Hunting down dementia
Dementia cases are surging globally, with more than 55 million people affected and nearly 10 million new diagnoses annually and so researchers are urgently decoding its hidden biological clues to combat this growing public health crisis.
It begins a subtle betrayal – an unnoticed pause in conversation, a missed appointment, a forgotten name, a change in gait. To the untrained eye, these are simple slips. But to a growing team of cognitive detectives at Monash University, these are possible clues; faint trails that might lead to a silent suspect long before it strikes.
Leading the chase are professors, neurologists, and data scientists, seasoned sleuths in suits and lab coats, investigating how the human brain ages. Their tools include blood pressure readings, MRI scans, sleep patterns, hospital records.
It’s all data, but to them, it’s a trail of breadcrumbs. And hidden within these is the possibility of foretelling cognitive decline, perhaps years before it shows its face.
Every year, the case is getting more urgent. Australians are getting older faster, and dementia is lurking in the shadows, picking at people’s minds until even a reflection in the mirror becomes a stranger.
The file is thick with projections. According to the Australian Bureau of Statistics, more than 4.4 million Australians were aged 65 and over in 2024. That’s about 17% of the population but, by 2050, it’s expected to swell to 22–25%.
Tailing that rise are dementia cases. In 2025 there were, according to Dementia Australia, 433,300 Australians living with dementia. That number is projected to nearly double by 2058, to 849,300.
But dementia doesn’t just stalk older people; younger-onset dementia also impacts nearly 29,000 Australians below 65, and that number is set to increase to 41,000 by 2054, an increase of 41%.
Globally, dementia affects more than 57 million people, is expected to rise to 153 million people by 2050, and is the seventh-leading cause of death.
In Australia, it’s the second-leading cause of death behind heart disease, and the leading cause of death among women.
A healthy adult brain contains about 86 billion neurons that communicate through tiny connections called synapses.
The human brain is like a supercomputer made up of nerve cells called neurons, which send and receive electrical and chemical signals, and glial cells, which support, protect and nourish those neurons. A healthy adult brain contains about 86 billion neurons that communicate through tiny connections called synapses.
It’s this intricate and complex interconnectedness that gives the brain its vast computational power and control over everything we do – how our muscles move, our heart beats, our eyes blink, and shapes what we think, feel, experience, and remember.
In healthy ageing, the brain shrinks slowly, almost politely. But in dementia, it withers, buckles under the weight of its own neural and vascular betrayal, and by the time symptoms surface the neurological damage is already done, impairing memory, thinking, and behaviour. Some of the key culprits include:
Alzheimer’s disease is the most prevalent form of dementia, accounting for 60-80% of cases. It involves the accumulation of amyloid plaques between the brain’s nerve cells, and tau tangles, found inside neurons.
Vascular dementia is caused by vascular injury to the brain, often following strokes or other more subtle vascular changes.
Lewy body dementia is characterised by abnormal protein deposits (Lewy bodies) in the brain, leading to cognitive decline and movement issues.
Frontotemporal dementia Involves the progressive degeneration of the frontal and temporal lobes, affecting personality, behaviour, and language. Hollywood actor Bruce was diagnosed with a form of this dementia, aphasia, in 2023.
But the pathologies of each of these dementia are not mutually exclusive.
“The situation is complicated by the fact that people often have multiple pathologies in the brain,” says Amy Brodtmann, a distinguished cognitive neurologist and the driving force behind the Cognitive Health Initiative at Monash University, which focuses on vascular determinants of brain health.
“Most people with Alzheimer’s, for instance, have vascular changes, and most people with Lewy body dementia have Alzheimer’s pathology.
“It’s even further complicated by the fact that some people can have the same level of brain pathology, like plaque build-up in Alzheimer’s, but show few or no outward dementia symptoms.”
She says it remains inconclusive why some people have higher cognitive resilience than others, but research suggests it may include, or be a combination of, genetics, lifestyle, education, and even where you live.
