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Epigenetic Basis of Lead-Induced Neurological Disorders

Author

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  • Tian Wang

    (School of Food and Bioengineering, Hefei University of Technology, Hefei 230009, China)

  • Jie Zhang

    (School of Food and Bioengineering, Hefei University of Technology, Hefei 230009, China)

  • Yi Xu

    (School of Food and Bioengineering, Hefei University of Technology, Hefei 230009, China)

Abstract

Environmental lead (Pb) exposure is closely associated with pathogenesis of a range of neurological disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), attention deficit/hyperactivity disorder (ADHD), etc. Epigenetic machinery modulates neural development and activities, while faulty epigenetic regulation contributes to the diverse forms of CNS (central nervous system) abnormalities and diseases. As a potent epigenetic modifier, lead is thought to cause neurological disorders through modulating epigenetic mechanisms. Specifically, increasing evidence linked aberrant DNA methylations, histone modifications as well as ncRNAs (non-coding RNAs) with AD cases, among which circRNA (circular RNA) stands out as a new and promising field for association studies. In 23-year-old primates with developmental lead treatment, Zawia group discovered a variety of epigenetic changes relating to AD pathogenesis. This is a direct evidence implicating epigenetic basis in lead-induced AD animals with an entire lifespan. Additionally, some epigenetic molecules associated with AD etiology were also known to respond to chronic lead exposure in comparable disease models, indicating potentially interlaced mechanisms with respect to the studied neurotoxic and pathological events. Of note, epigenetic molecules acted via globally or selectively influencing the expression of disease-related genes. Compared to AD, the association of lead exposure with other neurological disorders were primarily supported by epidemiological survey, with fewer reports connecting epigenetic regulators with lead-induced pathogenesis. Some pharmaceuticals, such as HDAC (histone deacetylase) inhibitors and DNA methylation inhibitors, were developed to deal with CNS disease by targeting epigenetic components. Still, understandings are insufficient regarding the cause–consequence relations of epigenetic factors and neurological illness. Therefore, clear evidence should be provided in future investigations to address detailed roles of novel epigenetic factors in lead-induced neurological disorders, and efforts of developing specific epigenetic therapeutics should be appraised.

Suggested Citation

  • Tian Wang & Jie Zhang & Yi Xu, 2020. "Epigenetic Basis of Lead-Induced Neurological Disorders," IJERPH, MDPI, vol. 17(13), pages 1-23, July.
  • Handle: RePEc:gam:jijerp:v:17:y:2020:i:13:p:4878-:d:381169
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    References listed on IDEAS

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    3. Johannes Gräff & Damien Rei & Ji-Song Guan & Wen-Yuan Wang & Jinsoo Seo & Krista M. Hennig & Thomas J. F. Nieland & Daniel M. Fass & Patricia F. Kao & Martin Kahn & Susan C. Su & Alireza Samiei & Nadi, 2012. "An epigenetic blockade of cognitive functions in the neurodegenerating brain," Nature, Nature, vol. 483(7388), pages 222-226, March.
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    Cited by:

    1. Giorgia Adani & Tommaso Filippini & Caterina Garuti & Marcella Malavolti & Giulia Vinceti & Giovanna Zamboni & Manuela Tondelli & Chiara Galli & Manuela Costa & Marco Vinceti & Annalisa Chiari, 2020. "Environmental Risk Factors for Early-Onset Alzheimer’s Dementia and Frontotemporal Dementia: A Case-Control Study in Northern Italy," IJERPH, MDPI, vol. 17(21), pages 1-18, October.
    2. Yifei Duan & Hua Shi & Yongmei Jiang, 2021. "The Blood Lead Levels of Children and the Loss of Ca 2+ from Neurons Owing to Lead," IJERPH, MDPI, vol. 18(22), pages 1-11, November.

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