A potential role for LPS-induced inflammation in the induction of Alzheimer's disease-related pathology and cognitive deficits [electronic resource] /Show full item record
|Title||A potential role for LPS-induced inflammation in the induction of Alzheimer's disease-related pathology and cognitive deficits [electronic resource] /|
|Author||Kahn, Marielle Suzanne|
|Abstract||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.|
|Description||Title from thesis title page (viewed May 9, 2011).
Thesis--Texas Christian University, 2011.
Department of Psychology; advisor, Gary W. Boehm.
Includes bibliographical references.
Text (electronic thesis) in PDF.
This item appears in the following Collection(s)
- Theses and Dissertations