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Brain Sciences
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Mechanistic and Therapeutic Crosstalk across Neurodegenerative Diseases: What Can We...
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Mechanistic and Therapeutic Crosstalk across Neurodegenerative Diseases: What Can We Learn from Each Other?

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (30 September 2018) | Viewed by 15829

Special Issue Editor

Dr. Melissa Bowerman

E-Mail Website1 Website2
Guest Editor
1.School of Medicine, Keele University, UK
2.Institute for Science and Technology in Medicine, Stoke-on-Trent, UK
3.Wolfson Centre for Inherited Neuromuscular Disease, RJAH Orthopaedic Hospital, Oswestry, UK
Interests: spinal muscuspinal muscular atrophy; amyotrophic lateral sclerosis; therapeutic development; metabolism; muscle; mouse models

Special Issue Information

Dear Colleagues,

The last decade has seen tremendous advancements in uncovering novel pathological mechanisms and developing new therapeutic tools and strategies in the field of neurodegenerative diseases, which include, but are not limited to, spinal muscular atrophy, amyotrophic lateral sclerosis, multiple sclerosis, Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, ataxia and spinal and bulbar muscular atrophy. While these pathologies are genetically distinct and for the most part display specific pathological hallmarks, accumulating evidence suggests that similar mechanistic perturbations can occur in two or more of these diseases and that treatment strategies developed for one disorder can have broader implications for other neurodegenerative diseases. 

This Special Issue will highlight these similarities ranging from histological features, molecular pathways, tissue/cell dysfunctions, diagnostic methods, biomarkers and therapeutic developments.

Dr. Melissa Bowerman
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. Brain Sciences 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 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

  • Neurodegenerative disease
  • Histology
  • Molecular pathway
  • Diagnostic
  • Biomarker
  • Therapy

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Published Papers (3 papers)

