Parkinson’s disease is, at its core, a dopamine problem – and dopamine, that elegant chemical messenger, is the brain’s way of translating intention into movement. When the nerve cells that produce it begin to break down, the body becomes increasingly difficult to direct. Movements slow. Muscles stiffen. A characteristic tremor develops: rhythmic, visible, and still, for many people, the first thing they picture when they hear the word Parkinson’s.
They are picturing only part of the story.
The famous faces alone suggest the condition’s reach: Michael J. Fox, Billy Connolly, Neil Diamond, Alan Alda of MAS*H. And then there is Jeremy Paxman – the BBC’s Grand Inquisitor, a man constitutionally unsuited to passive suffering. True to form, he has done what he knows best: made considerable noise about the failure of the NHS to help Parkinson’s patients manage their condition properly, delivered a charter to Downing Street, and committed to donating his brain to the Parkinson’s UK Brain Bank at Imperial College London. As advocacy goes, it is not a bad use of a diagnosis.
This line-up could give the impression that Parkinson’s is the older man’s disease of the popular imagination. In fact, around four in ten diagnoses are women. Janet Reno, the first woman to serve as US Attorney General under Clinton, coped with hers with characteristic directness. When asked whether she could still do her job, she was unequivocal: “I made a decision to continue doing my job.” She kept walking, kept swimming, and took up kayaking.
Margaret Bourke-White, one of the most celebrated war photographers of the twentieth century, faced a starker choice. From 1949 onwards, as her symptoms began to make themselves known – sudden lurches, fingers that refused to cooperate – she could have retreated from the work that defined her. She did the opposite. She had surgery. She danced. She did daily exercises to maintain the dexterity her cameras required. Parkinson’s was the enemy – if not in full retreat, then at least held at bay for the better part of a decade. Through the 1950s she continued travelling: documenting the violence between India and Pakistan, the conditions of apartheid in South Africa, and the war in Korea. She retired in 1969. Fellow photographers paid tribute with a photo essay in Life, and Bourke-White herself, writing in 1959, captured what that fight had cost and given back: “My fingers are more and more often loading my cameras, changing their lenses, and turning their winding buttons as I practise the simple blessed business of living and working again.”
Deborah Kerr largely withdrew from public view, but is known to have benefited greatly from levodopa – unavailable in the 1950s but in common use by the 1990s. She died at eighty-six. Joan Didion, misdiagnosed with MS in her thirties before the correct diagnosis came through, went on writing with ferocious precision until her death at eighty-seven.
And then there is Billy Connolly. Of all the responses to a Parkinson’s diagnosis, his may be the most instructive – and the most entertaining. He has spoken of forming a deliberately jocular relationship with the condition, of keeping it firmly in its place for as long as possible. He calls it a strange animal and maintains an ongoing dialogue with it, telling it on occasion: “I wish you’d fucking kept it to yourself.” He has also described a mental trick he developed to control the shaking – extending his arm as if steadying a gun sight, using the physical act of aiming to override the tremor. It worked. Whether or not it would work for anyone else, the underlying instinct – to engage, to invent, to refuse passivity – is one that research is increasingly finding has real neurological value.
Which brings us to something that is less well understood outside medical circles, and more important than it might initially appear. The tremor, the stiffness, the loss of motor control that most of us associate with Parkinson’s – these are not where the disease begins. They are where it eventually arrives. New research shows that Parkinson’s is foreshadowed, often years in advance, by symptoms with no obvious connection to movement at all: constipation, disrupted sleep, depression, a fading sense of smell. These can precede the tremor by a decade or more – sometimes considerably longer. That detail, as it turns out, is where the most important science is currently happening.
THE SECOND BRAIN
Your gut and your brain are in a running conversation. They have been since before you were born. The channel they use is the vagus nerve – a direct line running between your digestive system and your central nervous system so complex, so busy with signals, that researchers have taken to calling the gut the second brain. The trillions of bacteria living in your intestines are not passive tenants quietly going about their business. They influence mood, inflammation, immune response, and – as is now becoming clear – neurological health.
Here is the finding that stopped many researchers in their tracks. People who go on to develop Parkinson’s frequently experience constipation and other digestive problems up to twenty years before the tremors and movement difficulties most of us associate with the illness ever appear. A new study has found striking similarities between the gut microbiomes of Parkinson’s patients and those with inflammatory bowel disease – both groups showing seriously depleted levels of the bacteria that produce compounds essential to gut and brain health. The gut, in other words, appears to have been sending distress signals long before the brain showed any sign of trouble.
The gut, it is now emerging, may be the canary in the mine. In people with Parkinson’s, the gut lining becomes more permeable – what some people call “leaky gut” – allowing inflammatory substances into the bloodstream. A protein called alpha-synuclein, which forms the damaging deposits that are the hallmark of Parkinson’s, appears to originate in gut neurons before travelling to the brain along that same vagus nerve. By the time the tremor appears, the canary has been blasting out its message for years.
Which means it may also be among the first places we can act. Studies are already showing that probiotics – the live bacteria found in fermented foods and good-quality yoghurt – can reduce inflammation and may slow the accumulation of those harmful deposits. Researchers are exploring the transplantation of healthy gut bacteria into Parkinson’s patients, with encouraging early results. And the polyphenols found in berries, olive oil, and green tea are appearing with striking consistency in prevention research. None of this is a cure. But the dietary implications are clear enough – and the downside of eating better is, frankly, difficult to argue with.
