Aβ plaques do not protect against HSV-1 infection in a mouse model of familial Alzheimer's disease, and HSV-1 does not induce Aβ pathology in a model of late onset Alzheimer's disease.

ABSTRACT: The possibility that the etiology of late onset Alzheimer's disease is linked to viral infections of the CNS has been actively debated in recent years. According to the antiviral protection hypothesis, viral pathogens trigger aggregation of Aβ peptides that are produced as a defense mechanism in response to infection to entrap and neutralize pathogens. To test the causative relationship between viral infection and Aβ aggregation, the current study examined whether Aβ plaques protect the mouse brain against Herpes Simplex Virus 1 (HSV-1) infection introduced via a physiological route and whether HSV-1 infection triggers formation of Aβ plaques in a mouse model of late-onset AD that does not develop Aβ pathology spontaneously. In aged 5XFAD mice infected via eye scarification, high density o

SUBMITTER: Bocharova OV 

PROVIDER: S-EPMC9836376 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature