And although scientists have found several genes thought to increase the risk of Alzheimer’s, less than 5 per cent of cases are thought to be linked to a specific genetic change.
In search of early warning signs, scientists have increasingly been turning to blood-based biomarkers – or measurable indicators of disease progression that can be observed with simple blood tests.
With a range of clinical drug trials underway to test potential treatments, the need to catch the disease early and identify those most likely to benefit has become more pressing.
“We don’t yet know exactly when AD pathology begins to occur, although it’s thought to begin manifesting over a decade before symptoms become apparent,” Otago University researcher Dr Ashleigh Barrett-Young said.
“It’s thought that identifying people who are in the earliest stages of AD may help with mitigating symptoms.
“However, because the early symptoms of AD are so insidious, with memory loss beginning gradually and over an extended period of time, we need better ways to identify disease risk before symptoms are obvious.”
Throughout a Neurological Foundation-funded project, Barrett-Young and colleagues have been focusing on one particular biomarker, called pTau181, collected from participants of the world-famous Dunedin Study when they were aged 45.
Now, in a new study just awarded a $1.2 million Health Research Council grant, she and her team – including the Dunedin Study’s renowned director, Professor Richie Poulton, and Otago neuroscientist Professor Cliff Abraham – will reassess the participants at age 52, while measuring more biomarkers across the pool.
This would be done using an ultra-sensitive immuno-assaying device to measure tiny amounts of the target proteins in the blood, and only recently brought here by study collaborator Dr Erin Cawston, of the University of Auckland.
The new study’s two key questions, Barrett-Young said, were whether blood biomarkers like pTau181 were indeed linked with cognitive deficits in middle-aged people and whether there were factors that could raise or lower the risk.
“There’s been a lot of research in this area, looking at a variety of different markers, but so far it’s mostly been conducted in samples of people who already have a diagnosis of AD and comparing them to healthy controls,” she said.
“There are a few studies starting to look at biomarkers in pre-clinical samples, but we’ll be different in that our sample is relatively young, and it’s population-based, meaning we have participants from all walks of life.
“We also have a huge trove of data from across the study members’ lifetimes, meaning that we can look at risk and protective factors, from birth onwards.”
While finding biomarkers that could reveal the start of dementia would be game-changing, Barrett-Young acknowledged that not everyone would want to know if they were at risk – particularly as there wasn’t yet a cure.
“Ultimately, though, I would like to see these biomarkers used for screening the population, so that people who are at high risk of developing AD can start on pharmaceutical treatments that will extend their health-span and delay the onset of AD significantly – or maybe one day even prevent it,” she said.
“We’re a long way off from that reality at the moment, but I hope we’ll get there in my lifetime.”