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Toxics
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The Neuroexposome: Integrating Exposures with Physiology to Understand Brain Health...
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The Neuroexposome: Integrating Exposures with Physiology to Understand Brain Health and Disease

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Neurotoxicity".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 1561

Special Issue Editors

Dr. Megan Mahoney

E-Mail Website
Guest Editor
Comparative Biosciences, University of Illinois Urbana Champaign, Urbana, IL 61802, USA
Interests: sex differences; behavior; neurotoxicology; phthalates; mixtures; pesticides; cognition; anxiety section; exposome analysis and risk assessment
Dr. Jennifer L. Freeman

E-Mail Website
Guest Editor
School of Health Sciences, Purdue University, 550 Stadium Mall Dr., HAMP-1163D, West Lafayette, IN 47907, USA
Interests: environmental and molecular toxicology; developmental origin of health and disease; genome and epigenome alterations; molecular cytogenetics; neurotoxicology; toxicogenomics; zebrafish model system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The brain can be exquisitely sensitive to environmental exposures, particularly during periods of development. However, exposures occurring across the lifespan, from conception to old age, can impact the nervous system, resulting in neuroanatomical changes, compromised neural functions, and the development of disease. Exposures such as air pollution, chemicals, plasticizers, and heavy metals can lead to the occurrence of neurodevelopmental disorders, neurodegenerative diseases, and neuropsychiatric conditions. Furthermore, there is potential for environmental exposures to have a significant impact on brain health in individuals that are already susceptible to disease, such as those with a genetic predisposition and those experiencing psychosocial stressors. The “neuroexposome” can be described as the neurophysiological outcomes which occur as a result of the sum of the internal and external exposures experienced by an individual. Research in this area will provide important insights into how our environment shapes the onset and progression of brain disease and provide potential avenues for intervention. Thus, the goal of this Special Issue is to examine the relationships between environmental exposures and endogenous factors which lead to brain dysfunction and disease states, including neurodevelopmental conditions such as autism, neurodegenerative diseases including Parkinson’s or Alzheimer’s disease, or neuropsychiatric conditions. We invite original research articles or reviews in this area.

Dr. Megan Mahoney
Dr. Jennifer L. Freeman
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. Toxics 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 2600 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

  • exposome
  • exposomics
  • neuroexposome
  • neurodegeneration
  • neurotoxicology
  • neurodevelopment
  • developmental origins of health and disease (DOHAD)

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Published Papers (3 papers)

