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NeuroSci
Special Issues
Advances in Brain Development and Disease
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Advances in Brain Development and Disease

A special issue of NeuroSci (ISSN 2673-4087).

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 6138

Special Issue Editors

Dr. Frank Schubert

E-Mail Website
Guest Editor
School of Biological Sciences, University of Portsmouth, Hampshire, UK
Interests: developmental neurobiology; molecular mechanisms of brain development; neurogenesis; paediatric brain tumours; evolution of gene families
Special Issues, Collections and Topics in MDPI journals
Dr. Ricardo J. Rodrigues

E-Mail Website
Guest Editor
CNC—Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal
Interests: brain development; neurodegeneration; neuromodulation; purinergic receptors; NMDA receptors; adenosine; ATP; glutamate; neuronal migration; epilepsy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain development is achieved through a tightly controlled sequence of events—from neurogenesis, cell migration, differentiation, and neuritogenesis, to synapse formation and stabilization—in order to establish the neuronal network and a functional and healthy brain. Impairment of any of these critical stages of brain development, either by genetic variants or caused by extrinsic factors, can lead to long-term deleterious effects ranging from mild cognitive impairment to severe neurological and psychiatric conditions. Hence, it is essential to fully understand the mechanisms regulating the different processes governing brain development. In the last few decades, our knowledge on how the brain develops, particularly the molecular mechanisms involved or the relevance of the interactions between the different cells and extracellular matrix, has greatly improved. Yet, our current knowledge in this field is still at an “embryonic” stage. Furthermore, it will also be crucial to understand the spatial–temporal relevance of the different regulatory mechanisms and how they are integrated. In this Special Issue, we hope to gather contributions that highlight both the physiological mechanisms underlying brain development, and development-related brain disorders.

You may choose our Joint Special Issue in Biomolecules.   

Dr. Frank Schubert
Dr. Ricardo J. Rodrigues 
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. NeuroSci 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 1000 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.

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Published Papers (2 papers)

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12 pages, 671 KiB  
Review
P2Y1 Receptor as a Catalyst of Brain Neurodegeneration
by Ricardo J. Rodrigues, Ana S. Figueira and Joana M. Marques
NeuroSci 2022, 3(4), 604-615; https://doi.org/10.3390/neurosci3040043 - 31 Oct 2022
Cited by 4 | Viewed by 2864
Abstract
Different brain disorders display distinctive etiologies and pathogenic mechanisms. However, they also share pathogenic events. One event systematically occurring in different brain disorders, both acute and chronic, is the increase of the extracellular ATP levels. Accordingly, several P2 (ATP/ADP) and P1 (adenosine) receptors, [...] Read more.
Different brain disorders display distinctive etiologies and pathogenic mechanisms. However, they also share pathogenic events. One event systematically occurring in different brain disorders, both acute and chronic, is the increase of the extracellular ATP levels. Accordingly, several P2 (ATP/ADP) and P1 (adenosine) receptors, as well as the ectoenzymes involved in the extracellular catabolism of ATP, have been associated to different brain pathologies, either with a neuroprotective or neurodegenerative action. The P2Y1 receptor (P2Y1R) is one of the purinergic receptors associated to different brain diseases. It has a widespread regional, cellular, and subcellular distribution in the brain, it is capable of modulating synaptic function and neuronal activity, and it is particularly important in the control of astrocytic activity and in astrocyte–neuron communication. In diverse brain pathologies, there is growing evidence of a noxious gain-of-function of P2Y1R favoring neurodegeneration by promoting astrocyte hyperactivity, entraining Ca2+-waves, and inducing the release of glutamate by directly or indirectly recruiting microglia and/or by increasing the susceptibility of neurons to damage. Here, we review the current evidence on the involvement of P2Y1R in different acute and chronic neurodegenerative brain disorders and the underlying mechanisms. Full article
(This article belongs to the Special Issue Advances in Brain Development and Disease)
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Other

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8 pages, 1787 KiB  
Project Report
Lithium Prevents Telomere Shortening in Cortical Neurons in Amyloid-Beta Induced Toxicity
by Rafael M. Themoteo, Vanessa J. R. De Paula, Nicole K. R. Rocha, Helena Brentani and Orestes V. Forlenza
NeuroSci 2023, 4(1), 1-8; https://doi.org/10.3390/neurosci4010001 - 23 Dec 2022
Cited by 2 | Viewed by 2219
Abstract
Background: There is consistent evidence of the potential benefits of lithium attenuating mechanisms of neurodegeneration, including those related to the pathophysiology of Alzheimer’s disease (AD), and facilitating neurotrophic and protective responses, including maintenance of telomere length. The aim was to investigate the protective [...] Read more.
Background: There is consistent evidence of the potential benefits of lithium attenuating mechanisms of neurodegeneration, including those related to the pathophysiology of Alzheimer’s disease (AD), and facilitating neurotrophic and protective responses, including maintenance of telomere length. The aim was to investigate the protective effect of the pre-treatment with lithium on amyloid-beta (Aβ)-induced toxicity and telomere length in neurons. Methods: Cortical neurons were treated with lithium chloride at therapeutic and subtherapeutic concentrations (2 mM, 0.2 mM and 0.02 mM) for seven days. Amyloid toxicity was induced 24 h before the end of lithium treatment. Results: Lithium resulted in 120% (2 mM), 180% (0.2 mM) and 140% (0.02 mM) increments in telomere length as compared to untreated controls. Incubation with Aβ1-42 was associated with significant reductions in MTT uptake (33%) and telomere length (83%) as compared to controls. Conclusions: Lithium prevented loss of culture viability and telomere shortening in neuronal cultures challenged with Aβ fibrils. Full article
(This article belongs to the Special Issue Advances in Brain Development and Disease)
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