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Molecular Basis for the Environmental Promotion of Neurodegenerative Disease
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Molecular Basis for the Environmental Promotion of Neurodegenerative Disease

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

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 35111

Special Issue Editor

Prof. Dr. Stephen C. Bondy

E-Mail Website
Guest Editor
Center for Occupational and Environmental Health, Department of Medicine, University of California, Irvine 100 Theory, Suite 100, Irvine, CA 92617-1830, USA
Interests: neurotoxicology; nutririon; aging; protein aggregates
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,  

Most neurodegenerative diseases have a relatively minor genetic component. Huntington’s disease is the only major exception with the genetic penetrance being 100%. This implies that unknown environmental factors play a major role in determining the prevalence of defined neurological diseases in a specific population. Such agents consist of materials present in the general environment, such as those present in air, water, or surrounding terrains.

This special issue is focused on the possible molecular mechanisms by which these exogenous influences can initiate or accelerate processes associated with brain aging. Such expedition of normal events can lead to the premature emergence of distinctive disorders associated with brain aging. Mechanistic clues may be initiated by findings from clinical or epidemiological studies to be followed up using more detailed analyses of animal and isolated cell models. Each of the chapters will elaborate on some aspect of the more common neurodegenerative disorders toward better understanding the molecular disruption that is involved.

Prof. Dr. Stephen C. Bondy
Guest Editor

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Keywords

  • environmental toxicology
  • environmental neurotoxicology
  • neurodegenerative disease
  • neurological
  • idiopathic
  • environmental factors
  • brain disorder

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Published Papers (5 papers)

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Research

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17 pages, 2711 KiB  
Article
A Commonly Used Biocide 2-N-octyl-4-isothiazolin-3-oneInduces Blood–Brain Barrier Dysfunction via Cellular Thiol Modification and Mitochondrial Damage
by Donghyun Kim, Eun-Hye Kim, Sungbin Choi, Kyung-Min Lim, Lu Tie, Arshad Majid and Ok-Nam Bae
Int. J. Mol. Sci. 2021, 22(5), 2563; https://doi.org/10.3390/ijms22052563 - 4 Mar 2021
Cited by 9 | Viewed by 4076
Abstract
Isothiazolinone (IT) biocides are potent antibacterial substances commonly used as preservatives or disinfectants, and 2-n-Octyl-4-isothiazolin-3-one (OIT; octhilinone) is a common IT biocide that is present in leather products, glue, paints, and cleaning products. Although humans are exposed to OIT through personal and industrial [...] Read more.
Isothiazolinone (IT) biocides are potent antibacterial substances commonly used as preservatives or disinfectants, and 2-n-Octyl-4-isothiazolin-3-one (OIT; octhilinone) is a common IT biocide that is present in leather products, glue, paints, and cleaning products. Although humans are exposed to OIT through personal and industrial use, the potentially deleterious effects of OIT on human health are still unknown. To investigate the effects of OIT on the vascular system, which is continuously exposed to xenobiotics through systemic circulation, we treated brain endothelial cells with OIT. OIT treatment significantly activated caspase-3-mediated apoptosis and reduced the bioenergetic function of mitochondria in a bEnd.3 cell-based in vitro blood–brain barrier (BBB) model. Interestingly, OIT significantly altered the thiol redox status, as evidenced by reduced glutathione levels and protein S-nitrosylation. The endothelial barrier function of bEnd.3 cells was significantly impaired by OIT treatment. OIT affected mitochondrial dynamics through mitophagy and altered mitochondrial morphology in bEnd.3 cells. N-acetyl cysteine significantly reversed the effects of OIT on the metabolic capacity and endothelial function of bEnd.3 cells. Taken together, we demonstrated that the alteration of the thiol redox status and mitochondrial damage contributed to OIT-induced BBB dysfunction, and we hope that our findings will improve our understanding of the potential hazardous health effects of IT biocides. Full article
(This article belongs to the Special Issue Molecular Basis for the Environmental Promotion of Neurodegenerative Disease)
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Review

