The US Food and Drug Administration (FDA) has approved a second blood test to detect Alzheimer’s disease, potentially speeding diagnosis for millions of patients.

The Elecsys pTau181 test measures protein levels in blood plasma that act as biomarkers for the degenerative brain disorder, offering a simpler alternative to costly brain scans for people aged 55 and over with symptoms of cognitive decline.

The approval marks another step toward making Alzheimer’s detection more accessible through routine blood testing rather than specialist imaging that can take weeks or months for diagnosis.

Developed by Swiss biotech company Roche with Eli Lilly, the test builds on evidence that certain blood proteins can indicate brain changes linked to Alzheimer’s disease.

The pTau181 protein it measures is a biomarker — a biological indicator of disease activity.

“By bringing Alzheimer’s blood-based biomarker testing into primary care, we can help patients and their clinicians get answers sooner to support them earlier in their journeys,” said Brad Moore, CEO and president of Roche Diagnostics North America.

The FDA approved the first Alzheimer’s blood test, Lumipulse, earlier this year.

That test, made by Japanese company Fujirebio, detects different protein biomarkers linked to the disease.

Alzheimer’s is currently diagnosed using brain scans that detect toxic protein build-up and other hallmarks of the disease. These procedures are expensive, often involve long waiting times, and are not widely available.

Blood tests could make early screening easier in primary care, though experts stress they cannot provide a definitive diagnosis on their own.

“This is another important step toward expanding access to Alzheimer’s disease diagnostic tools,” said Dr Joanne Pike, president and CEO of the Alzheimer’s Association.

“At the same time, it is important to understand this test is designed to rule out the presence of amyloid plaques. It is not a test that will give an Alzheimer’s disease diagnosis, nor is it a standalone tool for detection.”

Amyloid plaques are abnormal protein deposits that form between brain cells and are a hallmark of Alzheimer’s.

The blood test helps determine whether these plaques are likely present, guiding doctors on whether further testing is needed.

Roche said a clinical study involving more than 300 participants showed the test correctly identified people without Alzheimer’s signs in nearly 98 per cent of cases.

his accuracy could help reduce unnecessary brain scans and related costs.

Researchers at UC San Diego recently reported that rises in blood proteins following brain inflammation and nerve cell damage were linked to cognitive decline — evidence supporting development of blood-based early detection tools.

Dr Richard Isaacson, who established one of the first Alzheimer’s prevention clinics in the US, told CNN that additional blood tests would likely be needed to give a full picture of brain health.

“This single Roche test is looking at pTau181 as a single protein marker,” he said.

“But for people who are at risk for Alzheimer’s, to truly have the best accuracy and the most granularity to understand what’s going on, we’re going to need a panel of tests.

“And then we’re going to need to follow these tests over time.”

The Alzheimer’s Association said the test could help avoid unnecessary and expensive diagnostic procedures.

The Elecsys pTau181 test is designed to be used alongside clinical evaluation and other diagnostic tools, not as a replacement for full medical assessment.

Patients with positive results would typically undergo additional testing to confirm a diagnosis.

Both approved blood tests represent progress in improving Alzheimer’s detection, though experts emphasise that diagnosis still requires a combination of clinical, imaging and laboratory assessments.

As blood-based biomarker research advances, scientists hope combining several markers will give a clearer picture of brain health and disease progression — potentially allowing earlier intervention and better patient outcomes.

Age Tech World explores the latest research developments in the world of ageing and longevity.

Pan-disease atlas maps molecular fingerprints of health, disease and ageing

A new study has mapped the distinct molecular “fingerprints” that 59 diseases leave in an individual’s blood protein, which would enable blood tests to discern troubling signs from those that are more common.

An international team of researchers mapped how thousands of proteins in human blood shift as a result of ageing and serious diseases, such as cancer and cardiovascular and autoimmune diseases.

The Human Disease Blood Atlas also reveals that each individual’s blood profile has a unique molecular fingerprint, which changes through childhood and stabilises in adulthood.

This provides a baseline for comparison that healthcare providers could one day use to flag early deviations.

The study used machine learning that enables information critical for building blood panels that would not misclassify patients in real world settings.

The mapping of molecular fingerprints of disease is a crucial step for building blood tests that work in the clinic, the researchers say.

For example, many proteins that rise in cancer or autoimmunity also rise in infections, reflecting shared inflammatory pathways, while other patterns such as liver-related conditions are clustered by organ systems.

The Disease Blood Atlas offers a path to solve the problem of identifying reliable, reproducible biomarkers for diseases – a process that to date has typically involved comparing new protein markers against a control, that is, a healthy profile.

The researchers point to the study’s success in identifying common biomarkers that are consistently altered in various conditions.

These shared molecular features could serve as universal diagnostic, prognostic or therapeutic targets.

