Breakthroughs in Alzheimer’s disease research signal meaningful progress against a historically intractable condition. These advances could reshape future mortality and morbidity trends and carry major implications for underwriting, product design, and long term claims experience as diagnosis shifts earlier and prevention strategies strengthen.
Alzheimer’s disease (AD) has long been one of the most challenging conditions to understand, diagnose, and treat, characterized by late clinical presentation and decades of therapeutic failure. As this begins to change, life and health insurers need to actively monitor developments in AD research because advances in diagnosis, prevention, and treatment have the potential to materially reshape future mortality and morbidity trends, underwriting practices, and long term claims experience.
Interpreting Alzheimer’s trends is particularly difficult because observed historical patterns reflect changes in diagnostic practices, data availability, and population aging as much as changes in underlying disease risk. For actuaries setting future assumptions, simply extrapolating past trends may therefore overstate future risk.
At the same time, advances in biomarkers, imaging, and genetics are enabling earlier and more precise detection of AD, while a growing understanding of risk – spanning biology, lifestyle, and comorbidities – is reshaping how the disease is conceptualized and studied.
Together with emerging disease modifying therapies, these developments point to a future that is cautiously but meaningfully brighter, marked by earlier intervention, improved patient stratification, and more targeted approaches to prevention and treatment.
These advances could slow disease progression and reduce age adjusted mortality, even as demographic aging continues to drive higher prevalence; that said, adverse lifestyle and environmental trends remain a material downside risk.
One particularly promising development is the emergence of blood based biomarkers for Alzheimer’s disease. While widespread adoption could transform diagnosis by enabling earlier and broader detection, it may also introduce material adverse selection risk – especially in critical illness and long term care insurance – by shifting the timing and distribution of observed incidence and claims.
AD is the most common form of dementia, leading to progressive cognitive decline and functional impairment. Advances in biomarkers, neuroimaging, and blood based diagnostic tools are improving the ability to identify AD earlier, while a new generation of therapies, with some targeting the underlying biology rather than just symptoms, is leading to more effective and personalized care.
Global figures show that AD currently affects an estimated 50 million people worldwide. This number is expected to triple by 2050.1
Historical data on AD prevalence, incidence, and mortality can be affected by diverse reporting biases, from diagnostic practices to death certificate coding, making the interpretation and modelling of trends far from straightforward. For example, the introduction of the International Classification of Diseases 10th revision (ICD-10) provided new classifications of disease for the coding of deaths, and changes in reporting practices affected recorded deaths for AD and other dementias.
Furthermore, varied and evolving case definitions have created substantial heterogeneity, making it difficult to track dementia prevalence consistently over time and across regions. Consequently, standardized epidemiological measures are essential to draw meaningful insights on historical trends.
Carefully designed studies have shown a declining age-standardized incidence in many countries, including the U.S., Canada, Denmark, and the UK. A meta-analysis of 49,202 individuals across seven studies in the U.S. and Europe found that the incidence rates of dementia declined by 13% per decade during 1988–2015. The age-specific dementia prevalence rates have also declined in the U.S., falling by around two-thirds during 1984–2024 at a relative rate of 2.5%–3.0%.3 It may be that these declines are because of changes in risk factors for the disease, such as declines in smoking, increased education levels and the use of statins.
Age standardized Alzheimer’s incidence is not declining everywhere, however. Trends are flat or rising in some high middle and middle income countries, particularly in East Asia. This region is consistently identified as an area with rising incidence burden not fully explained by aging alone. This may reflect unfavorable period and cohort effects, including worsening cardiometabolic mid‑life risk factors (obesity, high fasting glucose and smoking).
In contrast to incidence, age-standardized dementia-related mortality rates have surged in the U.S. and other countries. This sharp rise in mortality rates largely reflects greater recognition and reporting of dementia on death certificates. Depending on the data source, projecting historical AD trends to make forward-looking biometric assumptions (including mortality and morbidity improvement assumptions) could paint an overly pessimistic picture of future trends.
