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Brain Sciences
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Advanced Studies of the Neuron Model of Neurodegenerative Diseases
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Advanced Studies of the Neuron Model of Neurodegenerative Diseases

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neurodegenerative Diseases".

Deadline for manuscript submissions: closed (12 April 2024) | Viewed by 7271

Special Issue Editors

Prof. Dr. Antonella Cardinale

E-Mail Website
Guest Editor
Laboratory Experimental Neurophysiology, IRCCS San Raffaele Pisana, 00166 Rome, Italy
Interests: neurodegenerative diseases; neuroinflammation; neuroprotection; movement disorders; immunohistochemistry
Dr. Antonio De Iure

E-Mail Website
Guest Editor
Laboratory Experimental Neurophysiology, IRCCS San Raffaele Pisana, 00166 Rome, Italy
Interests: neurodegenerative disease; neuronal plasticity; molecular electrophysiology; neuroinflammation; movement disorders

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are characterized by progressive neuron damage and decreasing activity of synapses in the brain or peripheral nervous system, causing cognitive and motor symptoms and finally leading to human death.

Studies into the neurodegenerative mechanisms today represent the most complex and urgent challenge for neuroscience research. As research technologies continue to progress, several new experimental neuronal models are emerging. The different neuronal models attempt to deepen altered mechanism related to neurodegeneration and neuroinflammation. For this purpose, it will be interesting to analyze the experimental models that closely mimic clinical features of human neurodegenerative disease, such as induced pluripotent stem cells, trans-differentiated neurons, organoids, and three-dimensional culture. Understanding these disease processes assist in identifying new effective therapies and developing personalized medicine.

We invite authors to submit research articles and reviews at different levels of analysis, dealing with the state of the art in this field.

Prof. Dr. Antonella Cardinale
Dr. Antonio De Iure
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. 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 diseases
  • in vitro models
  • organotypic brain slice cultures
  • induced pluripotent stem cells
  • trans-differentiated neurons
  • organoids
  • three-dimensional culture

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Published Papers (4 papers)

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Research

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14 pages, 5842 KiB  
Article
Ultrastructural Changes of Neuroendocrine Pheochromocytoma Cell Line PC-12 Exposed In Vitro to Rotenone
by Manuel Belli, Mario Cristina, Valeria Calabrese, Marta Russo, Marisa Granato, Matteo Antonio Russo and Luigi Sansone
Brain Sci. 2024, 14(5), 476; https://doi.org/10.3390/brainsci14050476 - 8 May 2024
Cited by 1 | Viewed by 1449
Abstract
Rotenone is a pesticide used in research for its ability to induce changes similar, in vivo and in vitro, to those observed in Parkinson’s disease (PD). This includes a selective death of dopaminergic neurons in the substantia nigra. Nonetheless, the precise mechanism through [...] Read more.
Rotenone is a pesticide used in research for its ability to induce changes similar, in vivo and in vitro, to those observed in Parkinson’s disease (PD). This includes a selective death of dopaminergic neurons in the substantia nigra. Nonetheless, the precise mechanism through which rotenone modifies structure and function of neurons remains unclear. The PC12 cells closely resemble dopamine terminal neurons. This makes it a preferred model for studying the morphology of central dopamine neurons and predicting neurotoxicity. In this paper, we investigated the effects of 0.5 µM rotenone for 24–48 h on PC12 cell viability and ultrastructure (TEM), trying to identify primary and more evident alterations that can be related to neuronal damages similar to that seen in animal PD models. Cell viability decreased after 24 h rotenone treatment, with a further decrease after 48 h. Ultrastructural changes included vacuolar degeneration, mitochondrial mild swelling, decrease in the number of neuropeptide granules, and the loss of cell-to-cell adhesion. These findings are in agreement with previous research suggesting that rotenone, by inhibiting energy production and increasing ROS generation, is responsible for significant alterations of the ultrastructure and cell death of PC12 cells. Our data confirm the link between rotenone exposure, neuronal damage, and changes in dopamine metabolism, suggesting its role in the pathogenesis of PD. Full article
(This article belongs to the Special Issue Advanced Studies of the Neuron Model of Neurodegenerative Diseases)
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Review