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Research

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27 pages, 2012 KiB  
Article
Dual Effects of Maternal Diet and Perinatal Organophosphate Flame Retardant Treatment on Offspring Development, Behavior and Metabolism
by Ali Yasrebi, Catherine M. Rojas, Shabree Anthony, Samantha Feltri, Jamilah Evelyn, Kimberly Wiersielis, Samantha Adams, Veronia Basaly, Grace L. Guo, Lauren M. Aleksunes and Troy A. Roepke
Toxics 2025, 13(8), 639; https://doi.org/10.3390/toxics13080639 - 29 Jul 2025
Viewed by 334
Abstract
The maternal–fetal environment is influenced by multiple factors, including nutrition and environmental contaminants, which can impact long-term development. Perinatal exposure to organophosphate flame retardants (OPFRs) disrupts energy homeostasis and causes maladaptive behaviors in mice. Maternal obesity affects development by impairing blood–brain barrier (BBB) [...] Read more.
The maternal–fetal environment is influenced by multiple factors, including nutrition and environmental contaminants, which can impact long-term development. Perinatal exposure to organophosphate flame retardants (OPFRs) disrupts energy homeostasis and causes maladaptive behaviors in mice. Maternal obesity affects development by impairing blood–brain barrier (BBB) formation, influencing brain regions involved in energy regulation and behavior. This study examined the combined effects of maternal obesity and perinatal OPFR treatment on offspring development. Female mice were fed either a low-fat (LFD) or a high-fat diet (HFD) for 8 weeks, mated, and treated with either sesame oil or an OPFR mixture (tris(1,3-dichloro-2-propyl)phosphate, tricresyl phosphate, and triphenyl phosphate, 1 mg/kg each) from gestational day 7 to postnatal day 14. Results showed that both maternal diet and OPFR treatment disrupted blood–brain barrier integrity, energy balance, and reproductive gene expression in the hypothalamus of neonates. The expression of hepatic genes related to lipid and xenobiotic metabolism was also altered. In adulthood, LFD OPFR-treated female offspring exhibited increased avoidance behavior, while HFD OPFR-treated females demonstrated memory impairments. Metabolic assessments revealed decreased energy expenditure and nighttime activity in LFD OPFR-treated females. These findings suggest that maternal diet and OPFR treatment alter hypothalamic and liver gene expression in neonates, potentially leading to long-term metabolic and behavioral changes. Full article
(This article belongs to the Special Issue The Neuroexposome: Integrating Exposures with Physiology to Understand Brain Health and Disease)
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19 pages, 4063 KiB  
Article
Exposure to Mitochondrial Toxins: An In Vitro Study of Energy Depletion and Oxidative Stress in Driving Dopaminergic Neuronal Death in MN9D Cells
by Oluwatosin Adefunke Adetuyi and Kandatege Wimalasena
Toxics 2025, 13(8), 637; https://doi.org/10.3390/toxics13080637 - 29 Jul 2025
Viewed by 329
Abstract
Mitochondrial dysfunction is a key contributor to neurodegeneration, particularly in Parkinson’s disease (PD), where dopaminergic neurons being highly metabolically active are vulnerable to oxidative stress and bioenergetic failure. In this study, we investigate the effects of rotenone, a Complex I inhibitor, and antimycin [...] Read more.
Mitochondrial dysfunction is a key contributor to neurodegeneration, particularly in Parkinson’s disease (PD), where dopaminergic neurons being highly metabolically active are vulnerable to oxidative stress and bioenergetic failure. In this study, we investigate the effects of rotenone, a Complex I inhibitor, and antimycin A, a Complex III inhibitor, on mitochondrial function in MN9D dopaminergic neuronal cells. Cells were treated with rotenone (1.5 µM) or antimycin A (10 µM) for one hour, and key biochemical parameters were assessed, including ATP levels, reactive oxygen species (ROS) production, dopamine metabolism, and neuromelanin formation. Our results indicate significant ATP depletion and ROS accumulation following treatment with both inhibitors, with antimycin A inducing a more pronounced oxidative stress response. Dysregulation of dopamine biosynthesis differed mechanistically from vesicular monoamine transporter (VMAT2) inhibition by tetrabenazine, suggesting alternative pathways of catecholamine disruption. Additionally, oxidative stress led to increased neuromelanin accumulation, indicating a possible adaptive response to mitochondrial dysfunction. These findings provide insights into the cellular mechanisms underlying dopaminergic neurotoxicity and highlight mitochondrial electron transport chain inhibition as a key driver of PD pathogenesis. Future research should explore therapeutic strategies aimed at enhancing mitochondrial function to mitigate neurodegenerative progression. Full article
(This article belongs to the Special Issue The Neuroexposome: Integrating Exposures with Physiology to Understand Brain Health and Disease)
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Review

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22 pages, 2332 KiB  
Review
Glutamate-Mediated Neural Alterations in Lead Exposure: Mechanisms, Pathways, and Phenotypes
by Wagner A. Tamagno and Jennifer L. Freeman
Toxics 2025, 13(7), 519; https://doi.org/10.3390/toxics13070519 - 21 Jun 2025
Viewed by 567
Abstract
Lead (Pb) is a pervasive neurotoxicant with well-documented detrimental effects on the central nervous system, particularly in vulnerable populations such as children. Despite historical recognition of its toxicity, Pb exposure remains a significant public health concern due to its environmental persistence, historical industrial [...] Read more.
Lead (Pb) is a pervasive neurotoxicant with well-documented detrimental effects on the central nervous system, particularly in vulnerable populations such as children. Despite historical recognition of its toxicity, Pb exposure remains a significant public health concern due to its environmental persistence, historical industrial use, and ongoing applications in modern technologies. This review focuses on the mechanisms by which Pb disrupts glutamatergic signaling, a critical pathway for learning, memory, and synaptic plasticity. Pb’s interference with glutamate receptors (ionotropic NMDA and AMPA, as well as metabotropic receptors), transporters (EAATs, VGLUTs, and SNATs), and metabolic pathways (glutamate–glutamine cycle, TCA cycle, and glutathione synthesis) are detailed. By mimicking divalent cations like Ca2+ and Zn2+, Pb2+ disrupts calcium homeostasis, exacerbates excitotoxicity, and induces oxidative stress, ultimately impairing neuronal communication and synaptic function. These molecular disruptions manifest cognitive deficits, behavioral abnormalities, and increased susceptibility to neurodevelopmental and neurodegenerative disorders. Understanding Pb’s impact on glutamatergic neurotransmission offers critical insights into its neurotoxic profile and highlights the importance of addressing its effects on neural function. Full article
(This article belongs to the Special Issue The Neuroexposome: Integrating Exposures with Physiology to Understand Brain Health and Disease)
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