Significant progress continues to be made in understanding the risk and protective factors for AD, especially in:
Researchers have long focused on amyloid beta – a peptide that accumulates in the brain and forms plaques – as a central driver of dementia, but a growing body of science now points to the immune system and chronic inflammation as a critical piece of the puzzle. Indeed, inflammation and immune signaling are among the strongest emerging causal mechanisms. One especially intriguing observation is that vaccination may help lower the risk of dementia by modulating immune activity.
A wave of recent large scale studies has strengthened these ideas.
Further evidence has continued to build excitement. Multiple population level studies have now reported similar associations, including research showing that even vaccines for respiratory infections such as Respiratory Syncytial Virus (RSV) may be linked to reduced dementia risk.6 Together, these findings suggest that vaccination may help counter inflammatory or viral triggers that contribute to cognitive decline.
The most compelling development came in December, when a follow up study revealed that the shingles vaccine may not only prevent dementia but also slow its progression. In this analysis, the vaccine was associated with a lower risk of mild cognitive impairment among cognitively healthy adults and, notably, a reduction in mortality among people already living with dementia.7 This suggests that the vaccine’s benefits may extend beyond prevention to potentially modifying the disease trajectory itself.
Taken together, these studies mark a striking shift: certain vaccines long known for preventing infectious disease may also offer a promising new avenue for reducing dementia risk and improving outcomes for those already affected.
It has long been established that variants in the apolipoprotien E (APOE) gene are strongly associated with increased risk of AD. However, a recent study of individuals aged 60 and older found the proportion of all-cause dementia attributable to Ɛ3 and Ɛ4 APOE variants was 44.4% and 45.6% respectively. The research concluded that most AD could be prevented (or at least delayed) by reducing the risk conferred by differences in APOE expression or function.8
Research suggests that up to 45% of dementia cases could be delayed or reduced if 14 identified risk factors were eliminated via lifestyle changes or population-based policy changes.9
Implementing preventative measures such as increasing physical activity and socialization, stopping smoking, and decreasing alcohol consumption can reduce the risk of early diagnosis of AD.
Other risk factors include poor mental health, low level of early education, hearing loss, air pollution, diabetes, hypertension, obesity, traumatic brain injury, and two newly identified risk factors: high LDL cholesterol and poor vision. The U.S. POINTER trial showed structured lifestyle intervention (exercise, diet, cognitive stimulation, vascular risk control) improved cognition for at risk older adults.10
Hearing loss is also associated with cognitive decline and dementia risk, identified by the 2024 Lancet Commission as a major risk factor. In an analysis using data from the Framingham Heart Study, between January 2024 and August 2025, participants with mild or greater hearing loss (when compared to those with minimal or no hearing loss) had smaller brain volumes and reduced cognitive function. For those with minimal hearing loss compared to those with no hearing loss, risk of developing any dementia was 71% higher over a 15-year period, and even higher (186% higher) in those with at least one APOE Ɛ4 allele. Managing hearing loss with hearing aids may modify the risk for developing dementia for potentially 8% of new cases recorded each year.11
These findings are supported by other studies, including the Ishak et al’s study of incident dementia and hearing loss, where one in three dementia cases (32%) could potentially be attributed to significant hearing loss, whether mild (16.2%) or moderate or greater (16.6%).12 However, as yet it remains undetermined to what extent hearing loss may be an associative or causative factor.
Evidence continues to mount linking air pollution, specifically fine particulate matter (PM2.5), with an increased risk of developing dementia (see Alzheimer’s Disease: Epidemiology, Risks, and Testing | RGA). Despite the exact causation being largely unknown, PM2.5 exposure is associated with brain volume loss, atrophy, accelerated aging, worsening cerebrospinal fluid amyloid-beta42 biomarker levels, and increased amyloid positron emission tomography (PET) positivity. In a recent study of 602 deceased patients with dementia or movement disorders, higher PM2.5 exposure before death was associated with 19% increased odds of more severe AD neuropathic change.13 In a separate meta-analysis of 32 studies, dementia diagnosis was associated with long-term exposure to PM2.5, with a hazard ratio of 1.08 per 5µg/m3 increase in exposure.11
The rise of detectable and measurable blood-based biomarkers is set to transform the AD diagnostic process, which previously was primarily based on clinical symptoms and a process of elimination. A range of new and exciting developments in diagnostics announced last year could revolutionize the early diagnosis and treatment of AD. Newly approved diagnostics, as well as those still in development, could reduce AD-related mortality and significantly improve quality of life of patients. This, in turn, could influence claims payouts and pricing for multiple product lines.
