Controversial role of herpesviruses in Alzheimer's disease

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 DNA of human herpes simplex virus 1 (HSV1) in postmortem brain samples of AD patients at much higher levels than in healthy brains, hinting that viral infection could be somehow involved in the disease [1]. Since then, researchers have bolstered the association between AD and HSV1 as well as other pathogens, particularly human herpesvirus 6 (HHV6A and HHV6B), yet proving causality has remained elusive. Recent findings have shown that herpesvirus infections may induce amyloid beta (Aβ) production and deposition in the brain, resulting in antimicrobial activity [2]. Aβ oligomers might bind herpesvirus surface glycoproteins [3], possibly acting as a protective coating against neurotropic HSV1 and HHV6. Furthermore, the authors show that infection with herpesvirus seems to rapidly seed amyloid plaque deposition in a transgenic mouse model (5XFAD) and in a three-dimensional human neuronal cell-culture system [3]. These data lack confirmation by other groups.