A dementia diagnosis has long been a death sentence. But are things about to change?

At 9.30am on June 16, 2022, Megan* braced herself and clicked on the Zoom link. She was about to find out whether she had the gene mutation for early onset Alzheimer’s disease. She knew the condition was in her family; she’d watched her own mother – a woman who loved to cook and dance, who changed her curtains to match the seasons – die at 65, after almost 15 awful years. “She was a husk,” says Megan. “She couldn’t speak, she weighed 40 kilograms.” Two uncles and an aunt had also died of Alzheimer’s, and her maternal grandmother. There was a 50/50 chance she had the mutation – and if she did, there was a 100 per cent chance she’d get the disease.Twin sisters Megan (left) and Jillian tested positive for a gene mutation that causes Alzheimer’s. Peter TarasiukMegan was 55 years old at the time, with thick hair, blue eyes and unlined skin. Trained as a nurse, she was married, with three sons and an air of practical kindness: the sort of person who stops at the zebra crossing even if the pedestrian isn’t quite there yet; who says hello to everyone she sees on the street in her small home town in rural Victoria. She had no symptoms of cognitive decline, no signs of trouble at all. But a determinative mutation is like a time bomb. It will go off – the only question is when.The genetic counsellor joined the Zoom call. At 9.35, she broke the news. Megan has the same mutation as her mother – a pathogenic variation to her Presenilin 1 gene (PSEN1). She will get Alzheimer’s disease.Alzheimer’s is the most common form of dementia, accounting for up to 70 per cent of cases worldwide. The rest is split between frontotemporal lobe dementia, Lewy body dementia, vascular and mixed dementias, Huntington’s and Parkinson’s disease dementia, and various dementias caused by brain injury. There are even, rarely and tragically, more than 100 genetic conditions that cause dementia in children.Like every other form of dementia, Alzheimer’s is caused by the progressive death – often over years – of tens of billions of brain cells (at autopsy, the brain of someone with dementia may have a volume of up to 40 per cent less than that of a healthy person). It was first described in 1901, when Alois Alzheimer, a notably dedicated and meticulous German physician, took a 51-year-old woman called Auguste Deter, a seamstress, wife and mother, into his care. Alzheimer gave Deter some simple tests, including writing her own name. “Auguse”, she wrote, her pen trailing away on the “e”. “I have lost myself, so to speak,” she told him.Over the following years, Alzheimer could do nothing to help as Deter’s condition deteriorated. But he continued caring for her for free, and when she died in 1906 he conducted her autopsy, preparing the first microscope slides ever to reveal the two “peculiar substance[s]” now known to be the twin hallmarks of Alzheimer’s: amyloid-beta plaques and tau tangles.After Megan heard the news that winter morning, she got off Zoom, left her house, and started walking. After a few minutes, a car pulled up beside her. It was her sister, Jillian, who lives in the same town, on her way home from work. Jillian was also 55 years old, with thick hair, blue eyes and unlined skin. Also a trained nurse, also a mother to three children, she is six minutes younger than Megan, and her identical twin.Jillian leaned over, and Megan bent down to the window. “I took one look at her face,” says Jillian now, “and I knew. I went home and said to my husband, ‘I’ve got it. I’ve got it too.’ ”Why does dementia have such a grip on the human imagination? In surveys around the world, people – especially as they reach mid-life – routinely name it as their greatest health fear: greater than heart disease, greater even than cancer. Perhaps it’s because it feels so close: as simple as blanking on a word, misplacing the remote, getting lost in a sentence – and also so inconceivably far away. In what unimaginable world could we end up oblivious to the things we love, not knowing our own names, no longer recognising the faces of our children? Dementia, above all, is a disease of loss: how could we bear to know such losses are coming?This is exactly what Megan and Jillian are facing. Jillian’s own genetic counselling appointment was at noon on the same day as her sister’s. At 12.01, she confirmed she, too, had the PSEN1 mutation. Alzheimer’s was coming for her, too.The next few months were horrendous for both women. “I started walking in the dark,” says Megan. “Walking down dark laneways, hoping I would come across someone in a bad mood.” “And I just cried,” says Jillian. “Shane [her husband] and I just cried and cried for weeks.”Things are much better now – of which more later – but, as Jillian puts it, they’re always wondering if this might be the day Alzheimer’s symptoms begin. “You forget to do something, you do something stupid, and you go, ‘Is this it?’ ” she says. “I’ll say to Shane, ‘Is that it starting already?’ ”No wonder she’s worried. Last year, for the first time ever, dementia became the biggest cause of death in Australia: a 39 per cent rise in the past decade alone. Ninety thousand new dementia cases are now being diagnosed each year, and one in 12 Australians are either living with it, or looking after someone who is. As other fatal diseases – cancer, heart disease – have become increasingly treatable, dementia has not. Despite millions of research hours and billions of research dollars, there is still no cure. Just as it was 120 years go, dementia today is a death sentence.But now, finally, things are changing. In the past 12 months, two breakthrough new drugs have been approved, a new diagnostic blood test has become available, and new research about prevention and rehabilitation has been published. And so, for the first time in history, we can legitimately ask: can the future of dementia be different from the past?We’ve known for more than a generation that most dementia is caused by the mis-formation of proteins in the brain. These proteins – different in different forms of dementia – are all present in healthy brains, but in dementia they go rogue, destroying neuronal function. This process can begin years – even decades – before symptoms are evident. But eventually, as it progresses, the most fundamental processes of life – heartbeat, breathing, swallowing – are compromised. Most people with dementia die of aspiration pneumonia, when food is accidentally sucked into the lungs.What we haven’t known until recently, however, is that almost half of all cases are preventable – or at least delayable. Contrary to popular myth, less than one per cent of all dementia is inevitable, caused by determinative – 100 per cent guaranteed – gene variants like Megan’s and Jillian’s. Even “risk” genes, like the APOE4 gene variant Chris Hemsworth carries, only increase your susceptibility; they don’t cause disease outright. So for many of us, dementia is, to a greater or lesser extent, avoidable. And in July, the World Health Organisation updated its official dementia guidelines to reflect this fact, stating that “up to 45 per cent of the risks can be attributed to modifiable risk factors such as tobacco, alcohol use, social isolation, physical inactivity, air pollution and noncommunicable diseases, including high blood pressure and diabetes.”Many healthy people do get dementia; many risks are beyond our control. But if possible, why not try to modify the ones we can?Kaarin Anstey is the director of the UNSW Ageing Futures Institute. She studies non-pharmacological interventions for dementia. Drilling down on the WHO risk factors, she explains that type 2 diabetes “increases the risk of dementia by about 72 per cent for men. In women, it’s 77 per cent. Traumatic brain injury doubles the risk for men, and increases it by about 50 per cent for women. Untreated depression is an 82 per cent increased risk for men, and a 42 per cent increased risk for women.” Uncontrolled high blood pressure in middle age raises dementia risk by 20 to 30 per cent.Sharon Naismith is a clinical neuropsychologist at the University of Sydney who researches ageing, cognitive decline and dementia. She points out that the time to take action against many of these risks is exactly the time most people start worrying about dementia: in midlife. “So if you’re 50, you can start doing better things for your body and really lower dementia risk. All the research shows that.”What better things? The usual suspects: stop smoking, don’t drink to excess, get help for conditions like depression and high blood pressure. Maintain a healthy weight, eat sensibly, do exercise. Exercise, especially, is one of only “a few key neurotrophins we know”. Neurotrophins are factors that increase neurogenesis – the production of new brain cells. Neurogenesis itself will never solve dementia – even at high levels, the brain produces far fewer new cells than dementia destroys – but such cells are hyper-adaptable and efficient. Added to which, exercise also helps protect the brain from the blood-flow problems that cause vascular dementia.Another important protection is what’s known as cognitive reserve. The more active neurons and synapses in your brain, the more options you have to process information, and the more resilient the brain is to damage. Education in early life is particularly valuable for creating cognitive reserve, but so is social interaction, new skills acquisition and mental stimulation at any age.What about oestrogen? Caroline Gurvich is deputy director of the HER Centre at Monash University in Melbourne, a research centre dedicated to women’s mental health. Women are disproportionately affected by dementia: they account for about two-thirds of all diagnoses. And oestrogen is known to protect the brain in many ways. So could the loss of oestrogen at menopause be a risk factor for dementia? And if so, could menopause hormone therapy (MHT, which typically includes oestrogen and progesterone) help?