Connecting the dots
Matthew Pase, a professor at Monash University, is a man with one foot in the lab and the other deep in international networks of medical intelligence – the Framingham Heart Study, the Sleep and Dementia Consortium, MarkVCID (a consortium that develops biomarkers for vascular cognitive impairment).
He doesn’t just chase dementia clues; he connects the dots across global borders.
He’s also in charge of Monash University’s Epidemiology of Dementia research lab, and lead of the Ageing and Neurodegeneration Program, which are part of the School of Psychological Sciences.
And he was the lead on the Brain and Cognitive Health Cohort Study (BACH), a sprawling years-long investigation into the minds of ordinary Australians. Its mission? To predict the future – to catch dementia in the act before it steals another memory.
“Dementia is not an inevitable consequence of ageing,” he says. “Up to 50% of cases are theoretically preventable.
“Our research suggests health and lifestyle can influence a person’s brain health up to 40 years into the future, and since there’s no cure for dementia, research into risk and protective factors is critical.”
The The Lancet Standing Commission published its Dementia prevention, intervention, and care report last year.
The comprehensive report, led by British psychiatrist Gill Livingston from University College London (UCL) and including 27 of the world’s leading dementia experts, lists factors, starting in childhood, that could help prevent or delay dementia. Its message is clear. For many, brain health isn’t set in stone, but is sculpted by daily choices – exercise, connection, learning, purpose. And that prevention starts early, spans decades, and requires sweeping, systemic action.
Building on its 2020 dementia edition, The Lancet Commission’s latest report incorporates new evidence and two additional risk factors for dementia, high LDL cholesterol and uncorrected vision loss, bringing the list to 14. The full list includes:
Sharpened by dementia’s upward trajectory, the esteemed The Lancet Standing Commission last year published its Dementia prevention, intervention, and care report.
The comprehensive report, led by British psychiatrist Gill Livingston from University College London (UCL) and including 27 of the world’s leading dementia experts, lists factors, starting in childhood, that could help prevent or delay dementia. Its message is clear. For many, brain health isn’t set in stone, but is sculpted by daily choices – exercise, connection, learning, purpose. And that prevention starts early, spans decades, and requires sweeping, systemic action.
The 2024 update to the standing Lancet Commission on dementia prevention, intervention, and care adds two new risk factors (high LDL cholesterol and vision loss) and indicates that nearly half of all dementia cases worldwide could be prevented or delayed by addressing 14 modifiable risk factors.
The 2024 update to the standing Lancet Commission on dementia prevention, intervention, and care adds two new risk factors (high LDL cholesterol and vision loss) and indicates that nearly half of all dementia cases worldwide could be prevented or delayed by addressing 14 modifiable risk factors.
Building on its 2020 dementia edition, The Lancet Commission’s latest report incorporates new evidence and two additional risk factors for dementia, high LDL cholesterol and uncorrected vision loss, bringing the list to 14. The full list includes:
From grief to groundbreaking research
Preventing the possibility of dementia, or at the very least limiting its grip, occupies a significant amount of geriatrician Velandai Srikanth’s time and academic output, since his PhD thesis in 1998 on the link between strokes and dementia.
It’s also deeply personal. Dementia has already left its mark twice on his family. First, it was his maternal grandmother who suffered some strokes around age 70, and developed dementia a few years later.
“She passed away several years ago,” he says. “I remember how vibrant she looked in her 70s and how different she appeared in her late 80s. More importantly, despite appearances, by then she was unable to recognise her own great-grandchildren.
“My mother-in-law, too, was incredibly fit and active when my wife and I got married in 1996. She developed signs of dementia in her 80s and passed away in her early 90s. She needed more supportive care with time and thankfully enjoyed a reasonably good quality of life, but these experiences have given me a deep personal appreciation for what dementia means beyond the science.”
A professor of medicine at Monash University’s School of Translational Medicine, Professor Srikanth wears many hats. He’s also the director of research at Peninsula Health, and heads the National Centre for Healthy Ageing (NCHA), a partnership between Peninsula Health and Monash University that forms part of a federal initiative aimed at bridging academic expertise and clinical practice.
Together, these roles place him at the forefront of a national push to rethink how we understand, prevent or delay, and manage dementia.
His research centres on the critical relationship between vascular health and neurodegeneration, examining how conditions such as hypertension, diabetes and stroke contribute to brain cell loss and the onset of dementia.
There is no single cause of dementia, he says. It’s “a complex interplay” – a web of biological, vascular and metabolic factors working in concert, or sometimes in chaos.
“It often results from a mix of abnormal proteins like amyloid, tau, Lewy bodies, and TDP-43, damage to blood vessels from strokes or high blood pressure, and conditions like diabetes or obesity.”
In the past, research camps were divided. One side focused on the rogue proteins that disrupt brain function, the other on the vascular insults that starve brain tissue.
“The reality is most people with dementia have multiple pathologies,” he says. “It’s the convergence of these that tends to accelerate cognitive decline.
“Even those without a dementia diagnosis at death often show some level of pathology, though not enough to cross the threshold into clinical symptoms. The more pathologies a person has, the earlier and more severely symptoms tend to appear.
“Some people start with a higher brain reserve, or ‘buffer’, meaning it takes longer for symptoms to show. Others start with less reserve and may develop dementia sooner.”
This, he says, raises the question: Is brain ageing the same as dementia?
“The answer is no. Not everyone develops dementia as they age. In fact, even among those older than 80, between 60% and 80% do not have dementia. This is an important and often overlooked fact.”
He says that, as in paediatrics where growth charts help track physical development, there is now, thanks to a global study published in Nature in 2022, similar charts for the brain.
Using 120,000 brain scans from around the world, researchers created a detailed model of brain growth from before birth through old age. The data shows that the brain grows rapidly in early childhood and then slowly shrinks with age – mostly in the absence of disease.
He gestures to some brain scans that reveal that, in addition to brain shrinkage (atrophy), vascular disease can lead to changes in the brain that build up silently, such as white matter changes or tiny bleeds.
But what really matters, he says, given there’s no cure for dementia, is what influences the brain’s ageing process.
“Risk factors operate across the lifespan, from before birth, through childhood, adulthood, and into old age.
“For instance, good maternal health, avoiding smoking and alcohol during pregnancy, and proper childhood nutrition all help. In childhood, physical fitness and educational attainment are also linked to healthier brains later in life.”
“The reality is most people with dementia have multiple pathologies. It’s the convergence of these that tends to accelerate cognitive decline.” – Velandai Srikanth.
In one study he cites, led by Monash University and Peninsula Health researcher Jamie Tait, from Deakin University (formerly Monash University), and Associate Professor Michele Callisaya, from the National Centre for Healthy Ageing, 1200 children aged five to 17 were followed into adulthood. Those who were the fittest and leanest had the best cognitive score at age 40. The study included physical assessments such as running, sprinting and push-ups.
This, he says, indicates that there are things that can be done early in life that can protect against brain ageing, while others accelerate it.
Protective factors include physical activity, mental stimulation, education, and social engagement. These build what is called “reserve” or “resilience”. Harmful factors, such as smoking or unmanaged vascular disease, contribute to the development of abnormal proteins, silent strokes and, ultimately, dementia.
“Whether or not brain ageing progresses to dementia depends on the net sum of all these factors across a person’s life,” he says.
“No single cause dominates. The more positive factors you have, the more protected you are. The more harmful ones accumulate, the higher your risk.”
Yet Professor Srikanth’s vision extends beyond brain tissue and pathology. He’s a passionate advocate for holistic, person-centred care, a philosophy he champions at every level, from academic journals to policy roundtables.
