Antiviral drugs used to target the herpes virus could be effective at slowing the progression of Alzheimer's disease (AD), a new study shows.
The University of Manchester scientists have previously shown that the herpes simplex virus type 1 (HSV1) is a risk factor for Alzheimer's when it is present in the brains of people who have a specific genetic risk to the disease.
AD is an incurable neurodegenerative condition affecting about 18 million people worldwide. The causes of the disease or of the abnormal protein structures seen in AD brains - amyloid plaques and neurofibrillary tangles - are completely unknown.
The Manchester team has established that the herpes virus causes accumulation of two key AD proteins - β-amyloid (Aβ) and abnormally phosphorylated tau (P-tau) - known to be the main components of plaques and tangles respectively. Both proteins are thought by many scientists to be involved in the development of the disease.
"We have found that the viral DNA in AD brains is very specifically located within amyloid plaques," said Professor Ruth Itzhaki, who led the team in the University's Faculty of Life Sciences. "This, together with the production of amyloid that the virus induces, suggests that HSV1 is a cause of toxic amyloid products and of plaques.
"Our results suggest that HSV1, together with the host genetic factor, is a major risk for AD, and that antiviral agents might be used for treating patients to slow disease progression."
Currently available antiviral agents act by targeting replication of HSV1 DNA, and so the researchers considered that they might be successful in treating AD only if the accumulation of β-amyloid and P-tau accumulation caused by the virus occurs at or after the stage at which viral DNA replication occurs.
"If these proteins are produced independently of HSV1 replication, antivirals might not be effective," said Professor Itzhaki. "We investigated this and found that treatment of HSV1-infected cells with acyclovir, the most commonly used antiviral agent, and also with two other antivirals, did indeed decrease the accumulation of β-amyloid and P-tau, as well as decreasing HSV1 replication as we would expect.