In the second of a two-part series looking at crucial University of Auckland studies supported by the just-finished For All Our Futures campaign, science reporter Jamie Morton looks at three questions it's allowed researchers to answer.
Professor Ngaire Kerse thinks it's time we started treating our elderly better – if not for the simple fact there's going to be more older people around in the future.
Make that a lot more.
As it stands, there are now about 83,000 Kiwis aged 85 or over; by midcentury, that number will have grown to 383,000.
"The 75-plus age group is going to more than double, and the structure of our ethnic populations is going to change significantly," Kerse says.
"We already spend three to four times more on health and social services for our elderly than other groups - so there's going to be a significant impact.
"All of this means we need to understand, very well, how we can help our older people live more active, independent lives."
How can we age better?
Kerse spent years working as a GP in residential aged care, and is recognised as an international expert in boosting health and reducing falls for older people.
She was recently appointed the university's inaugural Joyce Cook Chair in Ageing Well – a role made possible by a $5m gift to the For All Our Futures campaign by Metlifecare founder Cliff Cook.
"Research about healthy, sustained wellbeing in ageing is really critical right now, because there are small things we can do our elderly that can make a huge difference."
Even checking in on them.
Findings from a world-first longitudinal study into advanced ageing that she co-leads with Dr Marama Muru-Lanning paints a stark picture of loneliness in old age.
Called the Life and Living in Advanced Age, a Cohort Study in New Zealand, or LiLACS NZ, the programme has been tracking nearly 1000 over-80-year olds in the Bay of Plenty.
More than 60 per cent of non-Māori women and more than half of Māori women in the study are living independently and alone.
Men are more often living with a wife.
The study found 40 per cent of Māori, and 28 per cent of non-Māori participants, reported feeling lonely always, often or sometimes.
Rates were particularly high among widowers.
The issue was much more important than we might think: loneliness is linked to poor mental and physical health, lower quality of life, cognitive decline and even dying sooner.
Older people were most at risk when they needed more emotional support, were suffering medical conditions and experiencing pain – or were always alone.
They fared better when living with a spouse, or viewed growing older as a positive experience.
"Encouraging mental wellbeing and good levels of physical activity is important – but we can do a lot more," Kerse says.
Some other obvious opportunities: improving access to parks and public transport; improving housing stock, and ending discrimination.
"Morally and ethically – that needs to change."
Do bad proteins bring on brain disease?
With an ageing population will also come a rise in rates of neurodegenerative diseases such as Parkinson's and Alzheimer's.
The number of people with Parkinson's in New Zealand has been steadily increasing, from an estimated 7300 in 2006 to 10,700 in 2017.
Researchers project that the number of Kiwis with the disease will double in the next 25 years.
That's not only due to the ageing population - which puts more people into the highest risk age groups – but also to the fact that people are now living longer
with the disease.
Getting to the crux of these complex conditions isn't easy.
New therapies to slow down the death of brain cells in Alzheimer's and Huntington's disease, particularly, first demand an understanding of how the disease affects various parts of the entire brain in the first place.
Currently, treatments available for Alzheimer's patients in New Zealand include medications like Aricept, Exelon and Reminyl, which are only modestly successful in some patients for improving memory and attention skills.
However, these medications can only manage the symptoms of dementia by helping the dying brain cells function.
The University of Auckland's Dr Malvindar Singh-Bains sees her mission as assessing disease across various brain regions, with help from samples from the Neurological Foundation of NZ's human brain bank.
The ultimate goal is to drive the discovery of new disease indicators - and potential drug targets for the future.
Her focus has been on a specific region of the brain, called the cerebellum, to reveal the most subtle of those molecular changes in Alzheimer's and Huntington's disease, with the hope of picking up the very earliest drivers of the diseases.
Located under the cerebral hemispheres at the back of the brain, the cerebellum packs in more brain cells than the rest of the brain put together - but comprises only 10 per cent of total brain volume, due to its complex folding.
"The role of the cerebellum in both Huntington's and Alzheimer's disease has been quite controversial, to the point of widely being considered 'unaffected', due to historical studies reporting lesser degrees of damage compared to more severely affected brain regions," Singh-Bains explains.
