New research adds to the mountain of evidence suggesting that the herpes virus may play a significant role in the development of Alzheimer’s disease, the sixth leading cause of death in the United States projected to affect nearly 14 million people by 2060.
Published last week in the journal Frontiers in Aging Neuroscience, the new study includes medical data on 99.9 percent of the population of Taiwan, all enrolled in the country’s National Health Insurance Research Database.
Researchers compiled observational information from three different studies of more than 8,000 subjects older than age 50, all of whom were either newly diagnosed with herpes simplex virus 1 (better known as the cause of cold sores) or herpes simplex virus 2, which typically leads to genital herpes.
When matching a control group of 25,000 subjects without the herpes infection — and following both groups over 10 years — the researchers found that those in the HSV1/HSV2 group were 2.5 times more likely to develop dementia than those in the control group. But the main effect was seen in those with HSV1 rather than HSV2 infections.
Additionally, HSV1-/HSV2-infected subjects that also underwent treatment with an anti-herpes drug were 10 times less likely to develop dementia than the untreated HSV1/HSV2 subjects, they found.
“The striking results include evidence that the risk of senile dementia is much greater in those who are infected with HSV, and that anti-herpes antiviral treatment causes a dramatic decrease in number of those subjects severely affected by HSV1 who later develop dementia,” study author Ruth Itzhaki said in a statement.
“It should be stressed that the results of these Taiwanese studies apply only to severe HSV1 (or VZV) infections, which are rare,” Itzhaki admitted. “Ideally, we would study dementia rates amongst people who have suffered mild HSV1 infection, including herpes labialis (cold sores) or mild genital herpes, but these are far less likely to be documented.”
Though the new research is primarily observational, and more work is needed to find a more causal link between HSV1 and Alzheimer’s, Itzhaki and her colleagues believe developing an HSV1 vaccine may be the most effective treatment.
“Probably the only way to prove that a microbe is a cause of a disease is to show that an occurrence of the disease is greatly reduced either by targeting the microbe with a specific anti-microbial agent or by specific vaccination against the microbe,” she wrote in for BBC.
Itzhaki’s work is only the most recent to suggest the link between herpes infections and Alzheimer’s.
In June, scientists at the Icahn School of Medicine at Mount Sinai, New York, used genetic data from three different brain banks to examine differences between healthy brain tissue and brain tissue from individuals who died with Alzheimer’s.
The medical community still doesn’t know what causes the disease, so the Mount Sinai scientists set out to try and identify new targets for drugs. Instead, they stumbled upon repetitive hints that the brain tissue of Alzheimer’s patients had higher levels of viruses.
While studying brain tissue of 622 people who had signs of the disease and 322 who weren’t affected by it, study author Joel Dudley and his team found significant evidence suggesting two specific strains of the human herpes virus (HHV-6A and HHV-7), both of which commonly cause skin rashes called roseola in young children, may have seeped into the Alzheimer’s patients’ brains and remained inactive for decades.
The team found that the herpes virus genes were interacting with specific genes known to increase risk for Alzheimer’s, but the mere presence of the virus isn’t enough to lead to the disease. Instead, Dudley said, something needs to be activating the viruses to cause replication.
The National Institute on Aging, which helped fund the new research, is working to back another study to test the effects of antiviral drugs on people in the early stages of Alzheimer’s with high levels of herpes virus in their brains.
“The data are very provocative, but fall short of showing a direct causal role,” Richard Hodes, director of the National Institute on Aging, which helped fund Dudley’s research, told NPR. “And if viral infections are playing a part, they are not the sole actor.”
The Atlanta-based Centers for Disease Control and Prevention on Thursday revealed that the country’s burden of Alzheimer’s disease and related dementias will double by the year 2060.
In 2014, 5 million Americans — or 1.6 percent of the population — felt the burden of the diseases. The figure is expected to grow to 13.9 million, equating to nearly 3.3 percent of the projected population in 2060.
Patients, caregivers and publicly funded long-term care facilities bear significant financial and societal costs due to increasing rates of Alzheimer’s deaths.
Experts recommend more federal funding toward caregiver support and education and toward research to find a cure.
This story has been updated. A previous version incorrectly stated the anti-herpes antiviral treatment was not as effective as authors noted.
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