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A potential role for LPS-induced inf...

Kahn, Marielle Suzanne.

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A potential role for LPS-induced inflammation in the induction of Alzheimer's disease-related pathology and cognitive deficits.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	A potential role for LPS-induced inflammation in the induction of Alzheimer's disease-related pathology and cognitive deficits./
作者:	Kahn, Marielle Suzanne.
面頁冊數:	61 p.
附註:	Source: Masters Abstracts International, Volume: 49-05, page: 3358.
Contained By:	Masters Abstracts International49-05.
標題:	Psychology, Behavioral. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1491006
ISBN:	9781124586977

A potential role for LPS-induced inflammation in the induction of Alzheimer's disease-related pathology and cognitive deficits.
Kahn, Marielle Suzanne.

A potential role for LPS-induced inflammation in the induction of Alzheimer's disease-related pathology and cognitive deficits. - 61 p.

Source: Masters Abstracts International, Volume: 49-05, page: 3358.

Thesis (M.S.)--Texas Christian University, 2011.

Alzheimer's disease (AD) is characterized by neuronal cell death in regions of the adult brain, including the hippocampus, due to formation of amyloid-beta plaques and neurofibrillary tangles. Inflammation has been implicated in the onset and progression of these pathologies. Our study was designed to create an animal model of peripheral inflammation-induced AD-like pathologies using the bacterial endotoxin Lipopolysaccharide (LPS). C57BL/6J mice were given intraperitoneal injections of LPS or saline for 7 days. Hippocampal tissue from animals receiving LPS contained significantly higher levels of amyloid-beta 1-42 than did control animals. We also demonstrated that one injection of LPS leads to sickness behavior, but 7 days does not, implicating endotoxin tolerance. To determine if elevation in amyloid-beta 1-42 might inhibit learning, cognitive testing in both MWM and CFC, revealed learning deficits in LPS treated mice. In summary multiple injections of LPS resulted in increased amyloid-beta 1-42, in the hippocampus and cognitive deficits in mice.

ISBN: 9781124586977Subjects--Topical Terms:

1017677
Psychology, Behavioral.

A potential role for LPS-induced inflammation in the induction of Alzheimer's disease-related pathology and cognitive deficits.
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520 $a Alzheimer's disease (AD) is characterized by neuronal cell death in regions of the adult brain, including the hippocampus, due to formation of amyloid-beta plaques and neurofibrillary tangles. Inflammation has been implicated in the onset and progression of these pathologies. Our study was designed to create an animal model of peripheral inflammation-induced AD-like pathologies using the bacterial endotoxin Lipopolysaccharide (LPS). C57BL/6J mice were given intraperitoneal injections of LPS or saline for 7 days. Hippocampal tissue from animals receiving LPS contained significantly higher levels of amyloid-beta 1-42 than did control animals. We also demonstrated that one injection of LPS leads to sickness behavior, but 7 days does not, implicating endotoxin tolerance. To determine if elevation in amyloid-beta 1-42 might inhibit learning, cognitive testing in both MWM and CFC, revealed learning deficits in LPS treated mice. In summary multiple injections of LPS resulted in increased amyloid-beta 1-42, in the hippocampus and cognitive deficits in mice.
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