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 2128

Special Issue Editors


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

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

Published Papers (1 paper)

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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 1 | Viewed by 1399
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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