In May 2025, the U.S. Food and Drug Administration (FDA) approved the first diagnostic blood test for early detection of amyloid plaques in AD, demonstrating more than 90% accuracy. If blood-based biomarker tests such as these were made widely available at an affordable cost, they could be carried out routinely by local physician services, replacing expensive and cumbersome tests such as amyloid and tau-based positron emission tomography (PET) scans and electroencephalography (EEG), reducing wait times to access specialist services. They also could be used in asymptomatic patients, offering the option for preventative treatment in high-risk individuals.14
Most recently, the international DROP-AD project has demonstrated the accuracy of a finger-prick blood test in detecting AD biomarkers, suggesting 86% accuracy in predicting cerebrospinal fluid biomarker positivity for AD.
While it will be some years before the test may be operative, it provides hope for early diagnosis that could completely shift the current projected trajectory of dementia incidence and mortality.
In addition, being able to monitor patients more regularly over time for personalized management would be life-changing for many individuals diagnosed with AD.15
Given these new developments, the U.S. National Institute on Aging (NIA) and the Alzheimer’s Association (AA) issued revised diagnostic criteria for AD, including that the disease should be defined biologically based on core biomarkers rather than based solely on clinical symptoms, and that the disease progresses from initial brain changes to progressive brain-related pathology accompanied by clinical symptoms.16 While a self-administered, at-home pre-screening tool could allow for early disease detection years in advance of the onset of symptoms, it could also allow for anti-selection in life, long-term care (LTC) and other insurance products.
Much has changed since June 2021, when it was announced that aducanamab (AduhelmTM) had been approved by the FDA as a disease-modifying therapy for AD (see New Medication for Alzheimer's Disease | RGA). Its approval was controversial at the time, following questions about its clinical benefits. Aducanamab was withdrawn by U.S. drug company Biogen in January 2024, reportedly due to lack of insurance coverage and low prescription rates.17
Older drug treatments include Donepezil, a cholinesterase inhibitor (ChEI) that blocks the breakdown of the neurotransmitter acetylcholine involved in memory and learning, and N-methyl-D-aspartate (NMDA) receptor agonists such as Memantine, which inhibit the action of NMDA receptors in the brain. Both are designed to delay the progression of cognitive decline, with modest effects. This figure shows changes in clinical dementia rating scores over a 15-year follow-up period, with higher values showing greater cognitive decline.
Growing evidence suggests that diabetics who use GLP-1 medications to manage their condition have a lower likelihood of developing dementia. While the biological pathways linking these medications to reduced dementia risk are not yet fully understood, the growing body of evidence is nonetheless promising. It suggests that, with further research, these drugs may ultimately be shown to confer a protective effect against dementia.
In November 2025, Novo Nordisk announced topline results from two Phase 3 clinical trials (Evoke and Evoke+) of their oral glucagon-alike peptide (GLP)-1 receptor agonist, semaglutide in early AD, stating that while semaglutide treatment improved AD-related biomarkers in both studies, this did not translate into a delay in disease progression. Full results are due to be published in March.24 Despite the failure of the Evoke and Evoke+ trials to meet their primary endpoints, semaglutide may still have relevance in AD research, particularly in prevention or earlier intervention rather than treating established disease.
