Occupational-like organophosphate exposure disrupts microglia and accelerates deficits in a rat model of Alzheimer’s disease

Occupational exposure to toxins may accelerate Alzheimer’s disease The interaction of genes and environment contributes to Alzheimer’s disease (AD). For example, agricultural workers, military personnel, industrial manufacturers, veterinarians, horticulturists, aircraft maintenance personnel, and pi...

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Autores principales:	Jaymie R. Voorhees, Matthew T. Remy, Claire M. Erickson, Laura M. Dutca, Daniel J. Brat, Andrew A. Pieper
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2019
Materias:	Geriatrics RC952-954.6
Acceso en línea:	https://doaj.org/article/97add60acab14939931cb8b2bbeb72e7
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spelling	oai:doaj.org-article:97add60acab14939931cb8b2bbeb72e72021-12-02T14:22:33ZOccupational-like organophosphate exposure disrupts microglia and accelerates deficits in a rat model of Alzheimer’s disease10.1038/s41514-018-0033-32056-3973https://doaj.org/article/97add60acab14939931cb8b2bbeb72e72019-01-01T00:00:00Zhttps://doi.org/10.1038/s41514-018-0033-3https://doaj.org/toc/2056-3973Occupational exposure to toxins may accelerate Alzheimer’s disease The interaction of genes and environment contributes to Alzheimer’s disease (AD). For example, agricultural workers, military personnel, industrial manufacturers, veterinarians, horticulturists, aircraft maintenance personnel, and pilots are all potentially at risk of occupational exposure to organophosphates (OPs), which are associated with increased risk of AD. We report here that occupational-like exposure of young animals to the OP chlorpyrifos (CPF) accelerates AD-like cognitive deficits and severe neurodegeneration in male, but not female, TgF344-AD rats, a genetic model of AD. CPF exposure also causes chronic dysregulation of brain microglial cells, while amyloid and tau pathology are not affected. Thus, microglial dysregulation after environmental toxin exposure may represent a second hit that advances the disease. Future therapies to preserve or restore normal microglia might help prevent AD in genetically vulnerable individuals exposed to CPF or other disease-accelerating environmental agents.Jaymie R. VoorheesMatthew T. RemyClaire M. EricksonLaura M. DutcaDaniel J. BratAndrew A. PieperNature PortfolioarticleGeriatricsRC952-954.6ENnpj Aging and Mechanisms of Disease, Vol 5, Iss 1, Pp 1-14 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	Geriatrics RC952-954.6
spellingShingle	Geriatrics RC952-954.6 Jaymie R. Voorhees Matthew T. Remy Claire M. Erickson Laura M. Dutca Daniel J. Brat Andrew A. Pieper Occupational-like organophosphate exposure disrupts microglia and accelerates deficits in a rat model of Alzheimer’s disease
description	Occupational exposure to toxins may accelerate Alzheimer’s disease The interaction of genes and environment contributes to Alzheimer’s disease (AD). For example, agricultural workers, military personnel, industrial manufacturers, veterinarians, horticulturists, aircraft maintenance personnel, and pilots are all potentially at risk of occupational exposure to organophosphates (OPs), which are associated with increased risk of AD. We report here that occupational-like exposure of young animals to the OP chlorpyrifos (CPF) accelerates AD-like cognitive deficits and severe neurodegeneration in male, but not female, TgF344-AD rats, a genetic model of AD. CPF exposure also causes chronic dysregulation of brain microglial cells, while amyloid and tau pathology are not affected. Thus, microglial dysregulation after environmental toxin exposure may represent a second hit that advances the disease. Future therapies to preserve or restore normal microglia might help prevent AD in genetically vulnerable individuals exposed to CPF or other disease-accelerating environmental agents.
format	article
author	Jaymie R. Voorhees Matthew T. Remy Claire M. Erickson Laura M. Dutca Daniel J. Brat Andrew A. Pieper
author_facet	Jaymie R. Voorhees Matthew T. Remy Claire M. Erickson Laura M. Dutca Daniel J. Brat Andrew A. Pieper
author_sort	Jaymie R. Voorhees
title	Occupational-like organophosphate exposure disrupts microglia and accelerates deficits in a rat model of Alzheimer’s disease
title_short	Occupational-like organophosphate exposure disrupts microglia and accelerates deficits in a rat model of Alzheimer’s disease
title_full	Occupational-like organophosphate exposure disrupts microglia and accelerates deficits in a rat model of Alzheimer’s disease
title_fullStr	Occupational-like organophosphate exposure disrupts microglia and accelerates deficits in a rat model of Alzheimer’s disease
title_full_unstemmed	Occupational-like organophosphate exposure disrupts microglia and accelerates deficits in a rat model of Alzheimer’s disease
title_sort	occupational-like organophosphate exposure disrupts microglia and accelerates deficits in a rat model of alzheimer’s disease
publisher	Nature Portfolio
publishDate	2019
url	https://doaj.org/article/97add60acab14939931cb8b2bbeb72e7
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Occupational-like organophosphate exposure disrupts microglia and accelerates deficits in a rat model of Alzheimer’s disease

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