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30 pages, 1166 KiB  
Review
Impact of Environmental Risk Factors on Mitochondrial Dysfunction, Neuroinflammation, Protein Misfolding, and Oxidative Stress in the Etiopathogenesis of Parkinson’s Disease
by Minhong Huang, Alejandra Bargues-Carot, Zainab Riaz, Hannah Wickham, Gary Zenitsky, Huajun Jin, Vellareddy Anantharam, Arthi Kanthasamy and Anumantha G. Kanthasamy
Int. J. Mol. Sci. 2022, 23(18), 10808; https://doi.org/10.3390/ijms231810808 - 16 Sep 2022
Cited by 32 | Viewed by 5895
Abstract
As a prevalent progressive neurodegenerative disorder, Parkinson’s disease (PD) is characterized by the neuropathological hallmark of the loss of nigrostriatal dopaminergic (DAergic) innervation and the appearance of Lewy bodies with aggregated α-synuclein. Although several familial forms of PD have been reported to be [...] Read more.
As a prevalent progressive neurodegenerative disorder, Parkinson’s disease (PD) is characterized by the neuropathological hallmark of the loss of nigrostriatal dopaminergic (DAergic) innervation and the appearance of Lewy bodies with aggregated α-synuclein. Although several familial forms of PD have been reported to be associated with several gene variants, most cases in nature are sporadic, triggered by a complex interplay of genetic and environmental risk factors. Numerous epidemiological studies during the past two decades have shown positive associations between PD and several environmental factors, including exposure to neurotoxic pesticides/herbicides and heavy metals as well as traumatic brain injury. Other environmental factors that have been implicated as potential risk factors for PD include industrial chemicals, wood pulp mills, farming, well-water consumption, and rural residence. In this review, we summarize the environmental toxicology of PD with the focus on the elaboration of chemical toxicity and the underlying pathogenic mechanisms associated with exposure to several neurotoxic chemicals, specifically 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, paraquat (PQ), dichloro-diphenyl-trichloroethane (DDT), dieldrin, manganese (Mn), and vanadium (V). Our overview of the current findings from cellular, animal, and human studies of PD provides information for possible intervention strategies aimed at halting the initiation and exacerbation of environmentally linked PD. Full article
(This article belongs to the Special Issue Molecular Basis for the Environmental Promotion of Neurodegenerative Disease)
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25 pages, 1567 KiB  
Review
Molecular Mechanism of Arsenic-Induced Neurotoxicity including Neuronal Dysfunctions
by Manisha Thakur, Mahesh Rachamalla, Som Niyogi, Ashok Kumar Datusalia and Swaran Jeet Singh Flora
Int. J. Mol. Sci. 2021, 22(18), 10077; https://doi.org/10.3390/ijms221810077 - 17 Sep 2021
Cited by 82 | Viewed by 13241
Abstract
Arsenic is a key environmental toxicant having significant impacts on human health. Millions of people in developing countries such as Bangladesh, Mexico, Taiwan, and India are affected by arsenic contamination through groundwater. Environmental contamination of arsenic leads to leads to various types of [...] Read more.
Arsenic is a key environmental toxicant having significant impacts on human health. Millions of people in developing countries such as Bangladesh, Mexico, Taiwan, and India are affected by arsenic contamination through groundwater. Environmental contamination of arsenic leads to leads to various types of cancers, coronary and neurological ailments in human. There are several sources of arsenic exposure such as drinking water, diet, wood preservatives, smoking, air and cosmetics, while, drinking water is the most explored route. Inorganic arsenic exhibits higher levels of toxicity compared its organic forms. Exposure to inorganic arsenic is known to cause major neurological effects such as cytotoxicity, chromosomal aberration, damage to cellular DNA and genotoxicity. On the other hand, long-term exposure to arsenic may cause neurobehavioral effects in the juvenile stage, which may have detrimental effects in the later stages of life. Thus, it is important to understand the toxicology and underlying molecular mechanism of arsenic which will help to mitigate its detrimental effects. The present review focuses on the epidemiology, and the toxic mechanisms responsible for arsenic induced neurobehavioral diseases, including strategies for its management from water, community and household premises. The review also provides a critical analysis of epigenetic and transgenerational modifications, mitochondrial oxidative stress, molecular mechanisms of arsenic-induced oxidative stress, and neuronal dysfunction. Full article
(This article belongs to the Special Issue Molecular Basis for the Environmental Promotion of Neurodegenerative Disease)
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23 pages, 326 KiB  
