SARS-CoV-2 Drives Neuroinflammatory Changes in Alzheimer’s Model Mice
Start Date
April 2026
Location
3rd floor - Library
Abstract
SARS-CoV-2 has links to prolonged inflammation and cognitive impairment suggesting the overlap with various neurodegenerative diseases like Alzheimer’s diseases (AD). This study investigated the connection between viral exposure and microglial activation in the AD mouse model (5xFAD) and wild-type (WT) mice. The genotypes were intranasally inoculated at 12 weeks old with either the SARS-CoV-2 Beta variant or a PBS control. With each condition, the process of perfusion was performed at either 2 days or 3 months post infection. Confocal microscopy and ImageJ methods were used to classify the quantified microglial morphology into four states: highly ramified/ramified, activated, rod-like, and amoeboid. Results revealed that SARS-CoV-2 increased activated and rod-like microglia, especially in the AD mouse model while the uninfected AD mice displayed heightened amoeboid morphology, reflecting neuroinflammation by predisposed genetic traits. The viral exposure is suggested to influence the accelerated microglial transformation associated with AD pathology, providing insight into how infection amplifies the neurodegenerative processes.
SARS-CoV-2 Drives Neuroinflammatory Changes in Alzheimer’s Model Mice
3rd floor - Library
SARS-CoV-2 has links to prolonged inflammation and cognitive impairment suggesting the overlap with various neurodegenerative diseases like Alzheimer’s diseases (AD). This study investigated the connection between viral exposure and microglial activation in the AD mouse model (5xFAD) and wild-type (WT) mice. The genotypes were intranasally inoculated at 12 weeks old with either the SARS-CoV-2 Beta variant or a PBS control. With each condition, the process of perfusion was performed at either 2 days or 3 months post infection. Confocal microscopy and ImageJ methods were used to classify the quantified microglial morphology into four states: highly ramified/ramified, activated, rod-like, and amoeboid. Results revealed that SARS-CoV-2 increased activated and rod-like microglia, especially in the AD mouse model while the uninfected AD mice displayed heightened amoeboid morphology, reflecting neuroinflammation by predisposed genetic traits. The viral exposure is suggested to influence the accelerated microglial transformation associated with AD pathology, providing insight into how infection amplifies the neurodegenerative processes.
