A recent study has suggested Shingrix, a relatively new vaccine given to protect older adults against shingles, may delay the onset of dementia.

This might seem like a bizarre link, but actually, research has previously shown an older version of the shingles vaccine, Zostavax, reduced the risk of dementia.

In this new study, published last week in the journal Nature Medicine, researchers from the United Kingdom found Shingrix delayed dementia onset by 17% compared with Zostavax.

So how did the researchers work this out, and how could a shingles vaccine affect dementia risk?

From Zostavax to Shingrix

Shingles is a viral infection caused by the varicella-zoster virus. It causes painful rashes, and affects older people in particular.

Previously, Zostavax was used to vaccinate against shingles. It was administered as a single shot and provided good protection for about five years.

Shingrix has been developed based on a newer vaccine technology, and is thought to offer stronger and longer-lasting protection. Given in two doses, it’s now the preferred option for shingles vaccination in Australia and elsewhere.

In November 2023, Shingrix replaced Zostavax on the National Immunisation Program, making it available for free to those at highest risk of complications from shingles. This includes all adults aged 65 and over, First Nations people aged 50 and older, and younger adults with certain medical conditions that affect their immune systems.

What the study found

Shingrix was approved by the US Food and Drugs Administration in October 2017. The researchers in the new study used the transition from Zostavax to Shingrix in the United States as an opportunity for research.

They selected 103,837 people who received Zostavax (between October 2014 and September 2017) and compared them with 103,837 people who received Shingrix (between November 2017 and October 2020).

By analysing data from electronic health records, they found people who received Shingrix had a 17% increase in “diagnosis-free time” during the follow-up period (up to six years after vaccination) compared with those who received Zostavax. This was equivalent to an average of 164 extra days without a dementia diagnosis.

The researchers also compared the shingles vaccines to other vaccines: influenza, and a combined vaccine for tetanus, diphtheria and pertussis. Shingrix and Zostavax performed around 14–27% better in lowering the risk of a dementia diagnosis, with Shingrix associated with a greater improvement.

The benefits of Shingrix in terms of dementia risk were significant for both sexes, but more pronounced for women. This is not entirely surprising, because we know women have a higher risk of developing dementia due to interplay of biological factors. These include being more sensitive to certain genetic mutations associated with dementia and hormonal differences.

Why the link?

The idea that vaccination against viral infection can lower the risk of dementia has been around for more than two decades. Associations have been observed between vaccines, such as those for diphtheria, tetanus, polio and influenza, and subsequent dementia risk.

Research has shown Zostavax vaccination can reduce the risk of developing dementia by 20% compared with people who are unvaccinated.

But it may not be that the vaccines themselves protect against dementia. Rather, it may be the resulting lack of viral infection creating this effect. Research indicates bacterial infections in the gut, as well as viral infections, are associated with a higher risk of dementia.

Notably, untreated infections with herpes simplex (herpes) virus – closely related to the varicella-zoster virus that causes shingles – can significantly increase the risk of developing dementia. Research has also shown shingles increases the risk of a later dementia diagnosis.

The mechanism is not entirely clear. But there are two potential pathways which may help us understand why infections could increase the risk of dementia.

First, certain molecules are produced when a baby is developing in the womb to help with the body’s development. These molecules have the potential to cause inflammation and accelerate ageing, so the production of these molecules is silenced around birth. However, viral infections such as shingles can reactivate the production of these molecules in adult life which could hypothetically lead to dementia.

Second, in Alzheimer’s disease, a specific protein called Amyloid-β go rogue and kill brain cells. Certain proteins produced by viruses such as COVID and bad gut bacteria have the potential to support Amyloid-β in its toxic form. In laboratory conditions, these proteins have been shown to accelerate the onset of dementia.

What does this all mean?

With an ageing population, the burden of dementia is only likely to become greater in the years to come. There’s a lot more we have to learn about the causes of the disease and what we can potentially do to prevent and treat it.

This new study has some limitations. For example, time without a diagnosis doesn’t necessarily mean time without disease. Some people may have underlying disease with delayed diagnosis.

This research indicates Shingrix could have a silent benefit, but it’s too early to suggest we can use antiviral vaccines to prevent dementia.

Overall, we need more research exploring in greater detail how infections are linked with dementia. This will help us understand the root causes of dementia and design potential therapies.

