Blood test to detect Alzheimer's could be available within two years

A new blood test to detect early signs of Alzheimer’s is being developed with the help of Irish scientists and could be on the market by 2026. This breakthrough is one of several significant advances in the battle to slow the progression of the debilitating disease
Blood test to detect Alzheimer's could be available within two years

Blood tests are becoming as reliable as scans in determining if potentially damaging plaques are present in the brain. Picture: iStock

Could a blood test for Alzheimer’s be within reach? Experts predict that it might be a reality within two years, since it has become possible to pinpoint the accumulation of toxic molecules in the brain through changes in the blood.

Alzheimer’s, the most common form of dementia, defined by memory loss and confusion, is associated with the formation of plaques and tangles in the brain, created by the accumulation of two proteins — amyloid and tau.

These plaques and tangles can be toxic to the brain, steadily killing cells.

In the last three years, University of Galway studies suggest that elevated levels of a particular protein, called p-tau181, in the bloodstream, reflect a concerning accumulation of these plaques in the brain.

Worrying changes can be first observed in the blood up to a decade before cognitive symptoms begin to show.

“These blood tests are showing themselves to be every bit as reliable at telling people that they have amyloid in their brain as advanced scans or cerebrospinal fluid tests, which are quite invasive,” says Professor Seán Kennelly, director of the Cognitive Clinical Trials Unit and Memory Service at Tallaght University Hospital (TUH).

Prof Kennelly’s research group at TUH is continuing to validate so-called blood-based bio-markers, such as p-tau181, which would likely form the basis of a coming test.

He believes such a test could be available by 2026.

However, the test is not likely to be rolled out as a population-level screening tool when people reach midlife, because amyloid is not the sole driving factor of Alzheimer’s. Prof Kennelly points to people in mid to later life who have significant amyloid accumulation on brain scans, but remain cognitively normal.

“We’ve still got a lot to figure out,” Prof Kennelly says. “Identifying this protein doesn’t mean that you’re absolutely going to develop dementia. There are a lot of nuances there, because not everyone progresses in the same way.

“So, first of all, these tests are more likely to be used in people who are already displaying mild symptoms to help accelerate the path to a diagnosis.”

Many people have cognitive resilience, the ability to withstand some of the ravages of ageing and to continue functioning, despite the presence of large amounts of amyloid and tau.

Picture: iStock
Picture: iStock

Cognitive resilience

Many of the factors that determine cognitive resilience are thought to be linked to lifestyle.

In 2020, the Lancet Commission estimated that 40% of dementia cases might be prevented by lifestyle alterations: Quitting smoking, increased social interaction; treatment of hearing loss; physical activity, and a healthy diet to prevent hypertension or obesity. More than 14 units of alcoholic drinks per week has also been associated with a greater risk of dementia, so it should be limited.

At TUH, consultant geriatrician Aoife Fallon runs a brain-health clinic to address potentially modifiable lifestyle factors for people in mid to late life.

“We should all be engaging in moderate to vigorous physical activity for 30 minutes at least five times a week,” says Fallon.

“Hearing loss can be addressed through reducing excessive noise exposure, or increasing cognitive stimulation with hearing age. Depression has also been associated with an increased risk of dementia, and treatment with antidepressants was shown to delay progression to dementia, in one study.”

Prof Kennelly is also interested in the protective effects of midlife vaccines, with growing evidence from population studies that influenza and shingles vaccines can reduce the risk of Alzheimer’s and other forms of dementia.

In 2022, a study from Houston found that over-65s who received an annual flu vaccination for three consecutive years reduced their dementia risk by 20% over the subsequent four to eight years, while six shots in a row led to a 40% reduction.

There are various theories as to why vaccines yield this protective effect. One idea is that they might boost the ageing immune system and prevent viruses from reaching the brain, where they could induce damage.

But there may also be a secondary effect, whereby vaccines help prevent the brain’s immune cells from overreacting to the presence of plaques and tangles and unleashing a wave of chronic inflammation that causes the loss of healthy brain tissue.

