| |
| author |
John Rinald
| | title |
Molecular Mechanism of DCP-LA in an Oxidative Stress Model of Alzheimer's Disease
| | abstract |
Alzheimer's Disease (AD) is a progressive neurodegenerative disease, that affects
more than 5 million Americans. Current methods to combat the progression of the disease
are only able to delay symptom progression, and cannot reverse the effects of the disease.
Dicyclopropyl Linoleic Acid (DCP-LA), has been shown to reduce deficits in spatial
memory in a model of AD in rats. However, the mechanism through which this
compound acts is not fully understood. In this study, two mechanisms for DCP-LA
activity are investigated in a primary neuronal culture model. These experiments used the
Ferrous-Amlyoid-Butionine (FAB) model of AD, which generates reactive oxygen
species, an important chemical aspect of sporadic AD. The effect of DCP-LA on cell
survival was analyzed through MTS assay and immunocytochemistry. The levels of PSD-
95 phosphorylation were not shown to increase in the long term, which indicates that
synaptogenesis through this mechanism may not be the causal pathway in DCP-LA's
cellular effects. Superoxide production was monitored through a fluorescent dye,
MitoSox Red, and was shown to decrease with exposure to DCP-LA. This implicated the
antioxidant activity of DCP-LA in mediating the preservation of memory in the model of
AD. When considering the pharmaceutical applications of previous findings, these
findings show that there may be options to optimize the clinical effects of this compound.
Future research will need to determine the signaling pathway that is mediating this
antioxidant effect.
| | school |
The College of Liberal Arts, Drew University
| | degree |
B.A. (2020)
|
| advisor |
Roger Knowles
|
| full text | JHRinald.pdf |
| |
