Controversial role of herpesviruses in Alzheimer’s disease
Roberta Rizzo
Abstract
The controversial hypothesis that microbes might trigger Alzheimer’s disease (AD) has been debated for decades. Around 30 years ago, researchers in the United Kingdom discovered \nDNA of human herpes simplex virus 1 (HSV1) in postmortem brain samples of AD patients at \nmuch higher levels than in healthy brains, hinting that viral infection could be somehow \ninvolved in the disease [1]. Since then, researchers have bolstered the association between AD \nand HSV1 as well as other pathogens, particularly human herpesvirus 6 (HHV6A and \nHHV6B), yet proving causality has remained elusive. \nRecent findings have shown that herpesvirus infections may induce amyloid beta (Aβ) production and deposition in the brain, resulting in antimicrobial activity [2]. Aβ oligomers \nmight bind herpesvirus surface glycoproteins [3], possibly acting as a protective coating against \nneurotropic HSV1 and HHV6. Furthermore, the authors show that infection with herpesvirus \nseems to rapidly seed amyloid plaque deposition in a transgenic mouse model (5XFAD) and \nin a three-dimensional human neuronal cell-culture system [3]. These data lack confirmation \nby other groups.