"Hence, my rationale for studying this region, compared to more severely affected regions of the brain - such as the cerebral cortex - is to discover new disease indications which would be more difficult to spot in regions that have massive cell death."
The discoveries he has been involved in include revealing brain cell death patterns within regions affected by Huntington's disease – something that had been generally neglected in medical research.
"These patterns can help explain why patients suffer from different symptoms in Huntington's disease," Singh-Bains says.
"For example, my studies into two brain regions, the globus pallidus and cerebellum, have shown these areas are affected in Huntington's disease, and have an important role in presenting the different and variable symptoms that patients with this disease experience."
The findings mean we are closer to fully unlocking how Huntington's affects the brain, which has implications for the development of treatments.
In Alzheimer's research, Singh-Bains recently published evidence that changes to our brain's immune cells, along with blood vessels in the cerebellum, are vital components of the disease's progression.
She's now working on some fresh projects to figure out how "bad proteins" that build up in brain cells may be contributing to the symptoms and other clinical features of Huntington's disease.
Can smell help us beat Parkinson's?
Singh-Bains colleague, Professor Maurice Curtis, is meanwhile exploring an intriguing link between our sense of smell and Parkinson's disease.
Six to 10 years before the characteristic features of the disease develops, that sense will already be lost – or at least be reduced.
At the same time as the loss of the sense of smell the olfactory bulb, where smell is first detected and processed in the brain, will have accumulated the disease-causing proteins.
This triggers a type of protein, called alpha synuclein, to spread to other parts
of the brain, causing those well-known symptoms like tremor.
So what's the link?
We know that the olfactory system begins in the roof of the nose, where small odour detecting neurons detect odorants as they're breathed in and out.
When an odorant binds to the olfactory sensory neuron, an impulse is generated that's carried in the nerve through small holes in the skull and into the olfactory bulb which is connected to the brain.
The olfactory sensory neurons are the only brain cells directly exposed to the outside world.
Curtis and colleagues are working on the idea that something in the environment or in the nasal cavity plays a part.
Whatever it is, it's thought to cause alpha synuclein to build up and spreads to the rest of the brain, eventually causing Parkinson's disease.
"The olfactory system is a great indicator that something isn't right in the brain, but loss of the sense of smell is quite non-specific and not everyone who loses their sense of smell will go on to develop Parkinson's disease," Curtis says.
About 60 per cent of those who do lose their sense of smell will develop Parkinson's disease or Alzheimer's disease.
With colleagues at Germany's famous Max Planck Institute, his team have been comparing bulbs from normal and Parkinson's disease brains from the Neurological Foundation Human Brain Bank; of which Curtis is the deputy director.
Having made 3D reconstructions, they've so far been able to show that the most exposed area of the olfactory system most exposed to the upper part of the nose experiences the greatest degeneration in Parkinson's disease.
"The disease erodes the functional units of the olfactory system and also leaves large deposits of clumped protein that the brain can't get rid of adequately."
"If we could treat these diseases when they first start, then people may not develop the movement disorder caused by neurodegeneration," Curtis says.
"The ultimate aim of our research is to stop the spread of alpha synuclein from the olfactory bulb to the rest of the brain."
His team is now trialling novel compounds that target the spread of the proteins.
'The ultimate gift'
None of these important insights would be possible without sufferers donating their brains after they die.
"It is a huge privilege to work with these precious samples, and I constantly feel humbled by the incredible contribution by the families for bequeathing their loved one's brain to our brain bank," Curtis says.
"It is their loved one who is providing scientists like myself the ultimate gift to unlock the secrets of these devastating diseases."
One of those donors happens to be Singh-Bain's former principal Waitakere College, Peter Garelja, who is now chair of Parkinson's New Zealand.
Garelja was diagnosed with Parkinson's in 2008 and hopes his offer will help provide vital clues about neurological diseases.
But he also wants to be a resource to researchers while still living, and keeps in contact with them.
"There are lots of people like me with Parkinson's still in the early stages – and so if they can tap into us, I think we'd be an amazing resource. We can be part of the solution," he says.
"I think that's important, because there's often a bit of a disconnect between researchers and people with the disease."
Garelja, a self-described workaholic, has made a point of keeping active with charity work, and looking after his health.
"I choose to live with, but still challenge it. The latest research gives you hope – and that's what keeps you going in the end."