Date of Submission


Document Type


Degree Name

Master of Science in Cellular and Molecular Biology


Biology and Environmental Sciences


Alireza G. Senejani, Ph.D.

Committee Member

Anna Kloc, Ph.D.

Committee Member

Eva Sapi, Ph.D.


Phospho-tau Protein, BE2C, Kelly Neuroblastoma Cell Lines, Menadione, Apoptotic Cells


Borrelia burgdorferi, Oxidative Stress, Vitamin K 3, Apoptosis


Alzheimer's disease, Neural networks (Neurobiology), Amyloid beta-protein, Borrelia burgdorferi, Oxidative stress, Flow cytometry, Apoptosis


In Alzheimer's disease (AD), the neurons are injured and mostly subjected to death throughout the brain, interconnections between neural networks may detach, and several regions of the brain begin to shrink in size. Amyloid-Beta (Aβ) and phospho-tau (p-Tau) are considered as main hallmarks of AD. Lyme-causing bacteria Borrelia burgdorferi can invade central nervous system resulting in neurological disorders. To evaluate how B. burgdorferi bacteria can contribute to the development and/or progress of AD, protein expression of Amyloid-Beta aggregates and p-Tau protein tangles were assessed before and after infection with B. burgdorferi in BE2C and Kelly neuroblastoma cell lines. To assess the sensitivity of these cell lines, they were subjected to the oxidative-stress effect of Menadione, which is a DNA-damaging agent and bacterial infection. Flow cytometry was performed for quantitative analysis of apoptotic cells before and after treatment. Results of this study shows significant increase in the expression of Amyloid-Beta and p-Tau proteins after infection of cell lines with Borrelia burgdorferi. A significant increase was observed in the apoptotic percentage of menadione-treated cell lines. Furthermore, infected cell lines were having elevated levels of apoptosis compared to non-infected cells. Henceforth, this study helps us understand better the correlation of the downstream effect of B. burgdorferi chronic infection along with oxidative stress, and contribute to understanding of the development and or progress of AD.

Available for download on Saturday, September 26, 2026