Among the findings was that specific protein profiles can change substantially as individuals approach a cancer diagnosis, with some proteins showing higher concentrations prior to diagnosis.

These findings suggest more study should be devoted to investigating the potential of using proteomics for early cancer detection.

Aging Well with AI report explores AI and the healthcare workforce

The “Aging Well with AI: Empowering Care through Innovation” whitepaper has been published, the first in a two-part white paper series exploring how artificial intelligence (AI) can strengthen the U.S. healthcare workforce and improve access to care.

As the US confronts a historic shortage of healthcare workers alongside a rapidly ageing population, the report outlines specific ways AI can reduce strain on clinicians and improve outcomes for older adults, without eroding the human relationships that are essential to high‑quality medicine.

HealthFORCE, a national alliance of leaders dedicated to addressing the root causes of America’s healthcare workforce crisis, along with the American Academy of Physician Associates (AAPA) and West Health, published the report.

The paper highlights five opportunities for AI to extend the healthcare workforce and improve care for older adults and calls on policymakers, health systems and innovators to invest in geriatric-focused tech innovation and prioritise AI tools that serve older adults.

It also calls for incentives for cross-specialty training in ageing care and AI use for all frontline providers, the establishment of national standards for AI integration across state lines and care settings and the promotion of interoperability and support value-based payment models that reward continuity, efficiency, and prevention.

The upcoming second report will focus on how AI can augment care delivery across all patient populations and help address the projected shortfall of 3.2 million healthcare workers by 2026.

It is set to be released later this month.

Lifelong companionship protects ageing rat brains from cognitive decline

A new research paper shows that aged rats who lived in socially enriched environments throughout life retained better memory and cognitive flexibility than those housed alone.

This study highlights the importance of social interaction in protecting the ageing brain.

Cognitive decline, such as memory loss and reduced problem-solving ability, affects many people over the age of 65.

While many factors contribute to age-related cognitive decline, this study suggests that one key factor may be surprisingly simple: long-term social connection.

To explore how social interaction might influence memory performance and brain activity, the researchers designed a study using rats as a model for ageing in humans.

The team compared three groups of rats: young adults, aged rats housed alone, and aged rats housed socially in groups.

All groups had access to the same physical enrichment, such as exercise and stimulating objects, but only some experienced lifelong social companionship.

The team tested these animals on a complex memory challenge known as the biconditional association task, which requires animals to make context-based decisions, an ability that typically declines with age.

The results showed that aged rats living in social groups performed just as well as young adults on the memory task, while those housed alone showed significant impairments.

Socially housed rats also made fewer working memory errors and required less effort to complete cognitive tasks, suggesting not only better performance but more efficient brain function.

These benefits were not observed in aged rats who received only environmental enrichment without social interaction.

Brain imaging revealed additional differences between the groups.

Socially housed aged rats showed increased activity in the hippocampus, particularly in the CA3 region, which plays a key role in forming and separating memories.

In contrast, aged rats that lived alone had lower activity in this region, which may explain their poorer performance.

Interestingly, socially housed rats also showed reduced overactivity in the anterior cingulate cortex, a brain area involved in attention and decision-making, suggesting a more balanced and efficient neural response.

This research provides new insight into how lifelong social experiences shape brain health during ageing.

While earlier studies have shown that physical activity and cognitive stimulation help preserve cognitive function, this study identifies social interaction as an independent and powerful protective factor.

The findings are consistent with human studies showing that older adults who remain socially active tend to experience slower cognitive decline and stronger brain function.

Overall, these results emphasise that brain ageing is not inevitable but may be influenced by our social environments.

This research suggests that fostering lifelong social connections could be a critical, low-cost strategy to protect memory and mental flexibility in older adults.

Service dogs slow cellular ageing in female veterans

New research has found that service dogs may help slow biological ageing in women.

This groundbreaking study, focused on female veterans in the United States, is among the first to examine the impact of working with service dogs on this often-overlooked population.

By measuring biological indicators of stress, the researchers have uncovered a key insight: the way stress is felt emotionally doesn’t always reflect how it affects the body at a cellular level.

Researchers conducted the study involving female veterans with post-traumatic stress disorder (PTSD), but instead of receiving service dogs, these women volunteered to train them for fellow veterans in need, offering support not just to others, but potentially to themselves.

The study examined whether this purposeful, mission-driven activity could reduce both biological and psychological stress, and whether previous combat exposure influenced those effects.

Until now, the emotional and therapeutic benefits of such unique relationships have been largely unexamined in female veterans.

To measure biological stress, researchers looked at telomere length (a marker of cellular ageing) using saliva samples, and heart rate variability (HRV), a sign of nervous system balance, using wearable monitors in participants in the service dog training program group or a comparison group that watched dog training videos.

Psychological stress was assessed using validated questionnaires measuring PTSD symptoms, perceived stress, and anxiety at multiple points during the study.

