximal to the CCI injury site diminished thermal hyperalgesia and inhibited pERK1/2 and c-Fos activation. These findings demonstrate that less severe pain-like behavior produced by PDR than CCI or CCD attributes to less activation of pERK1/2 and c-Fos. Such neurochemical activation partially relies on retrograde axonal transport of certain “injury signals” from the peripheral injured site to DRG somata. Full article
(This article belongs to the Special Issue Neurological Diseases: From Molecular Mechanisms to Therapy)
►▼ Show Figures

Figure 1

13 pages, 1029 KiB  
Article
Expression Analysis of Genes Involved in Transport Processes in Mice with MPTP-Induced Model of Parkinson’s Disease
by Margarita M. Rudenok, Maria I. Shadrina, Elena V. Filatova, Ivan N. Rybolovlev, Maxim S. Nesterov, Denis A. Abaimov, Ruslan A. Ageldinov, Anna A. Kolacheva, Michael V. Ugrumov, Petr A. Slominsky and Anelya Kh. Alieva
Life 2022, 12(5), 751; https://doi.org/10.3390/life12050751 - 19 May 2022
Cited by 5 | Viewed by 2126
Abstract
Processes of intracellular and extracellular transport play one of the most important roles in the functioning of cells. Changes to transport mechanisms in a neuron can lead to the disruption of many cellular processes and even to cell death. It was shown that [...] Read more.
Processes of intracellular and extracellular transport play one of the most important roles in the functioning of cells. Changes to transport mechanisms in a neuron can lead to the disruption of many cellular processes and even to cell death. It was shown that disruption of the processes of vesicular, axonal, and synaptic transport can lead to a number of diseases of the central nervous system, including Parkinson’s disease (PD). Here, we studied changes in the expression of genes whose protein products are involved in the transport processes (Snca, Drd2, Rab5a, Anxa2, and Nsf) in the brain tissues and peripheral blood of mice with MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-induced models of PD. We detected changes in the expressions of Drd2, Anxa2, and Nsf at the earliest modeling stages. Additionally, we have identified conspicuous changes in the expression level of Anxa2 in the striatum and substantia nigra of mice with MPTP-induced models of PD in its early stages. These data clearly suggest the involvement of protein products in these genes in the earliest stages of the pathogenesis of PD. Full article
(This article belongs to the Special Issue Neurological Diseases: From Molecular Mechanisms to Therapy)
►▼ Show Figures

Figure 1

Other

Jump to: Research

15 pages, 1304 KiB  
Systematic Review
The Allosteric Antagonist of the Sigma-2 Receptors—Elayta (CT1812) as a Therapeutic Candidate for Mild to Moderate Alzheimer’s Disease: A Scoping Systematic Review
by Anum Rasheed, Ahmad Bin Zaheer, Aqsa Munawwar, Zouina Sarfraz, Azza Sarfraz, Karla Robles-Velasco and Ivan Cherrez-Ojeda
Life 2023, 13(1), 1; https://doi.org/10.3390/life13010001 - 20 Dec 2022
Cited by 4 | Viewed by 1656
Abstract
Nearly 35 million people worldwide live with Alzheimer’s disease (AD). The prevalence of the disease is expected to rise two-fold by 2050. With only symptomatic treatment options available, it is essential to understand the developments and existing evidence that aims to target brain [...] Read more.
Nearly 35 million people worldwide live with Alzheimer’s disease (AD). The prevalence of the disease is expected to rise two-fold by 2050. With only symptomatic treatment options available, it is essential to understand the developments and existing evidence that aims to target brain pathology and dementia outcomes. This scoping systematic review aimed to collate existing evidence of CT1812 for use in patients with AD and summarize the methodologies of ongoing trials. Adhering to PRISMA Statement 2020 guidelines, PubMed/MEDLINE, Embase, Cochrane, and ClinicalTrials.gov were systematically searched through up to 15 November 2022 by applying the following keywords: CT1812, Alzheimer’s disease, dementia, and/or sigma-2 receptor. Three completed clinical trials were included along with three ongoing records of clinical trials. The three completed trials were in Phases I and II of testing. The sample size across all three trials was 135. CT1812 reached endpoints across the trials and obtained a maximum concentration in the cerebrospinal fluid with 97–98% receptor occupancy. The findings of this systematic review must be used with caution as the results, while mostly favorable so far, must be replicated in higher-powered, placebo-controlled Phase II–III trials. Full article
(This article belongs to the Special Issue Neurological Diseases: From Molecular Mechanisms to Therapy)
►▼ Show Figures

Figure 1

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