Single-Cell Analysis of ChP-BAM Co-cultured Organoids
Session Number
Project ID: BIO 17
Advisor(s)
Matti Lam, Tristan Philippe, Yanling Wang, RUSH University, Alzheimer’s Disease Center
Discipline
Biology
Start Date
17-4-2024 8:15 AM
End Date
17-4-2024 8:30 AM
Abstract
The choroid plexus (ChP) is a part of the blood-brain barrier that is responsible for cerebrospinal fluid (CSF) secretion, which washes out toxins and enables nutrient transport. Correspondingly, the ChP serves as a niche for immune cells (e.g. Border Associated Macrophages (BAMs). Studies suggest that ChP and immune dysfunction increases the incidence of Alzeimer’s Disease (AD), however, in vitro models are limited to induced microglia (iMGs). The human cell modeling group at the Rush Alzheimer’s Disease Center therefore created an in-vitro organoid ChP-iMG co-culture model to more accurately model BAMs. Single nuclei RNA sequencing (10X genomics kit) was used to characterize this new model. I performed data analysis within R using the Seurat package to clean, normalize, cluster, and visualize the data. I used proteinatlas.org and other scientific articles to identify unique cell types based on gene expression. We observed marked changes in gene expression (e.g. SPP1, CTSD, POSTN LPL) in immune cells that were co-cultured with the ChP (henceforth: iBAMs) compared to iMGs. These findings suggest that iBAMs are a better model to study the interaction between the ChP and immune system in Alzheimer’s disease and future treatments.
Single-Cell Analysis of ChP-BAM Co-cultured Organoids
The choroid plexus (ChP) is a part of the blood-brain barrier that is responsible for cerebrospinal fluid (CSF) secretion, which washes out toxins and enables nutrient transport. Correspondingly, the ChP serves as a niche for immune cells (e.g. Border Associated Macrophages (BAMs). Studies suggest that ChP and immune dysfunction increases the incidence of Alzeimer’s Disease (AD), however, in vitro models are limited to induced microglia (iMGs). The human cell modeling group at the Rush Alzheimer’s Disease Center therefore created an in-vitro organoid ChP-iMG co-culture model to more accurately model BAMs. Single nuclei RNA sequencing (10X genomics kit) was used to characterize this new model. I performed data analysis within R using the Seurat package to clean, normalize, cluster, and visualize the data. I used proteinatlas.org and other scientific articles to identify unique cell types based on gene expression. We observed marked changes in gene expression (e.g. SPP1, CTSD, POSTN LPL) in immune cells that were co-cultured with the ChP (henceforth: iBAMs) compared to iMGs. These findings suggest that iBAMs are a better model to study the interaction between the ChP and immune system in Alzheimer’s disease and future treatments.