A new review article published in the journal Frontiers in Aging Neuroscience has summarized the most recent evidence supporting the controversial hypothesis that Herpes Simplex Virus 1 (HSV1) is a major causal factor for Alzheimer’s disease. The article makes particular note of new population data out of Taiwan, finding that people infected with HSV1 are much more likely to develop senile dementia.
The idea that neurodegenerative disease could be spawned by viral infections is not new. For much of the 20th century the intriguing hypothesis sat on the fringes of neuroscience while the more popular amyloid hypothesis rose into common consensus by the end of the century.
A few scientists have recently rekindled the viral hypothesis, and Emeritus Professor Ruth Itzhaki has been one of the primary investigators in the area, working for over 25 years on the association. Itzhaki’s latest article offers a compelling overview of the science up to now, but perhaps the most interesting discussions are the ones surrounding newly released population data from Taiwan.
Taiwan is a treasure trove of data for scientists due to its National Health Insurance Research Database, which is composed of medical data from 99.9 percent of the population. Three recent studies have examined that data surrounding associations between viral infections and the development of senile dementia.
The most interesting data to come out of the Taiwan studies looked at more than 8,000 subjects over the age of 50 who were newly diagnosed with HSV1 or HSV2. That cohort was then matched against a control group of over 25,000 similarly aged subjects with no HSV infection. Over the next 10 years those in the HSV group were 2.5 times more likely to develop dementia than the control group. Perhaps even more interesting was the finding that those HSV-infected subjects that were treated with an anti-herpes drug were 10 times less likely to develop dementia than those infected, but untreated, subjects.
The evidence is still primarily observational, with no clear causal link reasonably established, but Itzhaki suggests the growing body of data is convincing enough to expand research into development of a HSV1 vaccine. Itzhaki also calls for broader investigation into antiherpes antivirals as a potential treatment for Alzheimer’s disease.
“Considering that over 150 publications strongly support an HSV1 role in Alzheimer’s, these Taiwan findings greatly justify usage of antiherpes antivirals – which are safe and well-tolerated – to treat Alzheimer’s disease,” says Itzhaki.
Not all researchers in the field are convinced of the veracity behind the association. John Hardy, from University College London, feels that the hypothesis is worthy of further research, but far from the stage of being seriously convincing.
“Dr Itzhaki has been ploughing a lonely furrow based on her belief that herpes infection is a risk factor for Alzheimer’s disease for a long time and most scientists, including me, have been skeptical,” says Hardy.
Tara Spires-Jones, from the University of Edinburgh, also questions whether there is any causal association between the virus and Alzheimer’s. “This is a literature review and does not add new data to the field,” says Spires-Jones. “The kind of studies discussed in this paper cannot determine whether the infection causes Alzheimer’s.”
Spires-Jones also questions whether the growing evidence of herpes infections in brains of Alzheimer’s subjects is more related to the disease damaging the blood-brain barrier allowing the virus to infect the brain.
The new article was published in the journal Frontiers in Aging Neuroscience.