dementia

Dementia Is Now Australia’s Leading Cause of Death: What Do New Alzheimer’s Blood Tests Actually Mean?

11 min read · Dr. Danny Cai · 8 September 2026

Dementia is Australia's leading cause of death. New blood tests for Alzheimer's are promising, but they're not for everyone. Here's what the evidence says.

Dementia, including Alzheimer's disease, is now Australia's leading cause of death. It has also been the leading cause of death among Australian women for several years. This makes progress in Alzheimer's testing, prevention and treatment deeply important.

One of the most significant developments is the arrival of blood based biomarkers that can help clinicians assess whether Alzheimer's related changes may be present in the brain. This is a genuine scientific shift. However, it is equally important to understand what these tests can, and cannot, tell us.

A blood test is not a diagnosis of dementia. It is not a crystal ball. And it is not currently recommended as a routine screening test for people who are well and have no cognitive symptoms.

The most useful question is not simply, "Should I have an Alzheimer's blood test?" It is:

"What clinical question are we trying to answer, and would the result change what we do next?"

A New Era in Alzheimer's Assessment

Alzheimer's disease develops over many years. Biological changes involving amyloid-beta and tau proteins may begin well before a person develops enough symptoms to meet criteria for dementia.

Traditionally, clinicians have used a combination of history, cognitive assessment, physical examination, blood tests, brain imaging and, when appropriate, specialist investigations to understand the cause of memory or thinking changes.

When confirmation of Alzheimer's pathology is needed, the established tools have been:

  • Amyloid PET, a brain scan that can demonstrate amyloid deposition

  • Cerebrospinal fluid testing, usually obtained by lumbar puncture, which measures amyloid and tau-related biomarkers

  • Comprehensive cognitive, functional and neurological assessment

These investigations can be highly informative, but access is limited by cost, availability and the need for specialist care. Blood biomarkers may help make the diagnostic pathway more accessible, particularly for people already being assessed for cognitive impairment.

The key point is that biomarker tests are designed to answer a clinical question. They do not replace a proper assessment of the person in front of us.

Which Blood Biomarkers Matter?

Not all blood tests described as "Alzheimer's tests" have the same evidence base. The biomarkers of greatest current interest relate to the two core pathological processes of Alzheimer's disease: amyloid and tau.

Amyloid-related biomarkers

Amyloid-beta is a protein that can accumulate in the brain as plaques. Blood measures related to the amyloid-beta 42/40 ratio may help estimate the likelihood of brain amyloid pathology.

A lower ratio may be associated with a higher probability of amyloid deposition, but there is an important caveat: numerical thresholds are assay specific.

A cut off used by one laboratory, analyser or test manufacturer cannot automatically be applied to another. Reference ranges, sample processing and the underlying patient population all influence how a result should be interpreted.

Tau-related biomarkers

Phosphorylated tau biomarkers, particularly p-tau217 and p-tau181, have become leading candidates for evaluating Alzheimer's-related pathology in blood.

In the appropriate clinical setting, abnormal p-tau results may increase the likelihood of underlying Alzheimer's pathology. However, a single elevated result does not establish that a person has dementia, predict exactly when symptoms will occur, or tell us how rapidly cognitive change may progress.

Markers of brain injury and inflammation

Other blood markers may offer additional context:

  • Neurofilament light chain, or NfL, is associated with axonal injury. It is not specific to Alzheimer's disease and may be influenced by several neurological, systemic and age related factors.

  • Glial fibrillary acidic protein, or GFAP, reflects astrocyte activation and may be associated with amyloid-related changes. It is also not specific enough to diagnose Alzheimer's disease in isolation.

The future is likely to involve combinations of markers, interpreted alongside symptoms, cognitive testing, medical history and, where indicated, imaging or cerebrospinal fluid analysis.

Why Testing Is Not for Everyone

The performance of a test depends not only on the test itself, but also on the person being tested.

This is called pre-test probability: the likelihood that a condition is present before testing. It is one of the most important principles in diagnostic medicine.

A blood biomarker may be useful when a person has objective cognitive impairment and is being assessed in a specialised memory care setting. In contrast, if the same test is used in a person with no cognitive symptoms and a low likelihood of Alzheimer's disease, a positive result is more likely to be difficult to interpret and may be misleading.