“Living with dementia is about more than memory loss,” he says. “It’s about mobility, dignity, social connection. We need models of care that look at the whole person. Their physical, mental and emotional needs.”
That vision is now helping shape national policy. Professor Srikanth, along with Professor Brodtmann, played a pivotal role in Australia’s National Dementia Action Plan 2024-2034, a 10-year federal government blueprint to transform how dementia is diagnosed, treated and lived with.
As part of the plan, the Albanese government last year committed $1.3 million to Monash University. The funding supports a major update to the Clinical Practice Guidelines and Principles of Care for People with Dementia – under the leadership of Professor Srikanth and Professor Simon Bell, from the Centre for Medicines Use and Safety at Monash’s Faculty of Pharmacy and Pharmaceutical Sciences – to help health professionals across Australia provide more consistent, evidence-based support.
The revised guidelines, due in 2026, promise to be more than a clinical manual. They aim to become a roadmap for care that is not only scientifically rigorous, but also deeply humane, with significant involvement from people with living experience of dementia.
“We’re not just studying disease,” Professor Srikanth says. “We’re working to ensure that people with dementia can live well, with clarity, compassion, and hope.”
AI is changing the landscape
For decades, diagnosing dementia has been handicapped by limited tools, subtle symptoms, and so, late detection. A master of disguise, it was able to sometimes elude cognitive tests, blood work, interviews, and doctor intuition. But artificial intelligence is quickly changing that.
With its ability to analyse vast amounts of hospital records, brain imaging, genetic data, and cognitive patterns in seconds, AI is now speeding up diagnosis and unearthing probative dementia evidence earlier than ever before.
A hunch that dementia clues might be hiding in the margins of medical records and buried in hospital databases led Dr Taya Collyer to develop a novel method for improving dementia detection in hospitals by combining traditional methods with artificial intelligence.
A senior research fellow and biostatistician at the National Centre for Healthy Ageing, Dr Collyer says improving the methods for counting people with dementia is critical to understanding the size of the problem and to effectively plan services.
“Routine health data that are currently used for this purpose probably underestimate the numbers of people with dementia,” she says.
“Currently, in hospitals, dementia is recorded based on gathering of information in the medical records by medical coders, who find it difficult to look through the vast amount of written information in the records.”
To address this, Dr Collyer earlier this year led a study involving more than 1000 people aged 60 and older in the Frankston-Mornington Peninsula area that combined traditional medical data analysis with natural language processing (NLP) to assess electronic health records.
The study participants included people already diagnosed with dementia and a comparison group without dementia.
The study, supported by grants from the National Health and Medical Research Council, the Medical Future Fund and the Department of Health and Aged Care, was published in the journal Alzheimer’s & Dementia, and demonstrated high accuracy in identifying whether or not a person may have dementia.
“Accessing high-quality curated electronic health records from our Healthy Ageing Data Platform helped assemble the data efficiently to address this problem,” she says. “Special software was used to harness the large amount of free text data in a way that NLP could then be applied.
“We then developed dementia-finding algorithms through a traditional stream for usual structured data, and an NLP stream for text records.”
Professor Srikanth says the future impact of this novel approach is exciting, “not only for the better counting of numbers of people with dementia, but also for the efficient identification of people with high probability of dementia who may need care and support but who may get missed otherwise”.
“Given that clinical recognition of people diagnosed with dementia presenting to hospitals is poor, using this new approach we could be identifying people earlier for appropriate diagnostic and clinical care.
“I’m sure that many people are missing out on good care because we’re not very good at identifying them or their needs.
“This new method offers a novel digital strategy for capturing and combining clues in written text, such as descriptions of confusion or forgetfulness, or alerts for distressed behaviour, to flag them for suitable care and support.
“Responsibly using AI in scientific research and dementia identification is potentially game-changing. The NCHA’s Healthy Ageing Data Platform, an Australian-first initiative, has been able to bring together various sources of data from electronic health records, safety and governance, and the technical capacity to enable such high-value projects.”