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15 pages, 918 KiB  
Review
The Association between Long Non-Coding RNAs and Alzheimer’s Disease
by Carson M. Black, Anneliesse A. Braden, Samia Nasim, Manish Tripathi, Jianfeng Xiao and Mohammad Moshahid Khan
Brain Sci. 2024, 14(8), 818; https://doi.org/10.3390/brainsci14080818 - 15 Aug 2024
Viewed by 1410
Abstract
Neurodegeneration occurs naturally as humans age, but the presence of additional pathogenic mechanisms yields harmful and consequential effects on the brain. Alzheimer’s disease (AD), the most common form of dementia, is a composite of such factors. Despite extensive research to identify the exact [...] Read more.
Neurodegeneration occurs naturally as humans age, but the presence of additional pathogenic mechanisms yields harmful and consequential effects on the brain. Alzheimer’s disease (AD), the most common form of dementia, is a composite of such factors. Despite extensive research to identify the exact causes of AD, therapeutic approaches for treating the disease continue to be ineffective, indicating important gaps in our understanding of disease mechanisms. Long non-coding RNAs (lncRNAs) are an endogenous class of regulatory RNA transcripts longer than 200 nucleotides, involved in various regulatory networks, whose dysregulation is evident in several neural and extraneural diseases. LncRNAs are ubiquitously expressed across all tissues with a wide range of functions, including controlling cell differentiation and development, responding to environmental stimuli, and other physiological processes. Several lncRNAs have been identified as potential contributors in worsening neurodegeneration due to altered regulation during abnormal pathological conditions. Within neurological disease, lncRNAs are prime candidates for use as biomarkers and pharmacological targets. Gender-associated lncRNA expression is altered in a gender-dependent manner for AD, suggesting more research needs to be focused on this relationship. Overall, research on lncRNAs and their connection to neurodegenerative disease is growing exponentially, as commercial enterprises are already designing and employing RNA therapeutics. In this review we offer a comprehensive overview of the current state of knowledge on the role of lncRNAs in AD and discuss the potential implications of lncRNA as potential therapeutic targets and diagnostic biomarkers in patients with Alzheimer’s disease. Full article
(This article belongs to the Special Issue Advanced Studies of the Neuron Model of Neurodegenerative Diseases)
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15 pages, 813 KiB  
Review
Neuroinflammation and Dyskinesia: A Possible Causative Relationship?
by Antonella Cardinale, Antonio de Iure and Barbara Picconi
Brain Sci. 2024, 14(5), 514; https://doi.org/10.3390/brainsci14050514 - 20 May 2024
Viewed by 1392
Abstract
Levodopa (L-DOPA) treatment represents the gold standard therapy for Parkinson’s disease (PD) patients. L-DOPA therapy shows many side effects, among them, L-DOPA-induced dyskinesias (LIDs) remain the most problematic. Several are the mechanisms underlying these processes: abnormal corticostriatal neurotransmission, pre- and post-synaptic neuronal events, [...] Read more.
Levodopa (L-DOPA) treatment represents the gold standard therapy for Parkinson’s disease (PD) patients. L-DOPA therapy shows many side effects, among them, L-DOPA-induced dyskinesias (LIDs) remain the most problematic. Several are the mechanisms underlying these processes: abnormal corticostriatal neurotransmission, pre- and post-synaptic neuronal events, changes in gene expression, and altered plasticity. In recent years, researchers have also suggested non-neuronal mechanisms as a possible cause for LIDs. We reviewed recent clinical and pre-clinical studies on neuroinflammation contribution to LIDs. Microglia and astrocytes seem to play a strategic role in LIDs phenomenon. In particular, their inflammatory response affects neuron-glia communication, synaptic activity and neuroplasticity, contributing to LIDs development. Finally, we describe possible new therapeutic interventions for dyskinesia prevention targeting glia cells. Full article
(This article belongs to the Special Issue Advanced Studies of the Neuron Model of Neurodegenerative Diseases)
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Other

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16 pages, 579 KiB  
Systematic Review
Investigating the Robustness of a Rodent “Double Hit” (Post-Weaning Social Isolation and NMDA Receptor Antagonist) Model as an Animal Model for Schizophrenia: A Systematic Review
by Khanyiso Bright Shangase, Mluleki Luvuno and Musa V. Mabandla
Brain Sci. 2023, 13(6), 848; https://doi.org/10.3390/brainsci13060848 - 24 May 2023
Cited by 4 | Viewed by 1969
Abstract
Schizophrenia is a debilitating psychiatric disorder comprising positive, negative, and cognitive impairments. Most of the animal models developed to understand the neurobiology and mechanism of schizophrenia do not produce all the symptoms of the disease. Therefore, researchers need to develop new animal models [...] Read more.
Schizophrenia is a debilitating psychiatric disorder comprising positive, negative, and cognitive impairments. Most of the animal models developed to understand the neurobiology and mechanism of schizophrenia do not produce all the symptoms of the disease. Therefore, researchers need to develop new animal models with greater translational reliability, and the ability to produce most if not all symptoms of schizophrenia. This review aimed to evaluate the effectiveness of the rodent “double hit” (post-weaning social isolation and N-methyl-D-aspartate (NMDA) receptor antagonist) model to produce symptoms of schizophrenia. This systematic review was developed according to the 2020 PRISMA guidelines and checklist. The MEDLINE (PubMed) and Ebscohost databases were used to search for studies. The systematic review is based on quantitative animal studies. Studies in languages other than English that could be translated sufficiently using Google translate were also included. Data extraction was performed individually by two independent reviewers and discrepancies between them were resolved by a third reviewer. SYRCLE’s risk-of-bias tool was used to test the quality and biases of included studies. Our primary search yielded a total of 47 articles, through different study selection processes. Seventeen articles met the inclusion criteria for this systematic review. Ten of the seventeen studies found that the “double hit” model was more effective in developing various symptoms of schizophrenia. Most studies showed that the “double hit” model is robust and capable of inducing cognitive impairments and positive symptoms of schizophrenia. Full article
(This article belongs to the Special Issue Advanced Studies of the Neuron Model of Neurodegenerative Diseases)
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