Is Neurodegenerative Disease a Long-Latency Response to Early-Life Genotoxin Exposure?

Western Pacific amyotrophic lateral sclerosis and parkinsonism-dementia complex, a disappearing neurodegenerative disease linked to use of the neurotoxic cycad plant for food and/or medicine, is intensively studied because the neuropathology (tauopathy) is similar to that of Alzheimer’s disease. Cyc...

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Autores principales: Kisby, Glen E., Spencer, Peter S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210588/
https://www.ncbi.nlm.nih.gov/pubmed/22073019
http://dx.doi.org/10.3390/ijerph8103889
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author Kisby, Glen E.
Spencer, Peter S.
author_facet Kisby, Glen E.
Spencer, Peter S.
author_sort Kisby, Glen E.
collection PubMed
description Western Pacific amyotrophic lateral sclerosis and parkinsonism-dementia complex, a disappearing neurodegenerative disease linked to use of the neurotoxic cycad plant for food and/or medicine, is intensively studied because the neuropathology (tauopathy) is similar to that of Alzheimer’s disease. Cycads contain neurotoxic and genotoxic principles, notably cycasin and methylazoxymethanol, the latter sharing chemical relations with nitrosamines, which are derived from nitrates and nitrites in preserved meats and fertilizers, and also used in the rubber and leather industries. This review includes new data that influence understanding of the neurobiological actions of cycad and related genotoxins and the putative mechanisms by which they might trigger neurodegenerative disease.
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spelling pubmed-32105882011-11-09 Is Neurodegenerative Disease a Long-Latency Response to Early-Life Genotoxin Exposure? Kisby, Glen E. Spencer, Peter S. Int J Environ Res Public Health Review Western Pacific amyotrophic lateral sclerosis and parkinsonism-dementia complex, a disappearing neurodegenerative disease linked to use of the neurotoxic cycad plant for food and/or medicine, is intensively studied because the neuropathology (tauopathy) is similar to that of Alzheimer’s disease. Cycads contain neurotoxic and genotoxic principles, notably cycasin and methylazoxymethanol, the latter sharing chemical relations with nitrosamines, which are derived from nitrates and nitrites in preserved meats and fertilizers, and also used in the rubber and leather industries. This review includes new data that influence understanding of the neurobiological actions of cycad and related genotoxins and the putative mechanisms by which they might trigger neurodegenerative disease. Molecular Diversity Preservation International (MDPI) 2011-10 2011-09-29 /pmc/articles/PMC3210588/ /pubmed/22073019 http://dx.doi.org/10.3390/ijerph8103889 Text en © 2011 by the authors; licensee MDPI, Basel, Switzerland http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Kisby, Glen E.
Spencer, Peter S.
Is Neurodegenerative Disease a Long-Latency Response to Early-Life Genotoxin Exposure?
title Is Neurodegenerative Disease a Long-Latency Response to Early-Life Genotoxin Exposure?
title_full Is Neurodegenerative Disease a Long-Latency Response to Early-Life Genotoxin Exposure?
title_fullStr Is Neurodegenerative Disease a Long-Latency Response to Early-Life Genotoxin Exposure?
title_full_unstemmed Is Neurodegenerative Disease a Long-Latency Response to Early-Life Genotoxin Exposure?
title_short Is Neurodegenerative Disease a Long-Latency Response to Early-Life Genotoxin Exposure?
title_sort is neurodegenerative disease a long-latency response to early-life genotoxin exposure?
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210588/
https://www.ncbi.nlm.nih.gov/pubmed/22073019
http://dx.doi.org/10.3390/ijerph8103889
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