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Neurodegenerative Disease: Looking for Oxidative Stress and Inflammation Mechanisms

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 May 2025 | Viewed by 1222

Special Issue Editor

Special Issue Information

Dear Colleagues,

Many papers about neurodegenerative diseases and their relationship with oxidative stress and inflammation have been published. In Alzheimer’s disease, Parkinson’s, Multiple Sclerosis and Amyotrophic Lateral Sclerosis, the mechanisms of illness are not well understood. The roles of different cells in the nervous system, such as neurons, astrocytes, microglia, and oligodendroglia, are also poorly understood. Moreover, studies on the influence of oxidative stress and inflammation in the nervous system will be a priority in the science future. We invite you to submit your latest research findings or review manuscripts to this Special Issue, which will bring together current research concerning oxidative stress and inflammation in the nervous system. Furthermore, manuscripts on new pharmaceuticals and/or techniques to improve these neurodegenerative diseases are encouraged.

Dr. Soraya L. Valles
Guest Editor

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Keywords

  • neurodegenerative disease
  • oxidative stress
  • inflammation mechanisms
  • neurons
  • astrocytes
  • microglia
  • oligodendroglia

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Published Papers (1 paper)

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Research

26 pages, 7621 KiB  
Article
Inflammatory Intracellular Signaling in Neurons Is Influenced by Glial Soluble Factors in iPSC-Based Cell Model of PARK2-Associated Parkinson’s Disease
by Tatiana Gerasimova, Daniil Poberezhniy, Valentina Nenasheva, Ekaterina Stepanenko, Elena Arsenyeva, Lyudmila Novosadova, Igor Grivennikov, Sergey Illarioshkin, Maria Lagarkova, Vyacheslav Tarantul and Ekaterina Novosadova
Int. J. Mol. Sci. 2024, 25(17), 9621; https://doi.org/10.3390/ijms25179621 - 5 Sep 2024
Viewed by 905
Abstract
Neuroinflammation is considered to be one of the driving factors in Parkinson’s disease (PD). This study was conducted using neuronal and glial cell cultures differentiated from induced pluripotent stem cells (iPSC) of healthy donors (HD) and PD patients with different PARK2 mutations (PD). [...] Read more.
Neuroinflammation is considered to be one of the driving factors in Parkinson’s disease (PD). This study was conducted using neuronal and glial cell cultures differentiated from induced pluripotent stem cells (iPSC) of healthy donors (HD) and PD patients with different PARK2 mutations (PD). Based on the results of RNA sequencing, qPCR and ELISA, we revealed transcriptional and post-transcriptional changes in HD and PD neurons cultivated in HD and PD glial-conditioned medium. We demonstrated that if one or both of the components of the system, neurons or glia, is Parkin-deficient, the interaction resulted in the down-regulation of a number of key genes related to inflammatory intracellular pathways and negative regulation of apoptosis in neurons, which might be neuroprotective. In PD neurons, the stress-induced up-regulation of APLNR was significantly stronger compared to HD neurons and was diminished by glial soluble factors, both HD and PD. PD neurons in PD glial conditioned medium increased APLN expression and also up-regulated apelin synthesis and release into intracellular fluid, which represented another compensatory action. Overall, the reported results indicate that neuronal self-defense mechanisms contribute to cell survival, which might be characteristic of PD patients with Parkin-deficiency. Full article
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