A test in time could save nine
What if there was a way of predicting dementia up to nine years before diagnosis? A way to look deep within the labyrinthine folds of the brain and its default mode network (DMN) before symptoms appear?
An international team of researchers did just that last year, providing a more accurate way to predict dementia than memory tests or measurements of brain shrinkage, two commonly-used methods for diagnosing dementia.
Published in Nature Mental Health, the researchers developed the predictive test by analysing functional MRI (fMRI) scans to detect changes in the brain’s default mode network. The DMN connects regions of the brain to perform specific cognitive functions and is the first neural network to be affected by Alzheimer’s disease.
Study co-author Professor Adeel Razi, from Monash University’s School of Psychological Sciences and the Turner Institute for Brain and Mental Health, says previous attempts at curing Alzheimer’s disease have failed because clinical trials often focus on advanced stages of the disease, when the damage to brain cells is irreversible.
“Our new method for predicting who will develop dementia well in advance will be a game-changer, enabling the development of therapies earlier in the disease process,” he says.
“By leveraging large datasets and advanced fMRI techniques, we can now identify individuals at high risk for dementia years before symptoms appear, paving the way for proactive and personalised healthcare strategies.
“This innovative approach bridges a critical gap in dementia diagnosis, offering a non-invasive biomarker that could transform early detection and treatment, ultimately improving patient outcomes.”
The study, led by Professor Charles Marshall from Queen Mary University of London, used fMRI scans from more than 1100 volunteers from the UK Biobank, a large-scale biomedical database and research resource containing genetic and health information from half a million UK participants, to estimate the effective connectivity between 10 regions of the brain that constitute the default mode network.
By measuring the connectivity, the team was then able to assign each participant a “probability of dementia” score, predicting with more than 80% accuracy who would go on to develop the disease.
More remarkably, in those who did later receive a dementia diagnosis, the model could estimate within just two years exactly how long it would take for the condition to manifest clinically.
The researchers also examined whether changes to the DMN might be caused by other known risk factors for dementia.
The study found that specific changes in the DMN were linked to genetic risk for Alzheimer’s, reinforcing the network’s central role in the disease. Even social isolation, the researchers discovered, seemed to erode this crucial network, pointing to an environmental route through which lifestyle could increase dementia risk.
“We hope that the measure of brain function that we have developed will allow us to be much more precise about whether someone is actually going to develop dementia, and how soon, so that we can identify whether they might benefit from future treatments,” Professor Marshall says.
Lead author Dr Samuel Ereira, also from the Queen Mary University of London, says using these analysis techniques with large datasets could also help researchers learn which environmental risk factors pushed these people into a high-risk zone.
The vital role of sleep
Sleep is fundamental to human health. The active, restorative process is a time our bodies enter a finely choreographed biological performance – the brain consolidates memories, the body repairs tissue, and hormones reset to keep our systems in balance.
It’s also a time that the glymphatic system flushes out the brain’s waste products and metabolic toxins – a kind of cerebral sanitation – that build up during the day, including amyloid beta, the protein strongly linked to Alzheimer’s disease.
Sleep can be divided into two states of consciousness – non-rapid eye movement (NREM), and rapid eye movement (REM).
On any given night, we enter NREM followed by a period of REM. The complete cycle for both is anywhere between 90-120 minutes and is played on a loop throughout the night.
Non-REM is further broken down into three stages.
Stage one is the lightest and lasts about 10 minutes, as a person drops off to sleep. It’s when a person can experience muscle jerks and that strange sensation of falling.
Stage two is also characterised by light sleep, though less light than stage one, and this is when a person’s heart rate and breathing slow, and body temperature drops.
Stage three is when a person enters deep sleep, and this is when the body begins to repair itself. It’s the stage when if you try to rouse someone, they’ll appear disoriented and groggy.
