Alzheimer’s disease is the most common form of dementia in the world with a new case of dementia diagnosed every 3.2 seconds. For over 25 years the amyloid cascade hypothesis has existed as a mechanism of understanding and diagnosing Alzheimer’s Disease. The amyloid cascade hypothesis suggests that Alzheimer’s Disease is sequential in protein progression and proliferative from the medial temporal lobe to the rest of the brain. Hypometabolism of brain regions has also been correlated to plaque deposition and hypometabolism is observed in brain regions that make up the default mode network, specifically the retrosplenial cortex, which is not accounted for in the amyloid cascade hypothesis. The default mode network is the series of brain regions that are activated when the brain is at rest To assess the validity of the amyloid cascade hypothesis, we tracked the rate of plaque progression in the retrosplenial cortex compared to other traditionally afflicted brain regions such as the hippocampus and entorhinal cortex with immunofluorescent staining of A plaques in APP/PS1 transgenic mouse brains at 13, 16, and 28 months. Results showed that there is a significant difference in plaque deposition over time and between brain regions. The rate of progression at this age range in the retrosplenial cortex is consistent and higher than traditionally afflicted brain regions. Results of this study gives more insight into the role of A of disease progression, as well as the validity of the amyloid cascade hypothesis.
Stavnezer, Amy Jo
Rashid, Maha H., "The Progression of Aβ Proteins in the Retrosplenial Cortex Using an APP/PS1 Alzheimer’s Disease Transgenic Rodent Model" (2019). Senior Independent Study Theses. Paper 8744.
Molecular and Cellular Neuroscience | Other Neuroscience and Neurobiology
Alzheimer’s Disease, Aβ, Default Mode Network, Hypometabolism, Retrosplenial Cortes, Amyloid Cascade Hypothesis
Bachelor of Arts
Senior Independent Study Thesis
© Copyright 2019 Maha H. Rashid