“We do know that a lot of menopause symptoms are risk factors for dementia,” says Gurvich: “poor sleep, depression, subjective cognitive decline. What we don’t know [despite several recent studies] is what MHT does in the long term for dementia prevention. There’s just not enough evidence either way.”What we also know, however, is that brain fog – a common experience of women around menopause – is not the start of dementia. Brain fog occurs in your 40s and 50s, explains Gurvich; unless you’re part of the guaranteed gene-mutation 1 per cent, that’s too early for dementia symptoms. Another point to bear in mind is that “often, people with dementia are not as aware of their own decline as their loved ones. Whereas with brain fog, women are usually really concerned: very aware of every tiny little symptom.”“Menopause is often seen as a window of vulnerability for women,” she concludes. “But it’s a window of opportunity, too. Both for more research, which we certainly need, but also for women to go, ‘OK, there are some simple things I can do – exercise, diet, sleep – that do have an evidence base for dementia, and can modify my trajectory.’”Does bad sleep affect our dementia risk? In 2024, British medical journal The Lancet published its influential Commission report on dementia prevention, intervention and care, and did not include sleep – due, explained the authors, to lack of evidence. Sleep researchers, however, point to a detoxifying process in the brain, occurring mostly during sleep, that seems to go to the root cause of dementia.“Basically, it’s like a waste-removal system for the brain,” Sharon Naismith explains. “The glial cells, which are the major support cells of the brain, shrink and expand, and that movement flushes cerebrospinal fluid through all the spaces in the brain, clearing toxins – including amyloid and tau [the malformed proteins of Alzheimer’s], and also alpha-synuclein [involved in Lewy body dementia and Parkinson’s]. And although we don’t have definitive human evidence yet – as you can imagine, it’s quite hard to test – certainly the animal data supports that it’s removing those toxic proteins.”There are other links between sleep and dementia. Untreated obstructive sleep apnoea, for instance, is believed to raise dementia risk by up to 40 per cent. “Sleep is a really significant process,” says Naismith. “It’s not just some small thing.”In April last year, perhaps the most surprising news about dementia prevention was published. A study of 280,000 older adults, published in Nature, found that the shingles vaccine reduces the chance of a new dementia diagnosis by about 20 per cent.And not just the shingles vaccine. “A number of vaccines appear to reduce risk,” says Michael Woodward, geriatrician and director of Aged Care Research and the Memory Clinic with Ramsay Health. “Particularly multiple vaccines. A combination of flu and pneumococcal vaccine, for instance.”Associate Professor Michael Woodward says a number of vaccines appear to reduce dementia risk.Jason SouthIt’s still not clear why vaccines lower dementia risk, but there are several theories. Obviously, they lower viral infection levels; perhaps they also reduce inflammation and swelling in the brain. They might also train the immune system to be more accurate and less reactive; they might protect the brain’s vascular function.Whatever the cause, Woodward is excited. “I think the one thing we can say that will absolutely increase vaccination rates in older people – which, at the moment, are abysmally low – is to be able to tell them that dementia, the most feared event in their life, and their main cause of death, is either preventable, or much less likely to happen. We’re not quite there. But that is exciting.”John Quinn was 51 when he first encountered “a few problems with my communication, driving, and processing things”. He seemed an unlikely candidate for dementia: young, healthy, fit, and mentally stimulated as a primary school principal. But his partner, Glenys Petrie, had two parents with dementia, and she knew John’s mother had died of Alzheimer’s in her 70s. For years, she watched as GPs, psychologists and psychiatrists suggested stress or depression as the root of John’s challenges.Glenys Petrie and John Quinn.Paul HarrisWhatever form dementia takes, early diagnosis is increasingly crucial: the success of any potential treatments depend on it. It’s also rare. GP training for dementia diagnosis is patchy, specialist assessment centres are few and far between, and