It’s this third stage of sleep that is of particular interest to Professor Pase, and a focus of much of his research into dementia, including the BACH cohort study and the Sleep-Dementia Consortium.
His Monash University Epi-D Research Lab is a hub that draws together international investigators and studies “to characterise risk and protective factors for cognitive decline and dementia, and [to] validate biomarkers for dementia prediction and diagnosis”.
The lab, his research page states, “… has a strong interest in understanding the role of sleep, vascular health, lifestyle, and neuroinflammation in dementia pathogenesis, including Alzheimer’s disease and vascular cognitive impairment”.
Many of his research projects draw on the rich data from The Framingham Heart Study, one of the most influential and long-running epidemiological studies in medical history. Launched by the US Public Health Service in Framingham, Massachusetts, in 1948, its original goal was to identify the risk factors for cardiovascular disease (CVD), at a time when little was known about what caused heart attacks and strokes.
The study gave rise to many of the standard risk factors for heart disease we now take for granted – high blood pressure, high cholesterol, smoking, obesity, physical inactivity, diabetes.
But more recently it expanded into neurology and dementia, giving researchers such as Professor Pase a trove of uniquely powerful, multi-generational data to conduct their own studies.
Among findings he’s unearthed is that as little as 1% reduction in deep sleep per year for people over 60 years of age translates into a 27% increased risk of dementia.
“Slow wave sleep, or deep sleep, supports the ageing brain in many ways, and we know that sleep augments the clearance of metabolic waste from the brain, including facilitating the clearance of proteins that aggregate in Alzheimer’s disease,” Professor Pase says.
“However, to date we’ve been unsure of the role of slow wave sleep in the development of dementia, but our findings suggest that slow wave sleep loss may be a modifiable dementia risk factor.”
In another study he conducted late last year, again using the Framingham Heart Study as his starting point, Professor Pase uncovered that people with high blood pressure who also lack sleep may be at increased risk of reduced cognitive performance and greater brain injury.
Published in the Journal of the American Heart Association, researchers assessed whether the combined effect of hypertension and short sleep duration had a negative impact on brain health.
They used data from 682 dementia-free Framingham Heart Study participants who completed overnight sleep recordings, self-reported sleep duration questionnaires, blood pressure and cognitive assessments; 637 underwent brain magnetic resonance imaging (MRI).
In those with high blood pressure, shorter sleep duration was associated with poorer executive functioning and markers of brain injury and accelerated brain ageing on MRI. These associations were not observed in people with normal blood pressure.
Professor Pase says that blood pressure normally dips during sleep, providing respite to the brain from high-pressure flow, which can potentially damage small blood vessels in the brain. However, for some people with poor sleep, blood pressure may dip, increasing the risk of adverse health outcomes.
These results were similar following adjustment for genetic, clinical and demographic variables.
“… to date we’ve been unsure of the role of slow wave sleep in the development of dementia, but our findings suggest that slow wave sleep loss may be a modifiable dementia risk factor.” – Professor Matthew Pase
Insights into the human condition
Professor Joanne Ryan’s dementia work stretches beyond neurons and neural networks, reaching into the everyday decisions we make. For her, dementia isn’t just a neurological mystery. It’s a window into the human condition.
“Our team conducts research to better-understand risk factors associated with dementia, and to identify preventative treatment and lifestyle interventions to reduce their incidence,” she says.
“But it’s also focused on the identification of biomarkers for dementia disorders, to improve the accuracy and timing of diagnosis, and to help assess the effectiveness of interventions.”
Just as Professor Pase is mining the Framingham Heart Study for clues to unlock dementia, Professor Ryan, who heads the Biological Neuropsychiatry and Dementia research unit in Monash University’s School of Public Health and Preventive Medicine, is sitting on a data goldmine, too. Only this time, it’s a sprawling, landmark study of older people, called the ASPREE Project.
