Special Issue "Molecular Signaling Pathways Associated with Neurotoxicity"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 31 October 2023 | Viewed by 191

Special Issue Editors

Albert Einstein College of Medicine, Yeshiva University, New York, NY, USA
Interests: neurotoxicity; neurological disorders; metals; natural small molecules; C. elegans
Graduation Program in Biochemistry, Universidade Federal do Pampa, Uruguaiana, Brazil
Interests: neurotoxicity; metals; pesticides; nanotoxicology; Caenorhabditis elegans
Special Issues, Collections and Topics in MDPI journals
Vanderbilt University Medical Center, Nashville, TN, USA
Interests: neurotoxicology; pesticides; metals; human-induced pluripotent stem cell models; microfluidic tissue chips

Special Issue Information

Dear Colleagues,

The rising incidence of neurodegenerative diseases and neurodevelopmental disorders is associated with an increasing social and financial global burden. The cause of neurodegenerative and neurodevelopmental disease is generally difficult to pinpoint, and they are largely due to a combination of genetic and environmental factors. Exposures to neurotoxicants, such as pesticides and heavy metals, are known to negatively impact the human CNS and have been implicated in the pathogenesis of CNS disease. Common molecular mechanisms of neurotoxicity, including oxidative stress, mitochondrial dysfunction and the alteration of protein homeostasis, are regulated via intracellular signaling transduction. Neurotoxicant-induced changes in signaling pathways may interfere with neural circuitry, the CNS immune system and/or blood–brain barrier function, eventually leading to neurological disorders. A considerable challenge to understanding the mechanistic basis of neurotoxicity is the lack of known molecular targets and/or the mechanism by which environmental toxicants affects these targets. Thus, there is an urgent need to investigate mechanistically relevant signaling pathways associated with the ever-growing number and levels of neurotoxicants in our environment. Therefore, we invite our colleagues in the field of neurotoxicology to submit either primary research findings or a review to this Special Issue, entitled “Molecular Signaling Pathways Associated With Neurotoxicity”.

Dr. Pan Chen
Prof. Dr. Daiana Silva Ávila
Dr. M. Diana Neely
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.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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.


  • neurotoxicity
  • signal transduction
  • heavy metals
  • environmental toxicants
  • neurodegeneration

Published Papers

This special issue is now open for submission, see below for planned papers.

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: p38- and ERK-MAPK signalling modulate developmental neurotoxicity of nickel and vanadium in the Caenorhabditis elegans model
Authors: Omamuyovwi M. Ijomone; Ann-Kathrin Weishaupt; Vivien Michaelis; Julia Bornhorst
Affiliation: 1) Food Chemistry, Faculty of Mathematics and Natural Sciences, University of Wuppertal, Wuppertal, Germany 2) The Neuro- Lab, Department of Human Anatomy, School of Basic Medical Sciences, Federal University of Technology Akure, Akure, Nigeria 3) Department of Anatomy, Faculty of Basic Medical Sciences, University of Medical Sciences, Ondo, Nigeria 4) TraceAge-DFG Research Unit on Interactions of Essential Trace Elements in Healthy and Diseased Elderly (FOR 2558), Berlin-Potsdam-Jena-Wuppertal, 14558 Nuthetal, Germany
Abstract: Nickel (Ni) and vanadium (V) are characteristic heavy metal constituents of many crude oil blends in Sub-Saharan Africa, and we have previously demonstrated their neurotoxic impact. However, molecular mechanisms driving Ni and V neurotoxicity are still being elucidated. The p38- and ERKs-MAPK pathways, which are mostly known for their involvement in human immune and inflammatory signalling, have been shown to influence an array of neurodevelopmental processes. In the present study, we attempt to elucidate the role of p38- and ERK-MAPK in neurotoxicity after early life exposures to Ni and V using the Caenorhabditis elegans model. Synchronized larvae stage-1 (L1) worms were treated with varying concentrations of Ni and V singly or in combination for 1 hour. Our results show Ni induces lethality in C. elegans even at very low concentrations. while much higher V concentrations are required to induce lethality. Furthermore, we identified that loss-of-function of pmk-1 and pmk-3 which are both homologous to human p38-α (MAPK14) are differentially affected by Ni and V exposures. Also, all exposure scenarios triggered significant developmental delays in both wild-type and mutant strains. We also see increased mitochondrial-derived reactive oxygen species following Ni and V exposures in wild-type worms with differential responses in mutant strains. Additionally, we observed alterations in dopamine and serotonin levels after metal exposures, particularly in the pmk-1 strain. Overall, our results suggest the p38- and ERK-MAPK signalling pathways may modulate Ni and V neurodevelopmental toxicity potentially affecting mitochondrial health, metal level dynamics and neurotransmitter levels.

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