EDTA Chelation Therapy for the Treatment of Neurotoxicity

Neurotoxicity can be caused by numerous direct agents, of which toxic metals, organophosphorus pesticides, air pollution, radiation and electromagnetic fields, neurotoxins, chemotherapeutic and anesthetic drugs, and pathogens are the most important. Other indirect causes of neurotoxicity are cytokin...

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Main Authors: Fulgenzi Alessandro, Ferrero Maria Elena
Format: Article
Language:English
Published: MDPI AG 2019-02-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/20/5/1019
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spelling doaj-0998c36616174aa6911862a60b139fff2020-11-25T01:33:49ZengMDPI AGInternational Journal of Molecular Sciences1422-00672019-02-01205101910.3390/ijms20051019ijms20051019EDTA Chelation Therapy for the Treatment of NeurotoxicityFulgenzi Alessandro0Ferrero Maria Elena1Department of Biomedical Sciences for Health, University of the Study of Milan, 20133 Milan, ItalyDepartment of Biomedical Sciences for Health, University of the Study of Milan, 20133 Milan, ItalyNeurotoxicity can be caused by numerous direct agents, of which toxic metals, organophosphorus pesticides, air pollution, radiation and electromagnetic fields, neurotoxins, chemotherapeutic and anesthetic drugs, and pathogens are the most important. Other indirect causes of neurotoxicity are cytokine and/or reactive oxygen species production and adoptive immunotherapy. The development of neurodegenerative diseases has been associated with neurotoxicity. Which arms are useful to prevent or eliminate neurotoxicity? The chelating agent calcium disodium ethylenediaminetetraacetic acid (EDTA)—previously used to treat cardiovascular diseases—is known to be useful for the treatment of neurodegenerative diseases. This review describes how EDTA functions as a therapeutic agent for these diseases. Some case studies are reported to confirm our findings.https://www.mdpi.com/1422-0067/20/5/1019neurotoxicityneurological diseasescardiovascular diseasesEDTA
collection DOAJ
language English
format Article
sources DOAJ
author Fulgenzi Alessandro
Ferrero Maria Elena
spellingShingle Fulgenzi Alessandro
Ferrero Maria Elena
EDTA Chelation Therapy for the Treatment of Neurotoxicity
International Journal of Molecular Sciences
neurotoxicity
neurological diseases
cardiovascular diseases
EDTA
author_facet Fulgenzi Alessandro
Ferrero Maria Elena
author_sort Fulgenzi Alessandro
title EDTA Chelation Therapy for the Treatment of Neurotoxicity
title_short EDTA Chelation Therapy for the Treatment of Neurotoxicity
title_full EDTA Chelation Therapy for the Treatment of Neurotoxicity
title_fullStr EDTA Chelation Therapy for the Treatment of Neurotoxicity
title_full_unstemmed EDTA Chelation Therapy for the Treatment of Neurotoxicity
title_sort edta chelation therapy for the treatment of neurotoxicity
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1422-0067
publishDate 2019-02-01
description Neurotoxicity can be caused by numerous direct agents, of which toxic metals, organophosphorus pesticides, air pollution, radiation and electromagnetic fields, neurotoxins, chemotherapeutic and anesthetic drugs, and pathogens are the most important. Other indirect causes of neurotoxicity are cytokine and/or reactive oxygen species production and adoptive immunotherapy. The development of neurodegenerative diseases has been associated with neurotoxicity. Which arms are useful to prevent or eliminate neurotoxicity? The chelating agent calcium disodium ethylenediaminetetraacetic acid (EDTA)—previously used to treat cardiovascular diseases—is known to be useful for the treatment of neurodegenerative diseases. This review describes how EDTA functions as a therapeutic agent for these diseases. Some case studies are reported to confirm our findings.
topic neurotoxicity
neurological diseases
cardiovascular diseases
EDTA
url https://www.mdpi.com/1422-0067/20/5/1019
work_keys_str_mv AT fulgenzialessandro edtachelationtherapyforthetreatmentofneurotoxicity
AT ferreromariaelena edtachelationtherapyforthetreatmentofneurotoxicity
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