After years of mostly benign negligence, I rolled up my sleeve for a round of the shingles vaccine early last year during a lull in the COVID pandemic. Tales of woe from seniors who had contracted the virus — including a neighbor who was rendered temporarily immobile by the bug — ultimately persuaded me to get jabbed. If I’d known then that the vaccine may also lower my risk of developing Alzheimer’s, I might’ve acted a bit sooner.
A certain portion of the scientific community has long theorized that viral infections, rather than the accumulation of amyloid plaque, may play a key role in neurodegeneration. And several studies in past years have focused on shingles (a.k.a. herpes zoster) as a likely culprit, suggesting that the live vaccine may be a viable tool in the fight against dementia.
But public health agencies in the United States and elsewhere have discontinued the use of the live vaccine, opting for a recombinant version, and thus rendering much of the earlier research moot. Recently, a team led by University of Oxford psychiatrist Maxime Taquet, PhD, ventured into that vacuum of knowledge. Taquet and his crew tracked the health records of more than 200,000 Britons who had received shingles vaccines: half were given the live vaccine before it was discontinued; the other half got the recombinant version.
The results, published this past July in the journal Nature Medicine, show that those who received the upgraded vaccine were less likely during the six-year follow-up period to develop dementia than their counterparts who got the live vaccine. The recombinant vaccine was also more protective against dementia than flu or tetanus-diphtheria-pertussis shots.
“These findings should stimulate studies investigating the mechanisms underpinning the protection and could facilitate the design of a large-scale randomized control trial to confirm the possible additional benefits of the recombinant shingles vaccine,” Taquet writes.
His study seems to have stimulated a renewed interest in the infection theory of Alzheimer’s, Rita Rubin reports in a November JAMA editorial. Despite what University of Colorado School of Medicine neurovirologist Maria Nagel, MD, describes as “a lot of skepticism” about the role of infectious diseases, researchers are becoming increasingly frustrated with the amyloid plaque theory, pointing to the modest benefits offered by the two FDA-approved medications currently on the market.
“If we could identify which infection is important, then we could prevent or treat it,” she tells Rubin.
But, prior to Taquet’s research, all attempts to explore the relationship between infectious diseases and dementia — and the efficacy of vaccines — have suffered from what’s known as “healthy vaccine bias.” Simply put, people who roll up their sleeves for their shots tend to be healthier than those who don’t. And they may be at less risk for cognitive dysfunction whether they get the vaccine or not.
That’s why Taquet’s approach may offer better evidence than that which has surfaced from earlier research. Both the live vaccine and the recombinant recipients his team studied consisted of people willing to get the shots, thus leveling the field. Still, this was an observational study and doesn’t prove cause and effect. “It might well be that the vaccine is delaying dementia rather than preventing it altogether,” he acknowledges.
Other researchers, however, are taking up the challenge. A paper presented at the 2024 Alzheimer’s Association International Conference reinforced Taquet’s findings among three groups of Americans who had received the live shingles vaccine, the recombinant version, and the pneumococcal shot. As in the Taquet study, the recombinant shingles vaccine offered more protection against dementia than did the live version and both outperformed the pneumococcal vaccine.
And a similar study in England and Wales mirrored those results and may have strengthened the infection theory. An international team led by Pascal Geldsetzer, MD, PhD, an assistant professor of medicine at Stanford University, tracked the health records of some 5 million people for nine years after the first shingles vaccine was made available to people 80 years old and older. Those who were eligible to receive the shot were 38 percent less likely to die from dementia than those who didn’t make the age-related cut.
Geldsetzer’s team can’t prove that those lucky octogenarians actually received the vaccine, but it does hint at some intriguing association, one that he tested further in a subsequent analysis focusing specifically on a cohort of Welsh seniors. Those results showed that, among people with no evidence of cognitive impairment, receiving the shingles vaccine slightly lowered the risk of developing symptoms over a nine-year period. And for those already living with dementia, the vaccine lowered their risk of dying as a result of the disease by nearly 30 percent.
How the vaccine might inhibit the development of the disease remains a mystery. Despite the growing consensus among researchers about the role infections play in neurodegeneration, it’s unclear whether the dementia-protecting benefits of vaccines occur because they’re clearing up the infections or for some other reason.
Neurodegenerative diseases defy simple antidotes, Nagel notes, because factors as various as genetics, lifestyle, viruses, and other environmental forces may combine to produce cognitive dysfunction. Recent research provides some hope, but demographics and low levels of vaccine acceptance suggest we’re losing the battle.
“Our aging population is growing, and it’s really concerning that one in nine people over 65 have Alzheimer’s,” she says. “It’s really critical that we figure out what to do about this disease.”
Maybe the shingles vaccine is part of the answer, or maybe it’s not. But either way, most U.S. seniors aren’t rolling up their sleeves. Only about a third of older adults had received the vaccine by 2020. I’m happy to have — even belatedly — joined that group.
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