Alzheimer’s disease (AD) is the most common cause of dementia worldwide, accounting for about two thirds of cases. It is a progressive neurodegenerative condition that slowly erodes memory, thinking, and the ability to manage daily life. Globally, tens of millions of people live with Alzheimer’s today — numbers expected to grow sharply as populations age. The personal toll on individuals and families is profound, and the economic burden runs into hundreds of billions annually when considering healthcare costs, social care, and lost productivity.

Early diagnosis remains one of the biggest challenges. Historically, clinicians relied on observing cognitive decline — often when the disease is already advanced and irreversible brain damage has occurred. Emerging tools, particularly biomarkers, are beginning to change this picture.

The value of biomarkers in Alzheimer’s disease

Biomarkers are measurable indicators of biological processes, disease activity, or treatment response. In Alzheimer’s disease, they help detect characteristic brain changes — such as beta amyloid plaques and tau protein tangles — long before symptoms appear. These can be identified through imaging, cerebrospinal fluid tests, and, increasingly, blood-based biomarkers.

Research shows that:

• Biomarkers can detect early pathological changes along the Alzheimer’s disease continuum, even in individuals without symptoms.1
• Blood-based biomarkers (BBMs) such as plasma amyloid and tau provide a low cost, accessible alternative to PET scans and lumbar punctures.2
• Updated diagnostic frameworks now define Alzheimer’s biologically, emphasizing that biomarker-detected pathology is equivalent to diagnosing the disease.3

This shift opens opportunities for earlier intervention, improved trial recruitment, and more personalized care.

What recent biomarker research tells us

1. Alzheimer’s is now considered a “biological disease” detectable long before symptoms.

Updated clinical criteria emphasize that identifying Alzheimer’s related proteins — through imaging, cerebrospinal fluid, or blood — is sufficient to diagnose the disease, even in people who feel cognitively normal. This reflects decades of evidence showing pathology accumulates silently before memory loss begins.4

2. Blood tests are emerging as game‑changers.

Advances in ultra‑sensitive technologies now allow scientists to detect minute amounts of proteins that leak from the brain into the blood. These tests measure markers like amyloid‑β and phosphorylated tau — proteins central to Alzheimer’s disease. Because they require only a simple blood draw, they enable repeated testing over time, making disease monitoring easier and more accessible.5

3. Blood biomarkers may revolutionize primary care detection.

Many people with early cognitive impairment go undiagnosed, especially in community settings. New blood-based biomarker tests can be integrated into routine care to flag individuals at high risk earlier, long before they reach a specialist.6

4. Early diagnosis enables better care and more timely treatment.

Because Alzheimer’s pathology starts decades before symptoms, identifying the disease early can help clinicians initiate supportive measures, guide lifestyle interventions, and offer patients and families time to plan. It also allows people to access relevant clinical trials at the most impactful disease stage.7

5. Biomarkers deepen scientific understanding of Alzheimer’s progression.

Different biomarkers reveal different aspects of disease — amyloid reflects early accumulation, tau correlates more strongly with neurodegeneration, and neurofilament light chain indicates nerve cell damage. Using multiple tests helps clinicians and researchers understand where a person lies along the disease continuum.8

Focusing on Amyloid Beta (Aβ)

I, along with my co-authors, recently published a study that investigated whether changes in amyloid beta (Aβ) can reliably predict whether a treatment will help patients think and function better, i.e., whether Aβ is a surrogate marker. Many new Alzheimer’s drugs reduce Aβ levels, and some have even been approved based on this effect. But the big question remains: Does lowering Aβ actually translate into meaningful clinical benefit?

We collected data from 23 clinical trials of seven different anti-amyloid monoclonal antibody drugs.

These trials reported treatment effects on both:

• Aβ levels (using brain scans such as PET SUVR or the Centiloid scale), and
• Clinical outcomes, including:
  • Clinical Dementia Rating – Sum of Boxes (CDR‑SOB)
  • Mini‑Mental State Examination (MMSE)
  • Alzheimer’s Disease Assessment Scale–Cognitive Subscale (ADAS‑Cog)

The team used a Bayesian meta-analysis, a statistical method that combines results across many studies to look for broad patterns.

The results showed that lowering amyloid‑beta often — but not always — leads to better clinical outcomes in Alzheimer’s disease. Aβ is a promising surrogate marker at the group level, but it is not reliable enough to predict benefit for individual drugs without additional evidence. Its use by health technology assessment agencies such as NICE and ICER to make decisions about the value of the new disease modifying treatments should take this into account.

The need for continued research into Alzheimer’s biomarkers

Biomarkers are reshaping the landscape of Alzheimer’s disease, offering hope for earlier, more accurate diagnosis and more tailored therapeutic strategies. But despite these advances, more work is needed.

Continued research is vital to:

• Improve the accuracy and reliability of blood-based tests
• Ensure tests are validated across diverse populations
• Link biomarker changes more precisely to clinical outcomes
• Support equitable access in primary care and low resource settings

As we enter an era of disease-modifying therapies, biomarkers will be indispensable — guiding diagnosis, monitoring response, and helping patients receive the right treatment at the right time.

The future of Alzheimer’s care will be biomarker driven, and ongoing research is the key to making that future accessible to all.

Interested in learning more?

Read “Evaluating amyloid-beta as a surrogate endpoint in trials of anti-amyloid-beta drugs in Alzheimer’s disease: A Bayesian meta-analysis.”

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