Meeting Abstract
Alzheimer’s disease (AD) is characterized by impaired cognitive and memory function, and behavioral changes. Associated neuropathology is marked by brain amyloid beta deposits and tau tangles. The underlying cause of AD is not fully understood, but, in-line with the glucocorticoid (GC) hypothesis of brain aging, elevated levels of stress and GC hormones are associated with severity and progression of the disease in humans and some mouse models. GCs can increase the production and toxicity of brain amyloid beta deposits and these deposits can promote GC release, suggesting a possible positive feedback between amyloid beta and GCs. However, this relationship has not been addressed in the commonly used APPswe/PS1dE9 mouse model of AD. APPswe/PS1dE9 mice produce human amyloid beta which accumulates in the brain and relates to memory and cognitive deficits. Here, we will determine if, compared to their non-transgenic littermates, 18-month-old transgenic (tg) mice: 1) have elevated baseline and post-stress GCs, 2) exhibit deficits in a short (1-hr) and longer (24-hr) term memory in the object recognition task, and 3) if GCs and memory performance are related to brain amyloid beta concentrations. We predicted that tg mice would have higher GCs and poorer memory performance, and that GCs would be positively correlated with brain amyloid beta levels. However, initial preliminary results suggest that baseline and post-stress GCs do not differ between genotypes nor do genotypes differ in object recognition performance. Additional data collection and analysis is underway. Our study will be the first to determine if GCs are related to memory and neuropathology in the APPswe/PS1dE9 mouse model of AD.
