The grand, high-ceilinged banquet hall of the Marigold restaurant in Sydney's Chinatown is a whirlwind of waiters, food trolleys and never-ending dishes as Sunday yum cha gets into full swing. Sitting at a large round table with his wife, Caroline, and their two children, aged 13 and 11, Peteris Ginters picks up his chopsticks and reaches over to pluck a prawn dumpling from a serving dish. The 44-year-old barrister finds himself chopstick-challenged as he struggles to apply the small pincer-like pressure between thumb and index finger required to pick up the dumpling. Taken aback – he's never had difficulty with chopsticks before – he winds up skewering the dumpling and dropping it in his mouth.

A few days later Peteris (pronounced "Petris") is emptying his dishwasher when a dinner plate slides out of his grip and smashes on the tiled floor. He dismisses it as a moment of uncharacteristic clumsiness. Over the next couple of weeks, he finds he can't turn the key in the heavy wooden door of his law chambers, nor fasten his top buttons for court without assistance. He's mystified about this worsening weakness between the thumb and index finger on his right hand. And what's with his handwriting? He's been using a fountain pen since he was a teen – while his cursive was never elegant, his sentences are now dissolving into an indecipherable squiggle.

It's late August 2016. Only recently, Peteris had cycled the 40-kilometre Akuna Bay West Head loop with his mates, which he did most Sundays. Always supremely fit – exercise was his means of combating the brutal stresses of the courtroom, and he also jogged regularly with his colleagues – he'd suffered his share of bruises and strained muscles over the years. Thus, when he feels an odd heaviness in his thighs, he chalks it up to a pinched nerve from one of those early-morning bike rides.

With the symptoms in his hand and legs getting worse, Peteris finally visits his GP, who sends him off for an MRI brain scan. It comes back all-clear, but the GP is troubled by Peteris's mysterious muscle weakness. "You need to see a neurologist," she advises, writing him a referral.

And so, on the sunny spring morning of November 7, 2016, Peteris finds himself on the M1 motorway driving towards Macquarie University Hospital, Caroline beside him in the passenger seat. Still convinced it's all related to a pinched nerve in his back, he's only attending this appointment at her urging (she'd looked up the neurologist's areas of expertise – Parkinson's disease and motor neurone disease [MND] – with some alarm). Peteris can only think of all the preparation he has to do for an appeal tomorrow. But he has a premonitory aww f... moment in the waiting room, when he spies a motor neurone disease poster on the wall.

Professor Dominic Rowe, a youthful-looking neurologist with a shaved head, barrel chest and bow tie, greets the couple and ushers them into his corner office, a casual, welcoming space with a Sherrin football and teddy bear perched on the window sill and sunlight streaming in. Rowe, 53, gets swiftly down to business; after Peteris runs through the set of strange symptoms, he asks him to remove his shoes for some strength and nerve tests. Rowe quietly watches Peteris as he fiddles awkwardly with his shoelaces and socks. On the examination table, he asks Peteris to push his hands as hard as he can against Rowe's, and to do the same with his feet. Things seem pretty normal to Peteris as the doctor bounces a weight on his knees, so he's surprised when Rowe says his responses are hypersensitive. Finally, Peteris's strength of grip is measured with a dynamometer.

While Peteris puts his shoes back on, Rowe pins the MRI scans on to his light box. "The radiologist's report says it shows nothing," says Peteris casually.

"That's not unusual," interjects Rowe without turning. "Sometimes changes can be very subtle." And there he sees it: dots that should be lined up are slightly out. He pauses. "I know this is a lot to take in, but I have absolutely no doubt you've got the most common form of motor neurone disease, sporadic amyotrophic lateral sclerosis [ALS]," he says.