until this year there have been no simple, accessible, accurate tests. In July, however, the PTau217 blood test was approved in Australia, which can accurately detect signs of Alzheimer’s up to 20 years before symptoms appear, with results available in less than 30 minutes. It’s expected to begin to become available for specialist referrals sometime this month.This test could be transformative. In John Quinn’s case, it took eight years for him to be diagnosed – which isn’t so unusual, says Loren Mowszowski, a clinical neuropsychologist with the memory and cognition clinic at Royal Prince Alfred Hospital in Sydney. Not all delays are due to clinical complexities, she points out: “There’s still a lot of stigma attached to dementia. There can be grief, there can be uncertainty, anger, sadness, confusion. All of these are very, very common reactions.” And so people put it off. “Delay is a global phenomenon. And it’s in the order of years.”By 2008, when Quinn was 57, “he was actually at a stage where he couldn’t work,” recalls Petrie. “He couldn’t make decisions; couldn’t organise himself. In the end, he was forced to leave work – and he still didn’t have a diagnosis.”‘Hopefully, one day there will be a cure. But I can’t afford to wait that long. I need to live well now.’John QuinnAround this time, he and Petrie went on a driving holiday in Victoria. “We were in the Dandenongs, and John started freaking out that we were going to run out of fuel,” recalls Petrie. She pauses. “I still get goosebumps just remembering it. To distract him, I got him to look at the map. We were approaching a T-intersection, and I asked him whether we should turn left or right. He suddenly became really, really concerned; a level of confusion I’d never seen. I said, ‘John, what’s the problem?’ and he said, ‘We’re going to fall off a cliff.’ He literally thought when the road ended on the map, we would just drop into space – his whole sense and perception of what a road map meant was confused.”When they got home, Quinn agreed to let Petrie make another doctor’s appointment, and asked her to attend with him. In 2010, he was finally referred to a neurologist and successfully diagnosed with (suspected genetically inherited young-onset) Alzheimer’s at 59. Despite initial relief, “I soon felt despair,” Quinn recalls. “I had a sense of being alone; I felt ashamed because I could no longer work and support my family. I descended into a state of mind which was very depressive.”This dark period lasted four years. What changed Quinn’s trajectory was developing a personal system of non-pharmacological interventions – strongly related to modifiable risk factors – that, according to experts, may well have dramatically slowed his decline.Quinn calls his system NAMES: Nutrition (and hydration), Art therapy, Mental activity (meditation, music and advocacy), Exercise (enjoyment), Social support (sleep, and setting goals). (The brackets are his.) He also takes a drug called galantamine, which can help cognitive symptoms in some people. Sixteen years after diagnosis, he still exercises every day, has coffee with friends, goes for walks on his own, and performs frequent advocacy work for those living with dementia. “Hopefully, one day there will be a cure,” he says cheerfully. “But I can’t afford to wait that long. I need to live well now.”The idea of living well with dementia is, in many circles, a depressingly recent concept. Yun-Hee Jeon is a professor of healthy ageing at the University of Sydney. She’s fought a long battle for the right of people with dementia to the kind of rehabilitation care common in conditions such as Parkinson’s or stroke. “Even if a person with dementia only lives two years, that’s a long time,” she points out. “Some people with cancer only live six months, but we do not abandon them and make them sit and wait for death! We spend a lot of money to make sure they live as well, and as independently as possible.”Jeon has led several world-first trials in dementia care, including an innovative rehabilitation model known as I-HARP (Interdisciplinary Home-Based Reablement Program), based on finding out what each patient really cares about and supporting them to do it.Rehabilitation is now recognised as a significant breakthrough: the 2025 World Alzheimer Report (which Jeon co-led) was devoted entirely to it. “It’s not sexy research, but I’ve seen first-hand how it helps. In terms of slowing cognitive decline, the scores that any new drugs can demonstrate are not very different from what you see by delivering one of these programs.” In a recent small study of people with early-stage dementia, only one participant in the rehab group went into residential care during 12 months of the study period, compared to six in the control group.It’s a strange concept – helping someone with a terminal condition get better. “It’s