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...

Descripción completa

Guardado en:
Detalles Bibliográficos
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:
Acceso en línea:https://doaj.org/article/97add60acab14939931cb8b2bbeb72e7
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
Descripción
Sumario: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.