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Research

9 pages, 456 KiB  
Article
MyomiRNAs Dysregulation in ALS Rehabilitation
by Valentina Pegoraro, Antonio Merico and Corrado Angelini
Brain Sci. 2019, 9(1), 8; https://doi.org/10.3390/brainsci9010008 - 10 Jan 2019
Cited by 27 | Viewed by 5299
Abstract
Amyotrophic lateral sclerosis (ALS) is a rare, progressive, neurodegenerative disorder caused by degeneration of upper and lower motor neurons. The disease process leads, because of lower motor neuron involvement, to progressive muscle atrophy, weakness, and fasciculations and for the upper motor neuron involvement [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a rare, progressive, neurodegenerative disorder caused by degeneration of upper and lower motor neurons. The disease process leads, because of lower motor neuron involvement, to progressive muscle atrophy, weakness, and fasciculations and for the upper motor neuron involvement leads to spasticity. Muscle atrophy in ALS is caused by a neural dysregulation in the molecular network controlling fast and slow muscle fibers. Denervation and reinnervation processes in skeletal muscle occur in the course of ALS and are modulated by rehabilitation. MicroRNAs (miRNAs) are small, non-coding RNAs that are involved in different biological functions under various pathophysiological conditions. MiRNAs can be secreted by various cell types and they are markedly stable in body fluids. MiR-1, miR-133 a miR-133b, and miR-206 are called “myomiRs” and are considered markers of myogenesis during muscle regeneration and contribute to neuromuscular junction stabilization or sprouting. We observed a positive effect of a standard aerobic exercise rehabilitative protocol conducted for six weeks in 18 ALS patients during hospitalization in our center. This is a preliminary study, in which we correlated clinical scales with molecular data on myomiRs. After six weeks of moderate aerobic exercise, we found lower levels in serum of myomiRNAs. Our data suggest that circulating miRNAs changed during skeletal muscle recovery in response to physical rehabilitation in ALS. However, no firm conclusions can be made on the ALS-specific effect of exercise on miRNA levels. Full article
(This article belongs to the Special Issue Mechanistic and Therapeutic Crosstalk across Neurodegenerative Diseases: What Can We Learn from Each Other?)
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22 pages, 10713 KiB  
Article
Multi-Study Proteomic and Bioinformatic Identification of Molecular Overlap between Amyotrophic Lateral Sclerosis (ALS) and Spinal Muscular Atrophy (SMA)
by Darija Šoltić, Melissa Bowerman, Joanne Stock, Hannah K. Shorrock, Thomas H. Gillingwater and Heidi R. Fuller
Brain Sci. 2018, 8(12), 212; https://doi.org/10.3390/brainsci8120212 - 4 Dec 2018
Cited by 15 | Viewed by 5174
Abstract
Unravelling the complex molecular pathways responsible for motor neuron degeneration in amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) remains a persistent challenge. Interest is growing in the potential molecular similarities between these two diseases, with the hope of better understanding disease [...] Read more.
Unravelling the complex molecular pathways responsible for motor neuron degeneration in amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) remains a persistent challenge. Interest is growing in the potential molecular similarities between these two diseases, with the hope of better understanding disease pathology for the guidance of therapeutic development. The aim of this study was to conduct a comparative analysis of published proteomic studies of ALS and SMA, seeking commonly dysregulated molecules to be prioritized as future therapeutic targets. Fifteen proteins were found to be differentially expressed in two or more proteomic studies of both ALS and SMA, and bioinformatics analysis identified over-representation of proteins known to associate in vesicles and molecular pathways, including metabolism of proteins and vesicle-mediated transport—both of which converge on endoplasmic reticulum (ER)-Golgi trafficking processes. Calreticulin, a calcium-binding chaperone found in the ER, was associated with both pathways and we independently confirm that its expression was decreased in spinal cords from SMA and increased in spinal cords from ALS mice. Together, these findings offer significant insights into potential common targets that may help to guide the development of new therapies for both diseases. Full article
(This article belongs to the Special Issue Mechanistic and Therapeutic Crosstalk across Neurodegenerative Diseases: What Can We Learn from Each Other?)
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16 pages, 1789 KiB  
Article
A Multidisciplinary Approach Reveals an Age-Dependent Expression of a Novel Bioactive Peptide, Already Involved in Neurodegeneration, in the Postnatal Rat Forebrain
by Giovanni Ferrati, Emanuele Brai, Skye Stuart, Celia Marino and Susan A. Greenfield
Brain Sci. 2018, 8(7), 132; https://doi.org/10.3390/brainsci8070132 - 10 Jul 2018
Cited by 5 | Viewed by 4829
Abstract
The basal forebrain has received much attention due to its involvement in multiple cognitive functions, but little is known about the basic neuronal mechanisms underlying its development, nor those mediating its primary role in Alzheimer’s disease. We have previously suggested that a novel [...] Read more.
The basal forebrain has received much attention due to its involvement in multiple cognitive functions, but little is known about the basic neuronal mechanisms underlying its development, nor those mediating its primary role in Alzheimer’s disease. We have previously suggested that a novel 14-mer peptide, ‘T14’, could play a pivotal role in Alzheimer’s disease, via reactivation of a developmental signaling pathway. In this study, we have characterized T14 in the context of post-natal rat brain development, using a combination of different techniques. Ex-vivo rat brain slices containing the basal forebrain, at different stages of development, were used to investigate large-scale neuronal network activity in real time with voltage-sensitive dye imaging. Subsequent Western blot analysis revealed the expression profile of endogenous T14, its target alpha7 nicotinic receptor and the familiar markers of Alzheimer’s: amyloid beta and phosphorylated Tau. Results indicated maximal neuronal activity at the earliest ages during development, reflected in a concomitant profile of T14 peptide levels and related proteins. In conclusion, these findings show that the peptide, already implicated in neurodegenerative events, has an age-dependent expression, suggesting a possible contribution to the physiological mechanisms underlying brain maturation. Full article
(This article belongs to the Special Issue Mechanistic and Therapeutic Crosstalk across Neurodegenerative Diseases: What Can We Learn from Each Other?)
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