While herpes simplex virus type 1 is implicated almost exclusively as the cause of oral herpes, and not infrequently as the cause of genital herpes, researchers are also exploring the role this common virus may have in the development of Alzheimer’s disease (AD). The latest findings on the link between HSV-1 and AD, recently published in the Journal of Pathology, implicate HSV-1 in the development of protein plaques found in the brains of those with AD.
Plaques, abnormal deposits of a protein fragment called beta-amyloid between nerve cells that interfere with the ability of nerve cells to communicate, are one of the telltale signs of AD. In this most recent study, researchers found 90 percent of plaques in the brains of AD sufferers contained HSV-1 DNA.
For study author Professor Ruth Itzhaki of the University of Manchester, this finding is just the latest in her research on viral on HSV-1 and AD. Her research team previous demonstrated that HSV-1 DNA is present, latently, in brain of a high proportion of AD patients and can reactivate. They also discovered, though, that HSV-1 was present in the brains of many seniors without AD. This led the team to explore further genetic factors.
What they found was a specific gene--apolipoprotein E (APOE), the type 4 allele (APOE-e4)—that appears to be a susceptibility factor for AD. Research showed that a strong association between HSV-1 in the brain and AD in those that carrier APOE-e4.
Results of this most recent research now link HSV-1 directly with the development of abnormal plaque typical of AD. As the authors of the research state, their recent work, combined with evidence from previous studies, “support the deduction that HSV-1 is a major cause of plaque formation. Obviously, association does not prove causality. However, alternative explanations for viral presence in plaques are very unlikely.”
With this knowledge, researchers are now interested in examining what role antivirals may play in treating AD. As study co-author Dr. Matthew Wozniak notes: “Antiviral agents would inhibit the harmful consequences of HSV-1 action; in other words, inhibit a likely major cause of the disease irrespective of the actual damaging processes involved, whereas current treatments at best merely inhibit some of the symptoms of the disease.”