Particulate matter increases beta-amyloid and activated glial cells in hippocampal tissues of transgenic Alzheimer's mouse: Involvement of PARP-1

Exposure to air pollutants, such as particulate matter (PM), has been implicated in neurodegenerative disorders including Alzheimer's disease (AD). However, direct effects of PM on production of β-amyloid (Aβ), a key pathogenic molecule in AD, and its underlying mechanism are still elusive. Giv...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2018-06, Vol.500 (2), p.333-338
Main Authors: Jang, Sooah, Kim, Eun Woo, Zhang, Yinhua, Lee, Jimin, Cho, So Yeon, Ha, Junghee, Kim, Hyunjeong, Kim, Eosu
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
AIR POLLUTION
Alzheimer's disease
Glial cell
HIPPOCAMPUS
MICE
PARP-1
Particulate matter
PATHOGENESIS
POLYMERASES
RIBOSE
TISSUE CULTURES
β-amyloid
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Summary:Exposure to air pollutants, such as particulate matter (PM), has been implicated in neurodegenerative disorders including Alzheimer's disease (AD). However, direct effects of PM on production of β-amyloid (Aβ), a key pathogenic molecule in AD, and its underlying mechanism are still elusive. Given PM's potential to induce oxidative stress in other tissues, we hypothesized that poly(ADP-ribose) polymerase (PARP-1) might be involved in PM-induced neurotoxicity. To address this, we used an ex vivo model of AD, the organotypic hippocampal slice tissue culture from old (12-14 months-of-age) triple transgenic 3xTg-AD mice. First, we observed that fine PM (aerodynamic diameter 
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2018.04.068