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Neurological Disorders: From Alcoholism to Environmental Pollution

A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601). This special issue belongs to the section "Toxicology and Public Health".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 8090

Special Issue Editor

Department of Experimental and Clinical Medicine, Anatomy Section, School of Human Health Sciences, University of Florence, 50121 Florence, Italy
Interests: blood–brain barrier; vitamin D; cadmium toxicity; cannabidiol; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

I am glad to announce the Special Issue titled “Neurological disorders: from alcoholism to environmental pollution”, in the International Journal of Environmental Research and Public Health.

This Special Issue aims to better understand the effects of alcohol and environmental pollutant exposure on the nervous system, ranging from neurodegeneration to neuroinflammation. It is my pleasure to invite researchers that are working in vitro, in vivo and ex vivo, to submit original research manuscripts focusing on neurological disorders related to alcoholism or environmental pollution. Despite the aetiology of these disorders still being poorly understood, the central role of environmental pollutants and alcohol as putative risk factors is gaining more and more importance. Neurotoxic heavy metal, pesticides, metal-based nanoparticles, polychlorinated biphenyls, polycyclic aromatic hydrocarbons and alcohol contribute to chronic neurodegenerative diseases and neurodevelopmental disorders that lead to enormous direct and indirect healthcare costs, and millions of deaths worldwide every year.

In this regard, a better understanding of the pollution- and alcoholism-associated neurodegeneration may improve the knowledge in the field, and ameliorate the public health outcomes.

Dr. Jacopo Junio Valerio Branca
Guest Editor

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. International Journal of Environmental Research and Public Health 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 2500 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

  • Alcohol exposure
  • environmental pollutants
  • neuroinflammation
  • neurodegeneration
  • neurodevelopmental disorders
  • neurological diseases

Published Papers (2 papers)

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Research

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14 pages, 4730 KiB  
Article
Alcohol-Induced Blood-Brain Barrier Impairment: An In Vitro Study
by Donatello Carrino, Jacopo Junio Valerio Branca, Matteo Becatti, Ferdinando Paternostro, Gabriele Morucci, Massimo Gulisano, Lorenzo Di Cesare Mannelli and Alessandra Pacini
Int. J. Environ. Res. Public Health 2021, 18(5), 2683; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph18052683 - 07 Mar 2021
Cited by 15 | Viewed by 2983
Abstract
In recent years, alcohol abuse has dramatically grown with deleterious consequence for people’s health and, in turn, for health care costs. It has been demonstrated, in humans and animals, that alcohol intoxication induces neuroinflammation and neurodegeneration thus leading to brain impairments. Furthermore, it [...] Read more.
In recent years, alcohol abuse has dramatically grown with deleterious consequence for people’s health and, in turn, for health care costs. It has been demonstrated, in humans and animals, that alcohol intoxication induces neuroinflammation and neurodegeneration thus leading to brain impairments. Furthermore, it has been shown that alcohol consumption is able to impair the blood–brain barrier (BBB), but the molecular mechanisms underlining this detrimental effect have not been fully elucidated. For this reason, in this study we investigated the effects of alcohol exposure on a rat brain endothelial (RBE4) cell line, as an in vitro-validated model of brain microvascular endothelial cells. To assess whether alcohol caused a concentration-related response, the cells were treated at different times with increasing concentrations (10–1713 mM) of ethyl alcohol (EtOH). Microscopic and molecular techniques, such as cell viability assay, immunofluorescence and Western blotting, were used to examine the mechanisms involved in alcohol-induced brain endothelial cell alterations including tight junction distribution, apoptosis, and reactive oxygen species production. Our findings clearly demonstrate that alcohol causes the formation of gaps between cells by tight junction disassembly, triggered by the endoplasmic reticulum and oxidative stress, highlighted by GRP78 chaperone upregulation and increase in reactive oxygen species production, respectively. The results from this study shed light on the mechanisms underlying alcohol-induced blood–brain barrier dysfunction and a better understanding of these processes will allow us to take advantage of developing new therapeutic strategies in order to prevent the deleterious effects of alcohol. Full article
(This article belongs to the Special Issue Neurological Disorders: From Alcoholism to Environmental Pollution)
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Review

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23 pages, 382 KiB  
Review
Epigenetic Basis of Lead-Induced Neurological Disorders
by Tian Wang, Jie Zhang and Yi Xu
Int. J. Environ. Res. Public Health 2020, 17(13), 4878; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph17134878 - 07 Jul 2020
Cited by 47 | Viewed by 4617
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Neurological Disorders: From Alcoholism to Environmental Pollution)
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