not about ‘getting better’,” Jeon corrects. Maybe “feeling better” is a more useful term – the possibility that through targeted assistance people can regain function they’ve lost, build abilities, find joy. “We don’t claim we can improve cognition,” says Jeon. “But we can improve resilience and function.”This kind of work also acknowledges the many unknowns that still surround dementia. Nobody can predict the course of its progression, or foretell its speed, or explain the precise calibration of what is lost – and also, what remains.Anita Plateris-Fraser’s beloved mother Walentyna Plateris was diagnosed with dementia – a mix of vascular and Alzheimer’s – in 2015, at 87 years old. Plateris-Fraser was her carer for much of the following eight years, until Walentyna died in 2023, aged 95. “I really didn’t know the enormity of it,” she reflects now. “It was the long, long, long, long haul.”Anita Plateris-Fraser’s mother, Walentyna. As time passed and the condition progressed, her mother – who was Polish, and spoke five languages – began to revert to her native tongue. Like Auguste Deter, she lost the ability to write her own name, her script changing from beautiful, flowing cursive to “just a tiny dot”. She stopped drawing the fairytale house in the pine woods, often including a little fox, that she remembered from her European childhood; she began having nightmares about soldiers at the end of her bed. “I feel lost,” she told her daughter – again, like Deter. “I am lost.”Plateris-Fraser could see that her mother was slowly shutting down. “It was the loss of this beautiful mind,” she says. “But it was also still Mama, living and breathing. We’re all complex human beings.”A proof of such complexity is a small area of recent dementia research which investigates “terminal lucidity”: moments of clarity and awareness in the end stages of dementia that don’t seem possible given the devastation of the disease. A fortnight before Walentyna died, Plateris-Fraser caught what might be such a moment on her phone video.“It was the loss of this beautiful mind,” says Anita Plateris-Fraser of her mother.Wolter PeetersHer mother had almost stopped speaking by this point. Mostly sleeping, barely eating, she seemed to have retreated far inside herself. She would look at her daughter with “a kind of helplessness, a vacancy; she wasn’t sure where she was”. Early on this particular evening, Plateris-Fraser had explained to her mother that she would put her to bed, then get herself something to eat. On video at 10.25pm, she’s settling the blankets over Walentyna’s unmoving form. You can hear her voice, filled with love, chatting quietly. “I think you should go sleep now, darling. You’re a bit tired. Close your eyes now, darling. Close your eyes and have a bit of rest. I’ll put [the heat pack] near your feet. There you go. Oh, that’s nice. Is that nice at your feet?”Suddenly, her mother’s voice comes from the nest of blankets, strong and determined. “Go!” she says firmly. “Go! Did you have anything to eat?!” Somehow, Walentyna had remembered her daughter’s words from hours before, understood their context, and was projecting both a lucid command and a relevant question: a whole series of complex thought processes presumed to be lost in end-stage dementia.What does such a moment mean? Do we explain it in biological terms: some long-dormant brain pathway suddenly firing? In consciousness terms: some point of awareness that endures beyond our general theory of mind-body connection? Or perhaps in emotional terms, as Plateris-Fraser certainly does. “That is a mother’s love,” she says.In the end, unsurprisingly, what everyone involved with dementia really wants is a cure. And last year, after a century of effort and failure, two revolutionary new drugs – donanemab and lecanemab – were approved by the Therapeutic Goods Association in Australia, the first of their kind in history.These drugs are not cures. Indeed, even their greatest proponents admit they’re far from perfect. They are designed only to destroy the amyloid-beta of Alzheimer’s, so they’re useless to other dementia sufferers, and only about 10-15 per cent of Alzheimer’s patients are eligible for them. They’re extremely expensive (close to $100,000 a year out-of-pocket including scans and infusion costs) and they’re high-risk (a one-in-50 chance of brain swelling or bleeding; a one-in-200 chance of death). All this, and they do not cure, stop, or reverse the disease.“They’re certainly not wonder drugs,” agrees Chris Rowe, Director of Australian Dementia Network (ADNET) at the University of Melbourne. “The benefit is to slow down the rate of progression. So overall, they reduce the rate at which you decline by about a third.”So the best drug available in the entire field of dementia is one in which a small proportion of people, with one type of dementia, might get worse more slowly?