For a moment Peteris and Caroline sit in stunned silence, processing those three words – motor neurone disease – knowing that in an instant, their universe has changed forever. ALS, known in the US as Lou Gehrig's disease after the former New York Yankees baseball star who died of it in 1941, is a progressive neurodegenerative disease that erodes motor neurons – cells in the brain and spinal cord that control muscular function – until it becomes difficult or impossible for a person to walk, talk, speak, swallow and breathe. ALS often begins with subtle muscle weakness in the hands or legs, creeping up like a stealth assassin as it wipes out hundreds of millions of nerves, leaving muscles to wither from being powerless to move limbs.

"I'm happy to refer you for a second opinion if you'd like one," Rowe adds gently. But Peteris instinctively trusts this doctor who so frankly, but compassionately, calls it as he sees it.

"Life expectancy?" Peteris asks quietly.

No two sufferers of ALS are exactly alike, answers Rowe, and there's no way to accurately predict how fast a sufferer's disease will progress. The grim truth is that ALS can move swiftly, one of the most traumatic aspects of the disease. Some can be on a cane within a month of diagnosis, which can turn into a walker and a wheelchair shortly after that. In others it can progress much more slowly, beginning with cramps, twitches and slurred speech. But he's sorry to say that on the list of diseases with the worst of prognoses, MND is near the top, with 75 per cent of the newly diagnosed dying within two-and-a-half to five years.

At this point, Peteris, who is not a crier, breaks down, his shoulders heaving. Rowe steps forward, and gives him a big hug. "It's a f…in' bastard of a disease," he says kindly.

But, he adds, Peteris is still in the early stages and while there's no cure, it can be managed with medication, physical therapy and speech therapy. The standard treatment for ALS is the drug riluzole, which can buy a little bit of time for some.

But there may be a better way of slowing the disease down, Rowe adds – a very promising one being trialled here at Macquarie University. If he's willing and able, Peteris may be a candidate.

On the drive back to the city, with the inevitable "What now?" questions thundering through their minds, Peteris and Caroline begin drafting a plan. They agree on the painful decision to close his legal practice immediately. He will wrap up the appeal tomorrow and pass his caseload over to other barristers. More traumatic will be how to prepare his son and daughter, two sisters and parents for the news.

But first, he has some urgent business to attend to. He asks Caroline to drop him off at Martin Place, where he walks to the Channel Seven building and takes the lift to State Chambers on the 36th floor.

Fiona Hayden, clerk of the chambers, takes one glance at the usually chirpy Peteris as he walks through the glass entrance doors and knows something awful has happened.

"Are you okay?" she asks. Peteris is due to sign on the dotted line for the purchase of new chambers – a single room on this floor – and wants to let the owner, who is in ill-health himself, know he can't proceed. "I've just been diagnosed with motor neurone disease," he tells Hayden with a trembling voice.

Moved to tears, Hayden gives Peteris a heartfelt embrace. The barristers on the floor had all been looking forward to Peteris joining them here. "Is there anything I – or any of us – can do for you?" she asks.

"That's kind of you, but no," replies Peteris, batting away fresh tears.

And with that he leaves the offices, his 18-year career as a barrister now over.

It's April 2018 and Rowe is standing in his office doorway, preparing for a busy Wednesday in what is the largest MND research facility and multi-disciplinary clinic in the country. Today, among his list of patients at various stages of MND, he'll be seeing a former sexual assault counsellor, a former Crown prosecutor and a former model.

"If you were to design the cruellest of diseases imaginable, this would be it," says Rowe. "It robs you of your ability to walk, to use your hands, wipe your bum, scratch your nose, swallow, hug your loved ones. Yet it leaves intact all your intellect and your special senses – sight, hearing, smell – so you're able to watch your body waste away."

What is it about the neurons controlling eye movement that makes them so resistant to ALS, a fact that enabled the late physicist Stephen Hawking to communicate? "The cells in the eyes, and the bladder and bowels, have different buffering capacities, more resistant to the process that destroys susceptible cells," he explains. Understanding how these cells stave off death may help scientists understand long-term survival.

