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

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.”

It’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.

Whatever 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 Quinn

Around 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.”

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.

Her 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.

The 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.

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