Current clinical guidance focuses on blood biomarkers in the diagnostic work up of suspected Alzheimer's disease in specialised care settings. It recommends that blood biomarker testing follows a comprehensive clinical evaluation and that results are interpreted in the full clinical context.

For this reason, blood biomarker tests are not currently recommended as:

  • A population wide screening test

  • A direct to consumer "brain health" check

  • A stand alone answer for people with no symptoms

  • A substitute for clinical assessment

  • A way to diagnose dementia from a number alone

This does not mean that family history, genetic risk or personal concern should be ignored. It means they should prompt a thoughtful clinical conversation rather than an automatic biomarker panel.

Positive, Negative and Intermediate Results

A responsible approach does not reduce biomarker testing to a simple "normal" or "abnormal" label.

Many specialists favour a two cut point approach that produces three broad result categories.

Negative result

A negative result means Alzheimer's related pathology is less likely in the clinical context in which the test was used. It does not rule out every possible cause of cognitive symptoms.

Intermediate result

An intermediate result is inconclusive. Further clinical review, repeat assessment, amyloid PET or cerebrospinal fluid testing may be appropriate, depending on the individual situation.

Positive result

A positive result means Alzheimer's related pathology is more likely, but the result must be interpreted alongside the person's symptoms, examination, cognitive profile and the assay-specific reference range. Confirmation may still be needed, especially if treatment is being considered.

This framework is safer than treating a single blood test value as a diagnosis.

Kidney function, age, body size and blood volume, acute illness, stroke, other neurological disease, specimen handling and the exact test platform may all affect biomarker interpretation. A result from one assay should not be directly compared with a value from another laboratory.

Genetics: Risk Is Not Destiny

Genetics can contribute to Alzheimer's risk, but genetic information needs careful interpretation.

The APOE ε4 variant is associated with increased susceptibility to late onset Alzheimer's disease. Carrying APOE ε4 does not mean a person will develop Alzheimer's disease. Conversely, people without APOE ε4 can still develop it.

Genetic information may be relevant in selected circumstances, including:

  • A strong family history of dementia, particularly when onset was unusually early

  • Specialist assessment of possible inherited dementia syndromes

  • Discussions about eligibility or safety considerations for certain amyloid-targeting treatments

  • Research participation

However, APOE testing should not be treated as a routine predictive test or a stand alone measure of individual destiny. It can have psychological and family implications, and genetic counselling may be appropriate.

Polygenic risk scores are an active research area but are not established as routine clinical tools for determining Alzheimer's risk or prescribing a personalised prevention programme.

Earlier Detection Does Not Mean Automatic Treatment

It is reasonable to feel optimistic about the progress in disease modifying therapy. A new generation of treatments is designed to act on specific aspects of Alzheimer's biology, including amyloid pathology, tau, inflammation and neurodegeneration.

Some anti-amyloid monoclonal antibody therapies are approved in certain jurisdictions for carefully selected people with early symptomatic Alzheimer's disease, typically mild cognitive impairment or mild dementia due to Alzheimer's disease, with confirmed amyloid pathology.

These therapies are not cures. They do not reverse established dementia. They are not general preventive medicines for people with a family history, genetic susceptibility or an isolated blood-test result.

Treatment requires specialist assessment, confirmation of Alzheimer's pathology, an informed discussion of likely benefit and limitations, and safety monitoring. Anti-amyloid therapies can be associated with amyloid related imaging abnormalities, including brain swelling or bleeding. The balance of benefit and risk varies between individuals.

The implication is not that people should lose hope. It is that more precise treatment requires more precise diagnosis.

What Supports Brain Health Now?

Even as biomarkers and medicines advance, the strongest population-level opportunities still involve protecting brain health across the life course.

The 2024 Lancet Commission identified 14 potentially modifiable risk factors that together could account for up to 45% of dementia cases worldwide at a population level. This is not a guarantee that any individual case of dementia can be prevented. It does show that dementia risk is shaped not only by age and genetics, but also by health, environment and opportunity.