Rowe's longest surviving patient with ALS has had the disease for more than 30 years, but he had one patient, a mother of two in her 40s, who died within two months of developing her first symptom – a weak ankle – while on an overseas trip. "It's this unpredictability that makes ALS one of the most feared diagnoses in medicine," he says.

Many will be surprised to learn that the number of MND diagnoses is as high as multiple sclerosis; the reason MND isn't as prevalent is that sufferers don't live nearly as long. At any one time, 2000 Australians have MND – 60 per cent male and 40 per cent female – and about 800 die each year. To put that number into context, the national road toll each year is around 1200. "The incidence [in cause of death] has almost tripled, from one in 500 in 1985 to one in 180 in 2014," notes Rowe. "Some argue that it's because of better diagnosis, but the diagnostic tools were the same in 2014 as they were in 1985."

The mystery at the heart of MND is this: what is the biological spark that sets off the deadly dance of nerve destruction? The human brain has about 100 billion nerve cells, which send signals to the muscles at speeds of up to 300 kilometres an hour. ALS is about the most pernicious form of MND, killing both the upper and lower motor neurons. About 10 per cent of sufferers have a family history of the disease, but for the vast majority the unknown cause is some complex interplay of genes and environment.

As he moves from room to room seeing patients, Rowe reminds me of an old-fashioned family doctor. With a warm, solicitous style, he frequently befriends the people in his care. "It's important to tell people the truth, not to withhold anything that they'll be dealing with," he says. "By the same token, you don't have to be some brutalist deliverer of the shit storm ahead." Rowe is known for his salty language, and on the morning I visit his clinic a patient hands him a swear jar. "Five bucks for every time I swear," he smiles. "But I defy anyone who works with MND not to swear." The jar already contains $10.

He has no patience with specialists who sit in their ivory towers and dole out impersonal medicine, nor does he have any truck with sugar-coating the truth. "Tomorrow is the first anniversary of my dad's death from renal cell carcinoma," he reveals. "He got sick four months before he died, and not one f...ing doctor involved in his care told him he was going to die. My dad asked me, 'Is this survivable?' and I told him no."

Rowe is the principal investigator in the trial of a new drug for MND, Copper ATSM (Cu-ATSM), which began in late 2016. While it's no cure, and cannot reverse pre-existing nerve death, the drug could be the most significant breakthrough yet in slowing the merciless march of the disease.

"We've finished one trial and we're in the middle of another trial of therapies that will dramatically slow and eventually stop MND, so we have rubber on the road for the first time," Rowe enthuses. The research, an Australian-first, involved the collaboration of a trio of professors from the University of Melbourne (Associate Professors Anthony White, Kevin Barnham and Paul Donnelly).

"There is actually a 20-year backstory to the trials and this is the first time they've been used on humans," he adds. Rowe has 70 scientists working solely on MND research, all of them paid for through fundraising efforts (Rowe and his wife, both accomplished cooks, have raised hundreds of thousands of dollars by auctioning off their dinners). In laboratory studies, Cu-ATSM extended the life of mice with ALS from two weeks to almost two years. "If we can slow down the progression of ALS by 50 per cent, we could potentially triple, or quadruple, people's survival," says Rowe.

Rowe's team has also been experimenting with a repurposed HIV/AIDS drug called Triumeq. A $1 million laboratory below his clinic contains tanks of transparent zebra fish, injected with the human gene that causes inherited MND. When motor neurons die, they glow yellow. "There has to be a biological reason why one ALS sufferer is dead in eight weeks and another lives for 30 years," Rowe muses.

Sucking in the mountain air, relishing the rush of adrenalin that comes with cycling in the inaugural L'Étape Australia, the largest Tour de France event held outside France, Peteris has shoved his diagnosis of a month earlier to the deepest recesses of his mind. It's December 2016, and he's been training for this moment since the beginning of the year. Head down as he peddles uphill, his thigh muscles strong from years of riding, he easily powers through the first stretch of the gruelling 157-kilometre course through the Snowy Mountains.