Ibrahim Javed, Enterprise and NHMRC Emerging Leadership Fellow, UniSA Clinical & Health Sciences, University of South Australia

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Over the past several days, the world has watched on in shock as wildfires have devastated large parts of Los Angeles.

Beyond the obvious destruction – to landscapes, homes, businesses and more – fires at this scale have far-reaching effects on communities. A number of these concern human health.

We know fire can harm directly, causing injuries and death. Tragically, the death toll in LA is now at least 24.

But wildfires, or bushfires, can also have indirect consequences for human health. In particular, they can promote the incidence and spread of a range of infections.

Effects on the immune system

Most people appreciate that fires can cause burns and smoke inhalation, both of which can be life-threatening in their own right.

What’s perhaps less well known is that both burns and smoke inhalation can cause acute and chronic changes in the immune system. This can leave those affected vulnerable to infections at the time of the injury, and for years to come.

Burns induce profound changes in the immune system. Some parts go into overdrive, becoming too reactive and leading to hyper-inflammation. In the immediate aftermath of serious burns, this can contribute to sepsis and organ failure.

Other parts of the immune system appear to be suppressed. Our ability to recognise and fight off bugs can be compromised after sustaining burns. Research shows people who have experienced serious burns have an increased risk of influenza, pneumonia and other types of respiratory infections for at least the first five years after injury compared to people who haven’t experienced burns.

Wildfire smoke is a complex mixture containing particulate matter, volatile organic compounds, ozone, toxic gases, and microbes. When people inhale smoke during wildfires, each of these elements can play a role in increasing inflammation in the airways, which can lead to increased susceptibility to respiratory infections and asthma.

Research published after Australia’s Black Summer of 2019–20 found a higher risk of COVID infections in areas of New South Wales where bushfires had occurred weeks earlier.

We need more research to understand the magnitude of these increased risks, how long they persist after exposure, and the mechanisms. But these effects are thought to be due to sustained changes to the immune response.

Microbes travel in smoky air

Another opportunity for infection arises from the fire-induced movement of microbes from niches they usually occupy in soils and plants in natural areas, into densely populated urban areas.

Recent evidence from forest fires in Utah shows microbes, such as bacteria and fungal spores, can be transported in smoke. These microbes are associated with particles from the source, such as burned vegetation and soil.

There are thousands of different species of microbes in smoke, many of which are not common in background, non-smoky air.

Only a small number of studies on this have been published so far, but researchers have shown the majority of microbes in smoke are still alive and remain alive in smoke long enough to colonise the places where they eventually land.

How far specific microbes can be transported remains an open question, but fungi associated with smoke particles have been detected hundreds of miles downwind from wildfires, even weeks after the fire.

So does this cause human infections?

A subset of these airborne microbes are known to cause infections in humans.

Scientists are probing records of human fungal infections in relation to wildfire smoke exposure. In particular, they’re looking at soil-borne infectious agents such as the fungi Coccidioides immitis and Coccidioides posadasii which thrive in dry soils that can be picked up in dust and smoke plumes.

These fungi cause valley fever, a lung infection with symptoms that can resemble the flu, across arid western parts of the United States.

A study of wildland firefighters in California showed high rates of valley fever infections, which spurred occupational health warnings including recommended use of respirators when in endemic regions.

A California-based study of the wider population showed a 20% increase in hospital admissions for valley fever following any amount of exposure to wildfire smoke.

However, another found only limited evidence of excess cases after smoke exposure in wildfire-adjacent populations in California’s San Joaquin Valley.

These contrasting results show more research is needed to evaluate the infectious potential of wildfire smoke from this and other fungal and bacterial causes.

Staying safe

Much remains to be learned about the links between wildfires and infections, and the multiple pathways by which wildfires can increase the risk of certain infections.

There’s also a risk people gathering together after a disaster like this, such as in potentially overcrowded shelters, can increase the transmission of infections. We’ve seen this happen after previous natural disasters.

Despite the gaps in our knowledge, public health responses to wildfires should encompass infection prevention (such as through the provision of effective masks) and surveillance to enable early detection and effective management of any outbreaks.

Christine Carson, Senior Research Fellow, School of Medicine, The University of Western Australia and Leda Kobziar, Professor of Wildland Fire Science, University of Idaho

This article is republished from The Conversation under a Creative Commons license. Read the original article.