The new study, reported in StatNews, is the first evidence of an association between herpesvirus HSV-1 and Alzheimer’s Disease using a lab model of a brain. Brain-like tissue infected with HSV-1 became riddled with amyloid plaques, one of the characteristic pathological findings in post-mortem studies of Alzheimer’s patients’ brains, along with tangles of tau protein. The plaques and other pathology that are generally thought to cause the disease may be the brain’s defensive response to viral infection long before the onset of symptoms. Amyloid is known to be antimicrobial but can disrupt brain structure and function. The finding may revitalize research on the connection between infectious agents and Alzheimer’s, a sort of backwater area of investigation, and the possibility that antiviral medications might offer treatment or prevention potential.
I am not a virologist, but it seems clear that some caution about these findings is indicated. The literature has see-sawed back and forth in recent years about whether viral etiologies are likely or not. Algorithms to analyze RNA and DNA sequencing data, and thus findings about viral presence in affected brains, can differ. More than 50% of us are estimated to be infected with HSV-1, far in excess of the proportion who will develop Alzheimer’s Disease. Indeed, non-demented patients may have considerable amyloid plaque at autopsy as well. The presence of higher levels of DNA strands of HSV-1 in postmortem studies of Alzheimer’s brains was first observed around 30 years ago but proving causality has not been easy. More recent studies have contradicted that findingas well, as well as putative links between Alzheimer’s and other herpesvirus or non-herpes viral genomes.
(Props to Abby)