“There’s massive evidence to support getting vaccinated for reducing your risk of dementia,” says Prof Kennelly. “It stops you from getting a primary infection, but, more importantly, it stops systemic inflammation in the brain.”

Slowing disease progress

There are more than practical ways to reduce our risk of Alzheimer’s. The first disease-modifying treatments that can slow the progression of the illness have started to emerge.

Last summer, phase-3 trials were completed for lecanemab and donanemab, both antibody infusion therapies that remove amyloid from the brain. Lecanemab slowed disease progression by 27% compared to a placebo, equivalent to a five-month delay in the disease progressing . In comparison, donanemab appears to slow progression by up to 48% in under-75s who have mild forms of Alzheimer’s.

While this isn’t perfect, and both treatments have concerning side effects, such as brain swelling and bleeding, researchers have lauded the trial results as a promising start.

“It does help to prove the concept of targeting amyloid in the brain treatment of Alzheimer’s, which has been a contentious scientific argument for some decades,” says David O’Connell, an associate professor at University College Dublin.

“These new drugs are not a cure, but they provide an opportunity to slow the disease and potentially provide a better quality of life for a little longer in the right patient.”

The success of these two drugs has accelerated a new wave of pharmaceutical investment in the field. Prof Kennelly says that 120 drugs are in development for Alzheimer’s, many of which are disease-modifying therapies, while numerous labatory studies are investigating novel ways of targeting amyloid to avoid the side effects of drugs lecanemab and donanemab.

O’Connell’s lab is attempting to use enzymes that can inhibit the development of amyloid plaques in the brain. It is also working with Enterprise Ireland to launch a spin-off company to begin a clinical trial.

“Alternative approaches that are safer and improve patient outcomes will be appearing in the clinic in the coming years, so the outlook is exciting,” he says.

However, other approaches target the inflammation that amyloid induces in the brain.

Prof Kennelly says that some researchers are developing one- or two-dose vaccine regimens that could dampen this neuro-inflammation.

TUH is also one of the centres for a clinical trial, called EVOKE, that is attempting to see whether certain doses of the drug semaglutide, better known as Ozempic, can have a protective effect on the brain in early Alzheimer’s.

“There are significant anti-inflammatory properties associated with it, which could potentially have a role in managing or reducing the progression of Alzheimer’s,” he says.

Overall, researchers are more optimistic that, over the next decade, we will start to see a succession of potentially game-changing treatments for the disease.

“We need to push beyond these two medicines, lecanemab and donanemab, which are very much just the start,” says Prof Kennelly.

“They’re definitely not where we’re going to end up. They reflect the complexity and the challenges that you have when looking for the first disease-modifying medicines in an area, as opposed to where I would hope we will be in five or 10 years.”

Five lifestyle changes to help reduce your risk 

1. Exercise: Regular exercise has been shown to cut your risk of developing all forms of dementia by nearly a third. This is because it protects against developing high blood pressure, which can damage fragile blood vessels in the brain, a contributing factor for many forms of the disease.

2. Minimising alcohol: Regularly consuming more than 14 units of alcohol per week can actively shrink parts of the brain which are involved in memory, predisposing those individuals to cognitive decline. Long-term heavy drinking can also lead to a lack of thiamine, a critical vitamin required by the brain, which impacts short-term memory.

3. Socialise: Research shows that lonely older adults are three times more likely to develop dementia. Social connections are known to play a major role in keeping the brain’s many networks stimulated and healthy, and prolonged isolation causes them to shrink in size, affecting cognitive functions like planning and decision-making.

4. Get a hearing test: Hearing loss is another dementia risk factor. The lack of stimulation to the auditory cortex, the part of the brain that processes sounds, causes it to degenerate slowly. Research has found that a hearing aid can stabilise cognitive function

5. Maintaining purpose: Retaining purpose in your latter years is essential for keeping your brain young by continuing to work for longer or finding regular part-time or volunteering roles. Studies of people who have lived past 100 have typically found that they have continued to find purpose throughout their lives.

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