Advantages:
- Advances viral neurology research by studying SARS-CoV-2's impact on the aging brain's choroid plexus.
- Identifies potential biomarkers for neurodegenerative diseases through cellular senescence and SASP factor analysis.
- Informs public health strategies regarding COVID-19-related neurological complications and preventive measures for vulnerable populations.
Summary:
This technology aims to study the effects of SARS-CoV-2 infection on the aging brain's choroid plexus, specifically focusing on cellular senescence and the release of senescence-associated secretory phenotype (SASP) factors into the cerebrospinal fluid (CSF). In vivo studies use SARS-CoV-2-infected aged mouse models with intranasal or systemic virus administration to mimic natural infection routes. This approach enables to observe and analyze the development of cellular senescence in the choroid plexus and other brain regions, as well as the secretion of SASP factors into the CSF. Additionally, in vitro experiments involve exposing primary human choroid plexus epithelial cells to SARS-CoV-2 to understand the cellular responses and molecular changes associated with senescence and SASP factor secretion. Overall, the research offers new directions for understanding the intricate relationship between SARS-CoV-2, cellular senescence, and Alzheimer's disease, potentially leading to novel therapeutic interventions and improved patient care.
Figure depicts the expression of senescence markers in the choroid plexus of the lateral ventricle in the brain, observed before the significant buildup of Tau tangles and beta-amyloid plaques in the hippocampus, which are known characteristics of Alzheimer's disease. Panels A, B, and C show specific markers, namely p21/Iba-1, Tau, and Aβ1-42, respectively, indicating the presence of cellular senescence and potential links to Alzheimer's pathology.
Desired Partnerships:
- License
- Sponsored Research
- Co-Development