The practical priorities are familiar:

  • Manage blood pressure, diabetes and cholesterol appropriately

  • Avoid smoking

  • Stay physically active, including aerobic and resistance exercise

  • Maintain social connection and meaningful engagement

  • Address hearing loss and vision impairment

  • Prioritise good-quality sleep and seek assessment for possible sleep apnoea when indicated

  • Limit harmful alcohol use

  • Treat depression and support mental wellbeing

  • Reduce risk of preventable head injury

  • Support education, cognitive stimulation and ongoing learning

  • Seek appropriate care for vascular and metabolic health

The Finnish FINGER study is an important example of this approach. In older adults at increased risk of cognitive decline, a two year programme combining diet, exercise, cognitive training and vascular risk monitoring improved or maintained cognitive performance compared with usual health advice.

It supports a multidomain approach rather than reliance on any single supplement, diet, exercise modality or biomarker.

No supplement has been proven to prevent Alzheimer's disease. Supplements may interact with medication, add cost and distract from more established foundations of health. They should not be used as a substitute for medical assessment or management of recognised risk factors.

When Should You Seek Assessment?

Consider a clinical review if you or those close to you notice persistent or progressive changes in memory, language, planning, behaviour, judgement or day-to-day function.

Examples include:

  • Repeatedly forgetting recent conversations or events

  • Asking the same questions frequently

  • Difficulty managing finances, medication, work or household tasks that were previously routine

  • New difficulty finding words, following conversations or planning multi-step tasks

  • Getting lost in familiar locations

  • Significant changes in mood, behaviour, social judgement or personality

  • Cognitive concerns noticed by family, friends or colleagues

There are many possible explanations for cognitive symptoms. Sleep disturbance, depression, anxiety, medications, alcohol, hearing impairment, thyroid disorders, vitamin deficiencies, cardiovascular disease and acute illness can all contribute.

This is why the first step should be a proper clinical assessment rather than self-diagnosis from an online risk score or isolated laboratory result.

Urgent assessment is required for sudden confusion, a rapid deterioration over hours or days, new focal neurological symptoms, fever, severe headache or a marked change in consciousness.

The Balanced Message

Blood-based biomarkers are a meaningful advance in the assessment of suspected Alzheimer's disease. They may help clinicians identify Alzheimer's-related pathology more accessibly and may become increasingly important as targeted treatments develop.

But precision matters.

A biomarker result is not a diagnosis. It must be interpreted in the context of the individual, the clinical question, the assay used and the likelihood of disease before testing. The best use of new technology is not to create fear in well people. It is to support careful assessment, clearer decision-making and better access to appropriate care.

For most people, the practical foundations remain the same: take persistent cognitive concerns seriously, seek an appropriate clinical assessment, protect cardiovascular and metabolic health, stay physically and socially active, treat sleep and sensory problems, and approach new tests with curiosity as well as healthy caution.

If you have concerns about your memory or thinking, or a family history of dementia, a consultation can help you understand what, if any, testing is appropriate for your situation. We focus on evidence-based assessment and clear, honest interpretation.

General information, not individual medical advice. Speak to your own doctor.

References

  1. Australian Bureau of Statistics. Causes of Death, Australia. Dementia, including Alzheimer's disease, is reported as Australia's leading cause of death. Accessed September 2026.

  2. Palmqvist S, Whitson HE, Allen LA, et al. Alzheimer's Association Clinical Practice Guideline on the use of blood-based biomarkers in the diagnostic workup of suspected Alzheimer's disease within specialized care settings. Alzheimer's & Dementia. 2025;21:e70535. PMID: 40729527.

  3. Livingston G, Huntley J, Liu KY, et al. Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission. Lancet. 2024;404(10452):572–628. PMID: 39096926.

  4. Ngandu T, Lehtisalo J, Solomon A, et al. A 2-year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial. Lancet. 2015;385(9984):2255–2263. PMID: 25771249.

  5. U.S. Food and Drug Administration. LEQEMBI (lecanemab-irmb) prescribing information. Treatment should be initiated only after confirmation of amyloid-beta pathology. Accessed September 2026.

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General education, not individual medical advice. No prescription medicines are advertised; personalised treatment follows clinical consultation.