Samin Hassan
Pronouns: she/her
Research Mentor(s): Benjamin Singer
Co-Presenter:
Research Mentor School/College/Department: Internal Medicine / Pulmonary and Critical Care Medicine / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 1 – 10am – 10:50am
Room: League Ballroom
Authors: Samin Hassan, Shiuan-Haur Su, Katsuo Kurabayashi, Benjamin Singer
Presenter: 113
Abstract
Alzheimer’s disease is explained and understood by specific forms of neuropathology, but the pathways that lead from that pathology to brain injury are not clearly understood. It is known from various epidemiologic studies that patients with Alzheimer’s disease usually have worsening symptoms after hospitalization for a systemic illness, such as urinary tract infection or pneumonia. The presence of Alzheimer’s neuropathology coupled with the presence of the brain’s response to infection causes the activation of microglia, which are important immune cells of the brain. The research project I will be taking part in this summer explores the activation of microglial cells in response to Alzheimer’s disease pathology and systemic infection. In order to study the activation of microglia cells, mice, either with or without AD neuropathology will be subjected to pneumonia and treated with antibiotics. Survivors are euthanized and perfused in order to isolate the brain. Then in order to isolate microglia cells in the brain, a series of enzymatic experimental isolations are conducted. A novel microfluidic cell culture platform and digital ELISA assay were developed to assay responses of microglia from mice that have been subjected to AD neuropathology and infection and mice without this neuropathology and systemic infection. The assay will then be analyzed to assess whether the presence of AD neuropathology increases the number of potentiated activation of microglia (Song et. al, 2021). Preliminary results examining the total tissue level of the microglial protein C1q in the digital ELISA device showed and effect of AD neuropathology, but not of infection. Results of microglial specific secretion have not been collected due to the ongoing nature of the experiment, but it is hypothesized that mice that are subjected to AD neuropathology and systemic infections will show more activation of microglia cells than pneumonia survivors without this pathology, or mice with AD neuropathology alone.
Biomedical Sciences