Professor Ryan is joint principal investigator of the project, a vast, bi-national study launched in 2010 that followed more than 19,000 healthy older adults across Australia and the United States. Originally designed to investigate whether low-dose aspirin could extend healthy, disability-free years, the project has evolved into one of the most comprehensive studies of ageing ever conducted.
With its unparalleled bank of biospecimens and meticulously tracked clinical data, ASPREE, and its ongoing successor ASPREE-XT, is giving researchers such as Professor Ryan the tools to decode the complex biology of ageing.
And what she’s finding is shifting long-held assumptions.
“In the face of an ageing population, these datasets provide vital information that can inform our understanding of illness and the ageing process, and potentially lead to important changes in clinical care,” she says.
Drawing on the rich, longitudinal data of the ASPREE Project, she’s exploring how lifestyle factors such as diet, exercise and cognitive tasks are linked to longevity and what it means to age healthily.
Already, she’s uncovered that men with high levels of belly fat are at increased risk of dementia.
The study, published in the journal Alzheimer’s & Dementia: Asessment & Disease Monitoring, also found that the risk for dementia is up to 38% lower in those with higher lean body mass and, perhaps surprisingly, more fat body mass.
“Our findings suggest that increased body weight in older age may confer protective effects on brain aging, regardless of body composition,” says Professor Ryan, who is a lead author of the study.
“However, abdominal adiposity may still be a risk factor for cognitive impairment in older individuals, particularly in men.
“These findings suggest that avoiding excess fat accumulation in the abdominal area and maintaining a balance between lean and fat mass may be beneficial to cognitive function in older age.”
Just as exercise and diet can contribute to combatting physical and metabolic saboteurs of brain health, there are, Professor Ryan says, many cognitive-related pastimes that can encourage neural firing and synaptic plasticity, and thus positive structural changes in brain matter.
In another study using the ASPREE dataset, she found that older participants who routinely engage in literacy and mental acuity activities, such as taking education classes, keeping journals, completing quizzes and doing crosswords, were 9-11% less likely to develop dementia than their peers. Creative pursuits such as crafting (knitting, woodworking) conferred a 7% decrease in risk.
The results remained significant even with adjustment for earlier education level, and socioeconomic status.
Curiously, the size of someone’s social network and the frequency of external outings to the cinema or restaurant were not at all associated with dementia risk reduction.
These findings, she says, point to a quiet revolution in how we approach dementia, not just as a disease of the brain, but as a condition shaped by how we live, move, and age.
Professor Ryan isn’t the only one unearthing hidden insights from the ASPREE archives. Suzanne Orchard, director of ASPREE-XT and an associate professor with Monash University’s School of Public Health and Preventive Medicine, previously used the study’s data to uncover an important link between age-related cognitive decline and physical decline.
The study found that walking speed and grip strength could be early indicators of dementia before the onset of other more noticeable symptoms.
“Poor physical function may be a marker of future risk of cognitive decline and dementia, and thus, understanding this association could enhance early detection and prevention strategies,” she says.
Hope for the future
Dementia is more than a clinical diagnosis – it’s a slow unravelling of memory, identity, and connection. For the millions living with it, and those walking beside them, it’s a daily negotiation between loss and love, between what’s fading and what remains.
And yet, in the midst of that uncertainty, there’s movement. Researchers are decoding the earliest biological signs, clinicians are learning to spot it sooner, and technological advances are pushing the boundaries of what’s possible.
But the future lies not only in medicine – it’s in how society chooses to respond. With empathy. With resources. With a willingness to see those affected not as forgotten patients, but as people with stories still unfolding.
This article was published by Lens.
Professor Srikanth is the Director of the National Centre for Healthy Ageing. His program of research spans several aspects of ageing health. These include dementia, cerebrovascular disease, metabolic health and brain ageing, gait and cognitive decline, and frailty and multimorbidity.