The other intervention requires no prescription and no waiting list: exercise. Vigorous aerobic activity, dance, resistance training – the research on these for protecting neurological function and improving quality of life in Parkinson’s is consistent, robust, and available right now. Not instead of medication. Alongside it.
WHAT’S COMING DOWN THE LINE
The gut is not the only front where the science is moving fast. When the photographer Margaret Bourke-White was first diagnosed, effective medication was essentially non-existent. The gold standard today – levodopa, which replaces some of the lost dopamine – was not even discovered until the late 1960s. But researchers are no longer content with managing symptoms. The goal now is to slow, stop, or even reverse the disease itself – and the pipeline of potential treatments is, at this moment, more promising than it has ever been.
Perhaps the most cutting-edge is a new once-daily pill called tavapadon, developed by AbbVie, designed to manage the tremor, stiffness, and slowness of Parkinson’s more smoothly and with fewer side effects than existing options. It was submitted to the FDA for approval in September 2025. The FDA typically takes around ten months to review an application of this kind – which means a decision could come as early as mid-2026.
Meanwhile, another drug – prasinezumab – tackles the problem from an entirely different angle. Rather than managing symptoms, it targets the toxic protein alpha-synuclein directly – the same protein that accumulates in the brain and drives much of the damage associated with Parkinson’s. It entered Phase 3 clinical trials in 2025 – the final stage before regulatory approval can be sought. If it succeeds, it would be the first therapy capable of slowing Parkinson’s progression at its biological source rather than simply managing its effects.
Brain surgery for Parkinson’s, once a blunt and irreversible procedure, has also been transformed. The FDA approved adaptive deep brain stimulation in 2025 – a system that makes real-time adjustments to the signals introduced into the brain, something that previously required a clinic visit to achieve. Focused ultrasound, which can now be applied to both sides of the brain in separate procedures, is offering relief to people for whom other options have not worked.
Perhaps the most striking frontier is stem cell research. A therapy called bemdaneprocel uses dopamine-producing neurons derived from stem cells, implanted directly into the part of the brain affected by Parkinson’s, with the aim of reconnecting correctly and restoring natural dopamine production. It is still in trials, and caution is warranted – there is no approved stem cell cure as of now, and anyone encountering expensive private clinics making dramatic promises should be sceptical. But the science is serious, and if successful it would represent the first therapy to repair the underlying damage of the disease rather than mask its symptoms.
Closer to home, a small molecule called HER-096, designed to support the survival of brain cells and reduce the clumping of alpha-synuclein, has shown positive results in its first human safety trial and is expected to move into larger Phase 2 studies in 2026.
Technology is changing what is possible for patients right now. Wearable devices and smartphone apps are giving researchers a continuous picture of symptoms rather than a fifteen-minute snapshot at a clinic every few months. The Michael J. Fox Foundation runs an ongoing online study in which patients log their daily experiences directly, feeding into research in real time. The more people engage – the more openly they speak about what living with the condition is actually like – the faster that research moves.
None of this is a cure yet. But the direction of travel is clear, and it is the right one.
THE LIVES THAT CARRY ON
What the science cannot fully capture is the human experience of refusal – of people who received a diagnosis and declined, in one way or another, to be defined by it. Bertrand Delhom became the first person with Parkinson’s to sail solo around the world, completing the Ocean Globe Race just days after World Parkinson’s Day 2024 – not despite the condition but, in some sense, in answer to it. Rune Vethe set up a Parkinson’s cycling club that now spans twelve countries. Artist Kanti Khanna, who had shown no particular gift for painting before her diagnosis, discovered one afterwards. In Peru, filmmaker Christine Jeyachandran made a documentary about living with the condition because, as she put it, stories reach people in ways that facts and scientific reports cannot.
New Zealand author Robyn Cotton wrote Mary and Me – a novel that follows two women living with Parkinson’s two hundred years apart, one of them drawn directly from her own experience of the condition. The earlier character, living in the nineteenth century, was considered by those around her to be drunk, insane, or worse. Thankfully that particular prejudice has largely had its day – though the fact that it needed a novel to make the point suggests there is still some distance to travel.
The pattern here – of people turning towards creativity, movement, and community rather than retreating from life – is too consistent to be coincidental. Emerging research suggests it may be more than attitude. Whether we stay active, creative, and socially connected after a Parkinson’s diagnosis appears to have measurable effects on how the condition progresses. The people doing the cycling and the sailing and the painting may, in some meaningful sense, be doing something neurologically useful. Billy Connolly’s gun-sight trick and Bertrand Delhom’s ocean crossing are not so very different in kind.
If you are caring for a parent with Parkinson’s, one practical consequence of all this research is worth holding onto. Digestive symptoms in older people – persistent constipation, bloating, gut discomfort – are habitually dismissed as minor inconveniences. In the context of Parkinson’s, they may be early signals worth raising with a doctor, and worth raising with some insistence. You are not catastrophising. You are paying attention at exactly the right moment.
Joan Didion kept writing. Bertrand Delhom kept sailing. The diagnosis, it turns out, is the beginning of the story, not the end of it.