“Exactly,” says Michael Woodward from Ramsay Health. “You’re buying time.” But for patients in their late 70s with mild cognitive impairment, “to buy an extra year or two of reasonable cognition is, I think, worthwhile. People might see a granddaughter graduate, a wedding, a grandchild.”“It’s a long way from perfect,” agrees Rowe. “But it’s a very important first step.” What he and many scientists believe is that, ultimately, a dementia cure will involve multiple therapies rather than a single silver bullet. “Take cancer,” says Janet van Eersel, group leader of the drug discovery research team within the Dementia Research Centre at Macquarie University. “When my father was diagnosed [with cancer], he immediately had three paths of treatment – surgery, chemo, immunotherapy. That’s what we need for dementia: better treatment options, and different combinations of options.”One possible joint target on the path towards a cure is amyloid-beta plus tau. Many scientists now believe tau may actually be the driver of cognitive decline in Alzheimer’s: as Michael Woodward puts it, “it’s the cataustrophe.” Combination trials are now occurring around the world. And two participants in one such trial – the DIAN-TU Tau NextGen trial – are Megan and Jillian.Megan and Jillian have been on a drug trial for four years. They show no symptoms of Alzheimer’s disease.Peter TarasiukThe years since their test results have been, by and large, positive ones for the sisters. They’ve retired (Megan); cut down on work (Jillian); travelled. They’ve talked to their adult kids about whether they might get tested; they’ve become part of the Dominantly Inherited Alzheimer’s Network, along with their younger sister, who also carries the gene mutation. They do daily crosswords and jigsaw puzzles and Sudoku to combat the moments when they forget if they’ve put cheese in the pasta. And they are grateful every fortnight for the trial infusions – of lecanemab, plus monthly doses of etalanetug (an experimental tau-targeting drug) or placebo – that make them feel like they’re doing something useful; something hopeful for the future.But none of this means they’re reconciled to what lies ahead. They both believe passionately that they should be able to control their own futures – up to and beyond the point at which they develop symptomatic Alzheimer’s. “We want to make the decision ourselves about whether we want to go on,” says Jillian. “When I can’t cook, or feed myself, I don’t want to be here,” adds Megan. “Not when I’m no longer me.”Both sisters have lobbied the Victorian state government to change the laws governing Voluntary Assisted Dying to encompass dementia. They recognise that this would involve a major shift in the way the law is applied. Currently, cognitive impairment precludes you from access: what Jillian and Megan want is access at exactly this point. “Our mother didn’t have any choices, and she would have hated to die how she did,” says Jillian. “But we know what path we’re on, and we can make that decision ourselves.”“We know it’s not easy to change the law,” concludes Megan. “But when you talk to dementia sufferers and their families, everyone wants it. Everyone wants control over their lives – and that’s their right. Why can’t they have their wishes written down, and when the time comes, have those wishes activated?”Here’s another wish: that people like Megan and Jillian never have to get to such a moment at all. “This could be a wonder drug we’re on,” jokes Jillian. “Who knows?” If that were true, the sisters (and other trial participants) might avoid dementia altogether. And if so, they would be the first people in human history to do so.Nobody can mention such a blue-sky, out-of-the-box, miracle-cure idea out loud, of course. “It will take years to see if [the trial] makes any difference,” says trial research co-ordinator Dr Katie Tran. “But Megan and Jillian are both doing very well. Their mother was in her early 50s when she began showing symptoms – they’re 60, on the trial four years, and still no cognitive impairment. It’s been such a joy to witness that. It will take time to empirically prove anything – but it’s wonderful to see.”* Megan and Jillian have chosen not to use their surnames due to the sensitive nature of familial dementia.Read more from Amanda Hooton in Good Weekend magazine: Banning nudification apps and tackling Big Tech: helping female MPs take back control of their feeds‘It was quite traumatic’: Hugo Weaving on overcoming a childhood diagnosis – and the secrets to a happy familyLiane Moriarty’s new book is nearly here – but first, she wants women to read these three sentencesYou’re in your 40s and suddenly people you know are dying. What’s going on?Get the best of Good Weekend delivered to your inbox every Saturday morning. Sign up for our newsletter.