Viral Investigation of Regulatory Human Astrocytes to Understand the Glymphatic System
Files
Publication or External Link
Date
Advisor
Citation
DRUM DOI
Abstract
Alzheimer's disease (AD), and other neurodegenerative diseases, results from an extracellular accumulation of beta-amyloid plaques, which are composed of misfolded peptide oligomers of beta-amyloid. The accumulation is thought to be due to the failure of the glymphatic system, a waste clearance system in brain, which uses aquaporin-4 (AQP4) protein water channels. This protein exists as heterotetramers of M1 and M23 isoforms from splice variants of AQP4. Previous studies suggested that Herpes Simplex Virus-1 (HSV-1) infection of the central nervous system (CNS) may be correlated to AD development. However, the effect of HSV-1 on the glymphatic system has not been definitively established. The objective of this study was to investigate HSV-1 infection on AQP4 expression in human brain-derived glial cells. Our preliminary results suggest that HSV-1 infection of the cells leads to lower protein levels of M23 isoform. These results suggest that HSV-1 infection may potentially interfere with the function of the glymphatic system through the reduction of the AQP4 protein.