Cellular and Molecular Mechanisms of Neurotoxicity

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 July 2026 | Viewed by 1208

Special Issue Editors


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Guest Editor
Department of Neuroscience, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy
Interests: temporal lobe epilepsy; glia; astrocyte; microglia; connexin; neuroinflammation; cytokines; chicken imprinting

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Guest Editor
Department of Veterinary Anatomy, University of Jos, Jos, Nigeria
Interests: neuroanatomy

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Guest Editor
1. Department of Cell Biology, Physiology and Immunology, Faculty of Biology and Institute of Neurosciences, Universitat de Barcelona (UB), Barcelona, Spain
2. Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED-CIBER), ISCIII, Madrid, Spain
Interests: syntaxin-1

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Guest Editor
Department of Veterinary Anatomy, University of Ibadan, Ibadan, Nigeria
Interests: comparative anatomy; morphometrics; veterinary anatomy; embryology; gross anatomy; cross-sectional anatomy; neuro-therapy; neurodegeneration; neurotoxicology; immunohistochemistry

Special Issue Information

Dear Colleagues,

Neurotoxicity is a widespread condition as we are exposed to neurotoxic agents on a daily basis. Neurotoxins from external sources may be present in air pollutants, industrial chemicals, volatile gases, heavy metals, drugs, and other agents. Endogenous toxins can be produced through the altered metabolism of endogenous substances. The effects of toxins on the central and peripheral nervous system can lead to the degeneration and death of neuronal cells, and exposure to these substances has also been linked to the development of neurodegenerative diseases. This Special Issue will explore and provide a more comprehensive overview of the cellular and molecular mechanisms behind neurotoxicity and their connection to neurodegenerative conditions. The role of glial cells in neurotoxic mechanisms and the mechanisms by which neurotoxins cross or damage the blood–brain barrier are also of interest. Researchers are invited to contribute original research articles and reviews on the interactions of exogenous or endogenous neurotoxins with the nervous system, as well as their link to neurodegenerative diseases. Contributions highlighting disease models, human neuropathology, neuroinflammatory conditions, and cellular and molecular studies are welcome. This Special Issue does not intend to include articles analyzing clinical trials or focusing on therapeutic interventions.

Dr. Anna Andrioli
Dr. Idris Azeez
Dr. Tiziana Cotrufo
Dr. Olumayowa Igado
Guest Editors

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Keywords

  • neurotoxicity
  • neurodegeneration
  • neuronal cell death
  • neurodegenerative disorders
  • nerve regeneration
  • heavy metals
  • air pollution
  • endogenous neurotoxins
  • oxidative stress
  • glutamate

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Published Papers (1 paper)

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Research

18 pages, 3605 KB  
Article
PCB 153 Modulates Genes Involved in Proteasome and Neurodegeneration-Related Pathways in Differentiated SH-SY5Y Cells: A Transcriptomic Study
by Aurelio Minuti, Serena Silvestro, Claudia Muscarà, Michele Scuruchi and Simone D’Angiolini
Cells 2026, 15(3), 217; https://doi.org/10.3390/cells15030217 - 23 Jan 2026
Viewed by 659
Abstract
Polychlorinated biphenyls (PCBs) are persistent environmental contaminants associated with neurotoxicity and increased risk of neurodegenerative diseases. PCB 153, a highly abundant non-coplanar congener, bioaccumulates in human tissues and impairs homeostasis. This study investigated the transcriptomic effects of PCB 153 (2,2′,4,4′,5,5′-Hexachlorobiphenyl) in retinoic acid [...] Read more.
Polychlorinated biphenyls (PCBs) are persistent environmental contaminants associated with neurotoxicity and increased risk of neurodegenerative diseases. PCB 153, a highly abundant non-coplanar congener, bioaccumulates in human tissues and impairs homeostasis. This study investigated the transcriptomic effects of PCB 153 (2,2′,4,4′,5,5′-Hexachlorobiphenyl) in retinoic acid (RA)-differentiated SH-SY5Y neuronal cells to identify early, sub-cytotoxic molecular alterations. Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay after 24 h exposure to increasing PCB 153 concentrations. RNA-Seq was performed on cells treated with 5 μM PCB 153, the highest non-cytotoxic dose. Sequencing reads were quality-filtered, aligned to the human genome, and analyzed with DESeq2. Functional enrichment was conducted using Gene Ontologies and KEGG pathways. Western blot analyses were performed to assess protein level changes in selected targets. RNA-Seq identified 1882 significantly altered genes (q-value < 0.05). Gene Ontology analysis revealed strong enrichment of proteasome-related terms, with most proteasomal subunits displaying coordinated upregulation. KEGG analysis further showed significant enrichment of Alzheimer’s (AD), Parkinson’s (PD), amyotrophic lateral sclerosis (ALS), and other neurodegenerative disease pathways. These findings indicate that PCB 153 triggers a pronounced proteostatic response in neuron-like cells, suggesting early disruption of protein homeostasis that may contribute to mechanisms associated with neurodegeneration. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Neurotoxicity)
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