Special Issue "Selected Papers from "Brainstorming Research Assembly for Young Neuroscientists (BraYn)"

A special issue of Neurology International (ISSN 2035-8377).

Deadline for manuscript submissions: 1 August 2024 | Viewed by 4865

Special Issue Editor

Special Issue Information

Dear Colleagues,

The 5th edition of the BraYn conference will take place in Rome (Italy) on September 28th-30th. The event is organized by the BraYn Association and is intended for young researchers under the age of 40 working in the field of Neuroscience. Young neuroscientists are often challenged with the difficulties of carrying out their research; the conference aims to help these researchers reach their full research potential through meeting, connecting, collaborating, and sharing with other scientists. The BraYn association aims to encourage cooperation among different research groups to broaden their horizons and improve the quality of neuroscience research. The BraYn conference is open to PhD students, post docs (juniors and seniors), junior PIs, residents in neurology, young neurologists, and clinicians from all around the world. For this conference Special Issue, we welcome original articles or reviews reporting new experimental or clinical data and promoting the understanding of biological processes from different disciplines of neuroscience, including neuroimmunology, neuronal plasticity, neurophysiology, neurodegeneration, neuro-oncology, epilepsy, neurodevelopment, neurogenetics, clinical neuroscience, and neuroimaging. We aim to provide a collection of high-impact manuscripts dissecting the unknown or lesser studied aspects of neuroscience. This Special Issue further hopes to help young neuroscientists to reconsider their basic knowledge. We invite young colleagues from all neuroscience disciplines to systematically exchange knowledge about their clinical or basic research.

Dr. Giovanni Ferrara
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. Neurology International is an international peer-reviewed open access quarterly 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 1600 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

  • neuroimmunology
  • neuronal plasticity
  • neurophysiology
  • neurodegeneration
  • neuro-oncology
  • paediatric neuroscience
  • epilepsy
  • neurodevelopment
  • neurogenetic
  • neuroimaging
  • basic research
  • clinical research
  • neurology
  • clinical neuroscience

Published Papers (3 papers)

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14 pages, 3981 KiB  
Article
FTD/ALS Type 7-Associated Thr104Asn Mutation of CHMP2B Blunts Neuronal Process Elongation, and Is Recovered by Knockdown of Arf4, the Golgi Stress Regulator
Neurol. Int. 2023, 15(3), 980-993; https://doi.org/10.3390/neurolint15030063 - 11 Aug 2023
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Abstract
Frontotemporal dementia and/or amyotrophic lateral sclerosis type 7 (FTD/ALS7) is an autosomal dominant neurodegenerative disorder characterized by the onset of FTD and/or ALS, mainly in adulthood. Patients with some types of mutations, including the Thr104Asn (T104N) mutation of charged multivesicular body protein 2B [...] Read more.
Frontotemporal dementia and/or amyotrophic lateral sclerosis type 7 (FTD/ALS7) is an autosomal dominant neurodegenerative disorder characterized by the onset of FTD and/or ALS, mainly in adulthood. Patients with some types of mutations, including the Thr104Asn (T104N) mutation of charged multivesicular body protein 2B (CHMP2B), have predominantly ALS phenotypes, whereas patients with other mutations have predominantly FTD phenotypes. A few mutations result in patients having both phenotypes approximately equally; however, the reason why phenotypes differ depending on the position of the mutation is unknown. CHMP2B comprises one part of the endosomal sorting complexes required for transport (ESCRT), specifically ESCRT-III, in the cytoplasm. We describe here, for the first time, that CHMP2B with the T104N mutation inhibits neuronal process elongation in the N1E-115 cell line, a model line undergoing neuronal differentiation. This inhibitory phenotype was accompanied by changes in marker protein expression. Of note, CHMP2B with the T104N mutation, but not the wild-type form, was preferentially accumulated in the Golgi body. Of the four major Golgi stress signaling pathways currently known, the pathway through Arf4, the small GTPase, was specifically upregulated in cells expressing CHMP2B with the T104N mutation. Conversely, knockdown of Arf4 with the cognate small interfering (si)RNA recovered the neuronal process elongation inhibited by the T104N mutation. These results suggest that the T104N mutation of CHMP2B inhibits morphological differentiation by triggering Golgi stress signaling, revealing a possible therapeutic molecular target for recovering potential molecular and cellular phenotypes underlying FTD/ALS7. Full article
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21 pages, 7322 KiB  
Article
Hesperetin Ameliorates Inhibition of Neuronal and Oligodendroglial Cell Differentiation Phenotypes Induced by Knockdown of Rab2b, an Autism Spectrum Disorder-Associated Gene Product
Neurol. Int. 2023, 15(1), 371-391; https://doi.org/10.3390/neurolint15010025 - 10 Mar 2023
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Abstract
Autism spectrum disorder (ASD) is a central nervous system (CNS) neurodevelopmental disorder that includes autism, pervasive developmental disorder, and Asperger’s syndrome. ASD is characterized by repetitive behaviors and social communication deficits. ASD is thought to be a multifactorial disorder with a range of [...] Read more.
Autism spectrum disorder (ASD) is a central nervous system (CNS) neurodevelopmental disorder that includes autism, pervasive developmental disorder, and Asperger’s syndrome. ASD is characterized by repetitive behaviors and social communication deficits. ASD is thought to be a multifactorial disorder with a range of genetic and environmental factors/candidates. Among such factors is the rab2b gene, although it remains unclear how Rab2b itself is related to the CNS neuronal and glial developmental disorganization observed in ASD patients. Rab2 subfamily members regulate intracellular vesicle transport between the endoplasmic reticulum and the Golgi body. To the best of our knowledge, we are the first to report that Rab2b positively regulates neuronal and glial cell morphological differentiation. Knockdown of Rab2b inhibited morphological changes in N1E-115 cells, which are often used as the neuronal cell differentiation model. These changes were accomplished with decreased expression levels of marker proteins in neuronal cells. Similar results were obtained for FBD-102b cells, which are used as the model of oligodendroglial cell morphological differentiation. In contrast, knockdown of Rab2a, which is another Rab2 family member not known to be associated with ASD, affected only oligodendroglial and not neuronal morphological changes. In contrast, treatment with hesperetin, a citrus flavonoid with various cellular protective effects, in cells recovered the defective morphological changes induced by Rab2b knockdown. These results suggest that knockdown of Rab2b inhibits differentiation in neuronal and glial cells and may be associated with pathological cellular phenotypes in ASD and that hesperetin can recover their phenotypes at the in vitro level at least. Full article
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82 pages, 628 KiB  
Conference Report
Abstracts of the Fifth Brainstorming Research Assembly for Young Neuroscientists (BraYn), Italy, 28–30 September 2022
Neurol. Int. 2023, 15(1), 415-496; https://doi.org/10.3390/neurolint15010028 - 14 Mar 2023
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Abstract
On behalf of the BraYn Association Ets, we are pleased to present the Abstracts of the Fifth Brainstorming Research Assembly for Young Neuroscientists, which was held in Rome, Italy from 28–30 September 2022. We congratulate all the presenters on their research work and [...] Read more.
On behalf of the BraYn Association Ets, we are pleased to present the Abstracts of the Fifth Brainstorming Research Assembly for Young Neuroscientists, which was held in Rome, Italy from 28–30 September 2022. We congratulate all the presenters on their research work and contribution. Full article
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