title: Developmental perfluorooctane sulfonate exposure results in tau hyperphosphorylation and β-amyloid aggregation in adults rats: Incidence for link to Alzheimer's disease.
abstract: With regard to the defects of the cognitive function observed after developmental exposure to perfluorooctane sulfonate (PFOS), and earlier studies on the developmental neurotoxicology, the aim of this study was to investigate the role of developmental PFOS exposure in neurodegenerative disorders in later life. Two pathological hallmarks of Alzheimer's disease (AD), Tau hyperphosphorylation and β-amyloid (Aβ) aggregation, were examined. SD rats were exposed to PFOS during only prenatal and/or postnatal period. Tau mRNA and protein levels were elevated by PFOS exposure. The phosphorylation of Tau at S199, T231 and S396 sites were also increased. Besides, PFOS exposure increased the Aβ1-42 levels, as well as the amyloid precursor protein (APP) regulation. The prenatal PFOS exposure caused alterations in the involved proteins at comparable levels with the postnatal and both prenatal and postnatal exposure. Thus, it has raised some evidence that early PFOS exposure can affect processes linked to neurodegeneration, enhancing the AD pathological risk. And PFOS exposures in early life may be of particular etiologic importance of neurodegenerative diseases.
authors.affiliation: Key Laboratory of Industrial Ecology and Environmental Engineering (MOE), School of Environmental Science and Technology, Dalian University of Technology, Dalian 116024, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Zhang
authors.affiliation: Key Laboratory of Industrial Ecology and Environmental Engineering (MOE), School of Environmental Science and Technology, Dalian University of Technology, Dalian 116024, China.
authors.forename: Huimin
authors.initials: H
authors.lastname: Zhao
authors.affiliation: Key Laboratory of Industrial Ecology and Environmental Engineering (MOE), School of Environmental Science and Technology, Dalian University of Technology, Dalian 116024, China. Electronic address: liu_wei@dlut.edu.cn.
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
authors.affiliation: Key Laboratory of Industrial Ecology and Environmental Engineering (MOE), School of Environmental Science and Technology, Dalian University of Technology, Dalian 116024, China.
authors.forename: Zhou
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Key Laboratory of Industrial Ecology and Environmental Engineering (MOE), School of Environmental Science and Technology, Dalian University of Technology, Dalian 116024, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Qin
authors.affiliation: Key Laboratory of Industrial Ecology and Environmental Engineering (MOE), School of Environmental Science and Technology, Dalian University of Technology, Dalian 116024, China.
authors.forename: Fang
authors.initials: F
authors.lastname: Luo
authors.affiliation: Health Management Center, The Second Hospital of Dalian Medical University, Dalian 116023, China.
authors.forename: Song
authors.initials: S
authors.lastname: Leng
mesh_terms: D017738:Alkanesulfonic Acids / Q000633:toxicity*; D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn; D005260:Female; D005466:Fluorocarbons / Q000633:toxicity*; D015994:Incidence; D010766:Phosphorylation / Q000187:drug effects / Q000502:physiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016875:tau Proteins / Q000378:metabolism*
chemical_list: D017738:Alkanesulfonic Acids; D016229:Amyloid beta-Peptides; D005466:Fluorocarbons; D016875:tau Proteins; C076994:perfluorooctane sulfonic acid
keywords: Alzheimer’s disease; Amyloid protein; Learning and memory; PFOS; Tau phosphorylation