Results evealed promising biological benefits associated with service dog training, particularly for veterans with combat experience, while improvements in psychological symptoms were seen across all participants, regardless of the intervention.

One of the most striking findings involved telomere length. Veterans who participated in the dog-training programme showed an increase in telomere length, suggesting a slowing of cellular ageing.

In contrast, those in the control group exhibited a decrease in telomere length, indicating accelerated ageing.

Combat experience significantly influenced these results: veterans with combat exposure who trained service dogs experienced the greatest gains in telomere length, whereas those with combat exposure in the control group saw the most pronounced declines.

On the psychological front, both groups, those who trained dogs and those in the control group, reported significant reductions in PTSD symptoms, anxiety and perceived stress over the eight-week period.

However, these mental health improvements were similar across groups, suggesting that simply participating in the study and receiving structured attention may have offered therapeutic value.

Unlike the biological findings, psychological outcomes did not appear to be affected by combat exposure.

The study also suggests that the skills learned during service dog training such as positive reinforcement and reading animal behavior may have strengthened participants’ bonds with their own pets at home, offering additional emotional support.

Unlike general volunteering, service dog training uniquely blends emotional healing with building a close relationship between veterans and their animals, providing therapeutic benefits that go beyond typical community engagement.

Female veterans aged 32 to 72 were randomly assigned to either the service dog training program group or a comparison group that watched dog training videos.

Both groups took part in one-hour sessions each week for eight weeks. Researchers measured outcomes before, during and after the programme.

These findings provide early evidence that non-pharmacological interventions – such as service dog training – may help reduce the physical toll of stress and slow cellular ageing in female veterans.

People with genetic variants that naturally lower cholesterol were found to have up to 80 per cent lower dementia risk in a study of more than one million participants.

The research analysed data from Denmark, England and Finland to assess how genes that mimic the effects of cholesterol-lowering drugs such as statins and ezetimibe influence dementia risk.

Scientists found that reducing blood cholesterol by one millimole per litre was linked to as much as an 80 per cent reduction in dementia risk for certain drug targets, suggesting possible benefits from cholesterol-lowering treatment.

The researchers used a method known as Mendelian randomisation, which allows scientists to study the effects of lowering cholesterol while avoiding confounding factors such as diet, weight and other lifestyle habits.

Dr Liv Tybjærg Nordestgaard led the research while at Bristol and now works at Copenhagen University Hospital–Bispebjerg and Frederiksberg hospital.

Dr Nordestgaard said: “What our study indicates is that if you have these variants that lower your cholesterol, it looks like you have a significantly lower risk of developing dementia.”

Some people are born with genetic variants that naturally affect the same proteins targeted by cholesterol-lowering drugs such as statins and ezetimibe.

By comparing these individuals with those without such variants, the researchers were able to measure differences in dementia risk.

Mendelian randomisation uses genetic variation as a natural experiment.

Because genes are inherited randomly at conception, this method can mimic randomised clinical trials and offer stronger evidence for cause-and-effect relationships than traditional observational research.

The findings suggest that having low cholesterol, whether due to genetics or medical treatment, could help reduce the risk of developing dementia. However, the study does not provide definitive evidence about the effects of the medicines themselves.

One of the main challenges in dementia research is that symptoms typically appear later in life, requiring decades of follow-up to detect meaningful changes. This makes long-term clinical trials difficult to conduct.

The biological link between high cholesterol and dementia is not yet fully understood. Dr Nordestgaard suggested that atherosclerosis — the build-up of cholesterol in blood vessels — may play a key role.

Dr Nordestgaard said: “Atherosclerosis is a result of the accumulation of cholesterol in your blood vessels.

“It can be in both the body and the brain and increases the risk of forming small blood clots—one of the causes of dementia.”

Blood clots can block small vessels in the brain, leading to vascular dementia — the second most common form of the condition after Alzheimer’s disease.

Even small clots can damage brain tissue over time and contribute to cognitive decline.

The study used data from large genetic research projects including the UK Biobank, the Copenhagen General Population Study, the Copenhagen City Heart Study, the FinnGen study and the Global Lipids Genetics Consortium.

These resources provide genetic and health information from diverse populations, improving the reliability of the findings across different ethnic and geographical groups.

The UK Biobank includes data from around 500,000 participants aged 40–69, while the Copenhagen studies have tracked Danish populations for several decades, providing detailed health records for long-term analysis.

“It would be a really good next step to carry out randomised clinical trials over 10 or 30 years, for example, where you give the participants cholesterol-lowering medication and then look at the risk of developing dementia,” Dr Nordestgaard added.

Such trials would provide direct evidence about whether cholesterol-lowering drugs can prevent dementia, rather than relying on genetic data.

However, their length and cost make them difficult to conduct.