Seeing Parkinson’s in a new light: Why we are studying tears

Parkinson’s disease is often described as a condition that creeps up quietly. In my work as a neuroscientist, I have seen how this slow and subtle beginning can mask years of underlying biological change. By the time the first tremor is noticed, or someone realises they are moving more stiffly than before, many of the brain cells that control movement have already been lost.

More than 12,000 people in Aotearoa live with Parkinson’s, and thousands more are affected indirectly through their whānau. Yet despite the scale of its impact, diagnosis still depends almost entirely on symptoms that appear only after significant damage has occurred. My team and I at Waipapa Taumata Rau, the University of Auckland, are working to change that by studying an unlikely source of information: human tears.

Understanding Parkinson’s symptoms

Although tremor is the symptom most commonly associated with Parkinson’s, it is only one part of a broader picture. People may experience slowed movement, stiffness, changes in handwriting, reduced facial expression, imbalance or quieter speech. These are often subtle at first and can appear so gradually that many people attribute them to ageing or tiredness.

There are also symptoms that have nothing to do with movement. Loss of smell, constipation, sleep disturbances, anxiety and depression can appear years before a tremor ever does. These non-motor symptoms remind us that Parkinson’s affects many parts of the nervous system, not just the brain regions responsible for movement.

The challenge is that none of these symptoms, on their own, provide definitive proof of Parkinson’s. They overlap with other conditions, and their gradual onset makes early recognition difficult, even for specialists.

How Parkinson’s is currently diagnosed

At present, Parkinson’s disease is diagnosed clinically. That means doctors assess symptoms, observe movement and rule out other causes. There is no blood test or brain scan that can confirm the condition reliably in its earliest stages. By the time a diagnosis is made, it is estimated that 60 to 70 percent of dopamine-producing neurons in a key part of the brain, the substantia nigra, have already been lost.

This diagnostic delay limits what we can do. While current medications can greatly improve quality of life, they treat symptoms rather than the underlying disease process. Treatments are much harder to develop and evaluate when we cannot identify the condition until the damage is well underway.

Why tears?

Tears, or roimata, hold emotional and cultural significance, but they are also a scientifically rich biological fluid. They are easy to collect in homes, marae or churches, and they carry proteins that reflect changes happening throughout the nervous system. One of these proteins, alpha-synuclein, plays a central role in Parkinson’s biology.

In a healthy brain, alpha-synuclein helps neurons communicate. In Parkinson’s disease, however, the protein can misfold and form clumps that spread from cell to cell. These clumps impair normal function and contribute to the progression of symptoms.

Importantly, these protein clumps take on different structural shapes, known as strains. Different strains may spread faster, cause earlier symptoms or influence how someone responds to medication. Understanding them could be key to explaining why no two people experience Parkinson’s in the same way.

Grounded in partnership

Our research also builds on a long-standing partnership with the South Auckland Pasifika Parkinson’s Support Group, spearheaded by Dr Christina Buchanan. Christina has worked closely with Samoan and Tongan families who carry a rare PINK1 gene mutation (c.1040T>C) that greatly increases the risk of early-onset Parkinson’s. Her dedication has created a unique and deeply engaged cohort, one that allows us to study the earliest molecular changes associated with the disease. By comparing tears from these individuals with those from people with idiopathic Parkinson’s disease, we can begin to map how specific alpha-synuclein strains relate to age of onset, symptom patterns and disease progression.

What we are trying to achieve

Advances in molecular amplification, such as real-time quaking-induced conversion (RT-QuIC), allow us to detect even minute traces of misfolded alpha-synuclein. My team has already shown that RT-QuIC can detect these protein clumps in tear fluid. This opens the door to the possibility of a simple, non-invasive diagnostic test that could identify Parkinson’s much earlier than is currently possible.

What earlier diagnosis could mean

Earlier diagnosis would not only change when we recognise Parkinson’s but how we respond to it.

• Better access to tailored treatments: Identifying Parkinson’s before major neuronal loss occurs could allow future therapies to target the disease at a stage when there is still much to protect.

• Improved clinical trials: Researchers could test new treatments on people who have early biological changes, not just those with established symptoms, improving the chances of finding disease-modifying interventions.

  
  

A shift toward prevention

If we can understand which protein strains drive different forms of Parkinson’s, we can also intervene long before symptoms appear. Early biological insights could open the door to personalised prevention strategies that draw on what we already know about lifestyle factors that improve outcomes for people with Parkinson’s.

Sleep, nutrition and regular physical activity each play an important role in supporting brain health. Better sleep can help stabilise mood, improve memory and support the brain’s natural repair processes. Eating a balanced diet rich in whole foods may reduce inflammation and support the gut–brain axis, which is increasingly recognised as relevant to Parkinson’s.

Growing evidence also shows that regular, intensive exercise may do more than improve mobility. A recent study of a high-intensity exercise programme for people with early Parkinson’s found increases in dopamine-related brain markers, suggesting that sustained physical activity could help counteract some of the neurological decline typically seen in the disease.

If we can identify Parkinson’s at the earliest molecular stages, individuals could begin these protective habits sooner and with clearer purpose. Over time, this shift toward prevention has the potential to change not only how we diagnose the condition but how we live with it, and perhaps even how we can stop the disease from ever manifesting.

Looking ahead

Parkinson’s is a complex condition, and no single test or discovery will solve every challenge it presents. But studying tears offers a promising and surprisingly accessible path toward earlier detection. The earliest biological signs of Parkinson’s may be present long before daily life is affected. Being able to detect these changes in a non-invasive way, and in familiar community settings, could shift our understanding of the disease from reactive to proactive.

For me and my team, the hope is simple. If we can diagnose Parkinson’s earlier, we can give people more time, more options and a better chance of holding off the symptoms for as long as possible. That is what drives this research, and why we continue to follow the science wherever it leads, even into something as unexpected as tears.

Dr Victor Dieriks