| dc.description.abstract | Alzheimer's Disease (AD) is the most common form of dementia and is currently estimated to affect over 5 million Americans. There is no treatment for AD, and the incidence is expected to increase as our population grows older. Many risk factors for AD have been identified, several of which involve stress. Our study aims to elucidate the connections between early-life stress and AD pathology in adulthood. Using a non-transgenic mouse line, maternal separation was implemented daily from post-natal day 2 or 3 (PND 2 or 3) to the time of weaning (PND 21-28) with the intention of modeling developmental stress. After weaning, the animals were allowed to age under regular conditions until adulthood. Before tissue collection, the animals were subjected to either 3 or 7 days of lipopolysaccharide (LPS) administration, modeling an acute stress event. LPS, a bacterial endotoxin, has previously been shown to exacerbate AD pathology in the form of amyloid beta and cognitive decline. After the period of LPS administration, contextual fear conditioning (CFC) was conducted to measure cognitive ability. Tissue was then collected and amyloid-beta evels were measured. Subtle sex differences were seen but overall, results were inconsistent. Maternal separation did enhance cognitive deficits, but only in one group of males. Additionally, maternal separation and LPS interacted to increase amyloid-beta load in females with 3 days of injections. Further studies must be completed to yield consistent results and identify a pathway of action. | |
