About this Research Topic
In recent years, environmental contaminants and pollutants have become a major public health concern. These substances, derived from sources such as chemical industries, automobile exhaust, research laboratories, agriculture, and clinical facilities, pose significant risks to both the environment and human health. Among these contaminants are nanoparticles, pesticides, nanoplastics, particulate matter, lipophilic vaporized toxicants, ultrafine particulate matter, and chemicals used in the production of polycarbonates and epoxy resins, including phthalates, Bisphenol A and its analogs.
These environmental contaminants are increasingly recognized for their potential role in the development or acceleration of neurological diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis. The high neurotoxic potency of these chemicals enables them to cross the blood-brain barrier, triggering stress and immune responses that activate astrocytes and microglia, ultimately leading to neuronal damage. There is evidence suggesting that these chemicals can induce neuroinflammation through mechanisms involving oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, myelin sheath disruption, and neurodegeneration, resulting in cognitive and motor impairments.
Reactive oxygen species (ROS) have been identified as mediators of redox signaling in neuronal damage, potentially stimulating inflammatory molecules that contribute to neuronal deterioration and oxidative stress. However, a detailed understanding of the impact of these environmental agents and the underlying mechanisms that regulate inflammatory responses and neuronal death remains elusive and requires further investigation.
Several in vitro and in vivo models have provided valuable insights at the preclinical and clinical stages, helping researchers explore potential therapeutic avenues. Understanding the mechanisms through which environmental pollutants provoke cellular stress and neuroinflammation is crucial for developing effective strategies to mitigate their impact on public health. Continued research is needed to elucidate these mechanisms and to formulate regulations and interventions that can enhance neurological health by minimizing exposure to these harmful substances.
There is still a scarcity of literature on the exact mechanisms of environmental contaminant-induced neurotoxicity, and there is an urgent need to investigate the interactions of these pollutants with the neuronal endogenous antioxidant defense system and inflammatory machinery, which may modulate neurodegeneration.
This Research Topic aims to gather original research articles and comprehensive reviews addressing the significance and impact of environmental contaminants on the brain and related neurological disorders.
We welcome submissions on the following themes:
o Mechanistic studies elucidating the pathways through which environmental pollutants induce neurotoxicity.
o The role of oxidative stress, mitochondrial dysfunction, and endoplasmic reticulum stress in pollutant-induced neuronal damage.
o In vitro and in vivo models developed to study the neurotoxic effects of environmental contaminants.
o The impact of specific contaminants, such as nanoparticles, nanoplastics, pesticides, and volatile organic compounds, on neuroinflammation and neurodegeneration.
o Biomolecular and cellular markers of neurotoxicity and their potential as therapeutic targets.
o Epidemiological studies linking exposure to environmental pollutants with the prevalence and progression of neurological disorders.
o Strategies for mitigating the neurotoxic effects of environmental pollutants, including potential pharmacological and non-pharmacological interventions.
o The interaction between environmental pollutants and the endogenous neuronal antioxidant defense system.
o The neurotoxic exposome and its influence on neurological health and disease progression.
o Regulatory approaches and policy recommendations to limit exposure to neurotoxic environmental contaminants.
These environmental contaminants are increasingly recognized for their potential role in the development or acceleration of neurological diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis. The high neurotoxic potency of these chemicals enables them to cross the blood-brain barrier, triggering stress and immune responses that activate astrocytes and microglia, ultimately leading to neuronal damage. There is evidence suggesting that these chemicals can induce neuroinflammation through mechanisms involving oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, myelin sheath disruption, and neurodegeneration, resulting in cognitive and motor impairments.
Reactive oxygen species (ROS) have been identified as mediators of redox signaling in neuronal damage, potentially stimulating inflammatory molecules that contribute to neuronal deterioration and oxidative stress. However, a detailed understanding of the impact of these environmental agents and the underlying mechanisms that regulate inflammatory responses and neuronal death remains elusive and requires further investigation.
Several in vitro and in vivo models have provided valuable insights at the preclinical and clinical stages, helping researchers explore potential therapeutic avenues. Understanding the mechanisms through which environmental pollutants provoke cellular stress and neuroinflammation is crucial for developing effective strategies to mitigate their impact on public health. Continued research is needed to elucidate these mechanisms and to formulate regulations and interventions that can enhance neurological health by minimizing exposure to these harmful substances.
There is still a scarcity of literature on the exact mechanisms of environmental contaminant-induced neurotoxicity, and there is an urgent need to investigate the interactions of these pollutants with the neuronal endogenous antioxidant defense system and inflammatory machinery, which may modulate neurodegeneration.
This Research Topic aims to gather original research articles and comprehensive reviews addressing the significance and impact of environmental contaminants on the brain and related neurological disorders.
We welcome submissions on the following themes:
o Mechanistic studies elucidating the pathways through which environmental pollutants induce neurotoxicity.
o The role of oxidative stress, mitochondrial dysfunction, and endoplasmic reticulum stress in pollutant-induced neuronal damage.
o In vitro and in vivo models developed to study the neurotoxic effects of environmental contaminants.
o The impact of specific contaminants, such as nanoparticles, nanoplastics, pesticides, and volatile organic compounds, on neuroinflammation and neurodegeneration.
o Biomolecular and cellular markers of neurotoxicity and their potential as therapeutic targets.
o Epidemiological studies linking exposure to environmental pollutants with the prevalence and progression of neurological disorders.
o Strategies for mitigating the neurotoxic effects of environmental pollutants, including potential pharmacological and non-pharmacological interventions.
o The interaction between environmental pollutants and the endogenous neuronal antioxidant defense system.
o The neurotoxic exposome and its influence on neurological health and disease progression.
o Regulatory approaches and policy recommendations to limit exposure to neurotoxic environmental contaminants.
Keywords: neurotoxicology, environmental contaminants, pollutants
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