Separately, in December 2025, results from a phase 2b clinical trial of the GLP-1 drug liraglutide showed promising results in people with early to moderate AD, with roughly half as much brain volume loss and an 18% slower decline in cognitive function. The trial found that injectable liraglutide entered the brain – one of the key challenges for any new potential AD treatment – albeit in small amounts.25
Oral semaglutide (treatment in Evoke and Evoke+ trials) is optimized for stability and absorption in the gut and for prolonged systemic exposure, properties that also appear to reduce its ability to enter the brain. This may explain why these two trials produced different results.
Trials of other disease-modifying therapies include the use of monoclonal antibodies such as trontinemab, which is specifically designed to cross the blood-brain barrier and rapidly remove amyloid plaques in the brain. In a Phase 1b/2a trial in 114 subjects, 91% of patients on the highest dose of trontinemab achieved amyloid negativity at 28 weeks. Importantly, the drug incurred a rate of less than 5% for brain bleeds or swelling – three to five times lower than existing immunotherapies.
Trials are continuing to assess the efficacy and safety of trontinemab in patients displaying early signs of AD.26
These breakthroughs raise important strategic questions for insurers:
For actuaries setting trend assumptions, it is important to again note the difficulties interpreting and extrapolating historical AD trend data. Depending on the data source, projecting historical data trends forward could paint an overly pessimistic picture of future dementia trends.
Experts believe that shifting AD diagnosis earlier is critical to improving mortality and quality of life outcomes. Early diagnosis expands the window during which patients may benefit from therapies that reduce symptoms or slow disease progression. This shift alone could significantly decrease disease progression and AD mortality trends in future.
In short, wide access to an accurate blood test for AD diagnosis could be transformative.
By the early to mid-2030s, dementia prevalence is expected to accelerate, as large segments of the population enter advanced age. However, ongoing improvements in the modifiable risk factors that increase dementia risk might help to reduce incidence rates. In this period, age-adjusted mortality rates might dip if new diagnostic tools successfully shift diagnosis earlier coupled with increased use of disease-modifying treatment strategies.
Over a 10- to 20-year horizon, significantly reducing disease progression and mortality will likely rely on treating asymptomatic patients. While evidence is currently very limited, increased use of GLP-1 drugs and targeted vaccination efforts could help to prevent or delay AD onset over the next several decades. Conversely, worsening environmental hazards (such as air pollution) and unhealthy lifestyle trends leading to obesity and diabetes could create higher-than-expected dementia incidence, particularly in vulnerable populations.
It should be noted that reducing AD‑specific mortality does not translate one‑for‑one into gains in life expectancy. Individuals who avoid dying from AD will still remain exposed to cardiovascular disease, cancer, infections, frailty‑related concerns, and other age‑associated risks. This is known as “competing risk” theory. In other words, a gain in survival from one disease may be partially or wholly offset by deaths from other causes that occur later in life.
From an underwriting perspective, earlier diagnosis and early intervention could improve the ability of younger lives to access life insurance, critical illness cover, and LTC cover. It also increases the likelihood of anti-selection by applicants who fail to disclose a positive biomarker result but who display no symptoms of AD.
Clarity of critical illness definitions for payout upon diagnosis of AD is imperative to ensure that it includes the requirement of a significant reduction of cognitive function, not just a diagnosis from a positive biomarker test.
As a result, insurers may need to review and tighten up definitions for both CI and LTC. Challenges also present for annuity underwriters who receive applications from individuals with positive biomarker results for AD but who are completely asymptomatic.
Life and health insurers must closely track the fast moving landscape of AD and monitor how emerging breakthroughs translate to mortality, morbidity, underwriting assessment, and long term claims patterns. As blood based biomarkers look set to enable earlier detection, insurers face new opportunities and new challenges – from improved risk stratification to heightened anti selection pressures.
If biomarker testing for AD becomes commonplace, it could trigger adverse selection, particularly in CI and LTC insurance. Similarly, the rapid evolution of disease modifying therapies and preventative interventions, public health recommendations, and regulatory approvals can reshape life expectancy projections, requiring insurers to continuously recalibrate pricing, product design, and reserve assumptions.
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