Support Alzheimer's Research at Cal Poly

Hello! My name is Sophie Biehler, and I am a current third year Biology major with a minor in Chemistry on the pre-medicine track at Cal Poly Pomona. I am involved in Neuroscience Research at my University, where I am conducting an independent research project regarding the inverse correlation between Alzheimer’s Disease and Cancer. Alzheimer’s Disease is classified as the degeneration of neurons due to the over-accumulation of β-amyloid plaques and phospho-tau within cognitive processing areas of the brain, such as the hippocampus and entorhinal cortex, where learning and memory occurs. Cell cycle reentry (CCR) is a process that occurs within both cancer cells and neurons, and can be stimulated by a variety of genetic, viral, or inflammatory processes. In cancer cells, cell cycle reentry allows somatic cells to metabolically switch over to an embryonic active growth (anabolic) and proliferative state, creating serious problems for the survival of the host. In neurons, neuroinflammatory stress-inducing factors (such oxidative and metabolic stress) can trigger neural cells into reentering the cell cycle in order to achieve protection against neurodegenerative processes. This is problematic for neurons, as it alters their ploidy level, essentially creating an overabundance in DNA for the cell, leading to cell malfunction and neurodegeneration. There is evidence that the p-tau loaded neurons that have reentered the cell cycle are much more vulnerable to neurodegeneration than p-tau loaded neurons that have not reentered the cell cycle. Individuals with a higher amount of CCR end up with more neurodegeneration and dementia, while those with lower levels of CCR end up with an abundance of resilient p-tau labeled neurons that survive and end up with less neurodegeneration and remain nondemented throughout their life. I am primarily providing research to demonstrate that the Non Demented Alzheimer’s Neuropathy (NDAN) patients have a lower percentage of cells reentering the cell cycle with specific CCR markers/antibodies, such as PIN1 and CDK5-P25. Understanding this correlation will create undiscovered treatment methods that will block neurons from reentry into the cell cycle that leads to this neurodegeneration, and could increase the percentage of dementia-free individuals (NDAN), even if they have Alzheimer’s neuropathy (plaques and tangles). My research is not funded by the University, and in order to proceed with the experimental trials, I must purchase 12 samples of hippocampal tissue and the PIN1 and CDK5/P25 antibodies, which is quite costly. Any donation is greatly appreciated, thank you!