Review
Microglia in Neurodegenerative Events—An Initiator or a Significant Other?
by Gaylia Jean Harry
Int. J. Mol. Sci. 2021, 22(11), 5818; https://doi.org/10.3390/ijms22115818 - 29 May 2021
Cited by 24 | Viewed by 3897
Abstract
A change in microglia structure, signaling, or function is commonly associated with neurodegeneration. This is evident in the patient population, animal models, and targeted in vitro assays. While there is a clear association, it is not evident that microglia serve as an initiator [...] Read more.
A change in microglia structure, signaling, or function is commonly associated with neurodegeneration. This is evident in the patient population, animal models, and targeted in vitro assays. While there is a clear association, it is not evident that microglia serve as an initiator of neurodegeneration. Rather, the dynamics imply a close interaction between the various cell types and structures in the brain that orchestrate the injury and repair responses. Communication between microglia and neurons contributes to the physiological phenotype of microglia maintaining cells in a surveillance state and allows the cells to respond to events occurring in their environment. Interactions between microglia and astrocytes is not as well characterized, nor are interactions with other members of the neurovascular unit; however, given the influence of systemic factors on neuroinflammation and disease progression, such interactions likely represent significant contributes to any neurodegenerative process. In addition, they offer multiple target sites/processes by which environmental exposures could contribute to neurodegenerative disease. Thus, microglia at least play a role as a significant other with an equal partnership; however, claiming a role as an initiator of neurodegeneration remains somewhat controversial. Full article
(This article belongs to the Special Issue Molecular Basis for the Environmental Promotion of Neurodegenerative Disease)
27 pages, 1286 KiB  
Review
Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update
by Alexey A. Tinkov, Monica M. B. Paoliello, Aksana N. Mazilina, Anatoly V. Skalny, Airton C. Martins, Olga N. Voskresenskaya, Jan Aaseth, Abel Santamaria, Svetlana V. Notova, Aristides Tsatsakis, Eunsook Lee, Aaron B. Bowman and Michael Aschner
Int. J. Mol. Sci. 2021, 22(9), 4646; https://doi.org/10.3390/ijms22094646 - 28 Apr 2021
Cited by 61 | Viewed by 6690
Abstract
Understanding of the immediate mechanisms of Mn-induced neurotoxicity is rapidly evolving. We seek to provide a summary of recent findings in the field, with an emphasis to clarify existing gaps and future research directions. We provide, here, a brief review of pertinent discoveries [...] Read more.
Understanding of the immediate mechanisms of Mn-induced neurotoxicity is rapidly evolving. We seek to provide a summary of recent findings in the field, with an emphasis to clarify existing gaps and future research directions. We provide, here, a brief review of pertinent discoveries related to Mn-induced neurotoxicity research from the last five years. Significant progress was achieved in understanding the role of Mn transporters, such as SLC39A14, SLC39A8, and SLC30A10, in the regulation of systemic and brain manganese handling. Genetic analysis identified multiple metabolic pathways that could be considered as Mn neurotoxicity targets, including oxidative stress, endoplasmic reticulum stress, apoptosis, neuroinflammation, cell signaling pathways, and interference with neurotransmitter metabolism, to name a few. Recent findings have also demonstrated the impact of Mn exposure on transcriptional regulation of these pathways. There is a significant role of autophagy as a protective mechanism against cytotoxic Mn neurotoxicity, yet also a role for Mn to induce autophagic flux itself and autophagic dysfunction under conditions of decreased Mn bioavailability. This ambivalent role may be at the crossroad of mitochondrial dysfunction, endoplasmic reticulum stress, and apoptosis. Yet very recent evidence suggests Mn can have toxic impacts below the no observed adverse effect of Mn-induced mitochondrial dysfunction. The impact of Mn exposure on supramolecular complexes SNARE and NLRP3 inflammasome greatly contributes to Mn-induced synaptic dysfunction and neuroinflammation, respectively. The aforementioned effects might be at least partially mediated by the impact of Mn on α-synuclein accumulation. In addition to Mn-induced synaptic dysfunction, impaired neurotransmission is shown to be mediated by the effects of Mn on neurotransmitter systems and their complex interplay. Although multiple novel mechanisms have been highlighted, additional studies are required to identify the critical targets of Mn-induced neurotoxicity. Full article
(This article belongs to the Special Issue Molecular Basis for the Environmental Promotion of Neurodegenerative Disease)
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