An old stalwart for treating cold sores and other conditions related to the herpes virus could have a new life as an Alzheimer’s disease therapy, suggest researchers from the UK’s University of Manchester.

A team from the University’s Faculty of Life Sciences and Manchester Royal Infirmary, led by Professor Ruth Itzhaki, had previously shown that herpes simplex virus type 1 (HSV1) was a strong risk factor for Alzheimer’s disease in people with the type 4 allele of the apolipoprotein E gene.

In their latest research, published in the Journal of Pathology (Volume 217, Issue 1), Itzhaki et al discovered that DNA for HSV1 was located specifically in the amyloid plaques characteristic of Alzheimer’s. Evidence of viral implication in the disease points to a possible role for antivirals such as aciclovir (GlaxoSmithKline’s Zovirax).

Notably, 90% of plaques in the brains of people with Alzheimer’s disease contained the viral DNA and 72% of the DNA was associated with plaques, the researchers reported. In aged normal brains, where amyloid plaques are also found but at a lower frequency, 80% of plaques contained HSV1 DNA yet only 24% of the viral DNA was plaque-associated.

The Manchester team had previously demonstrated that HSV1 infection of nerve-type cells induced deposition of beta amyloid, the main component of amyloid plaques. Taken together, “these findings strongly implicate HSV1 as a major factor in the formation of amyloid deposits and plaques, abnormalities thought by many in the field to be major contributors to Alzheimer’s disease”, Manchester University stated.

The researchers’ theory is that HSV1 “enters the brain in the elderly as their immune systems decline and then establishes a dormant infection from which it is repeatedly activated by events such as stress, immunosuppression and various infections”, Itzhaki explained. “The ensuing active HSV1 infection causes severe damage in brain cells, most of which die and then disintegrate, thereby releasing amyloid aggregates which develop into amyloid plaques after other components of dying cells are deposited on them.”

In preliminary experiments the Manchester team has shown that aciclovir reduces amyloid deposition and also certain other features of Alzheimer’s disease found to be caused by HSV1 infection. “Antiviral agents would inhibit the harmful consequences of HSV1 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,” team member Dr Matthew Wozniak commented.

The researchers hope they can now secure funding to take their work further, which would involve investigating in detail the effect of antiviral agents on the Alzheimer’s disease-associated changes that occur during HSV1 infection, as well as the nature of these processes and the role of apolipoprotein E gene.