After grabbing a mouthful of water, he reaches to put the bottle back in its cage when his hand freezes. In a split second, his front wheel arrows into the back wheel of the cyclist in front, and both riders tumble on to the hard bitumen. His fellow rider is fine, but his bike is a write-off. Peteris, who has landed on his left shoulder and snapped his collarbone, gallantly gives his bike, which is intact, to his mate to finish the race and waits for the ambulance that has been trailing the 4000 cyclists. Sitting in the cabin with two other injured comrades, Peteris shares a joke or two; inside, his heart is breaking.

"It was a huge reality check," he reflects, sitting perfectly upright at the dining table of his spacious apartment in Sydney's Woolloomooloo. "I realised for the first time that limitations had really come into force, that I couldn't hold off the ALS, that my cycling days were over. It was very confronting."

At 46, Peteris still has a youthful, sweet-tempered face. He slowly grasps a flask of water with both hands, lifts it up and takes a sip. "My hands and arms are of no use to me now. I can use my hands as claws, but I can't use a knife or fork. I can't press the buttons on my mobile phone, so I use Siri."

The six months after the cycling accident were a tsunami of physical weakening. Within six weeks, while on holiday with his family in Japan, he'd developed a limp in his right leg; his hands had lost so much dexterity he couldn't do up a zip. By March 2017 he was using a cane – a fetching black number with a silver handle – but he soon became so unsteady he had a couple of falls. By April he was no longer able to drive; by June he'd traded his cane for a walker.

The assaulting weakness slowed considerably after August, when he was given a slot on the Cu-ATSM trial, and slowed further still after February this year, when his dose was upped to 72 milligrams a day. Every morning he swallows six of these shiny blue pills before breakfast, the dosage soon to double, having received an all-clear in liver tests.

Still, it has slowed rather than stopped progress. By November 2017, Peteris had to use a wheelchair whenever he ventured out of the house. By early this year, the stairs of the family's much-loved terrace house in Paddington had become a nightmare – hence the move to this single-level apartment in Woolloomooloo.

I ask how well he's coping. "Surprisingly well," he replies. "The first few months after the diagnosis were difficult; there were times when I was uncontrollably sensitive, dissolving into tears for no apparent reason." No shaking your fist at the sky? "No," he smiles. "Shock and anxiety about the future, yes, but not anger. Part of that initial shock is, 'This isn't supposed to happen to someone like me', but of course it can happen to anyone. Caroline and I came to the conclusion there's no point being morbid or depressed about it."

The couple met in 1995 as law students and were married in 2000. "I would never have been able to get through this without her love and assistance," Peteris says quietly.

He doesn't miss the long, ruthless hours of his job, when he would sometimes rise at 4am on Sundays and put in four or five hours' work, so he could be at home by 10am to spend the day with his kids. "That's what you had to do to prepare for cases properly. I wanted to be on top of everything."

He comes from a high-achieving family. Born and bred in Sydney's Cammeray to a migrant father from Latvia and an Australian-born mother, Peteris has two older sisters, Laura, a lecturer in performance studies at the University of Sydney, and Anna, an account director in real estate. The family have always been close.

He didn't wind up telling his children about his diagnosis until April 2017, when Rowe told him he'd be a candidate for the next cohort of the Cu-ATSM drug trial. "I wanted to give the kids some positive news," he explains. "How could I tell them when I was having difficulties coping with it myself?"

"This is a disease of nice people," says Dr Stanley Appel, a world authority on MND from Houston Methodist Hospital's department of neurology in the US, and a mentor to Dominic Rowe. He's speaking to a packed hall of neurologists and students at Macquarie University. "Often they are in exceptional health, high achievers who tend to be more empathetic than most." This doesn't mean a cause-and-effect relationship between being nice and getting MND, he hastens to add.

As scientists inch closer to an understanding of the mechanism behind MND, they're also coming across a tantalising – and hideously complicated – range of possible culprits. Surveys of death certificates of former NFL players by New York's Columbia University have found they're four times more likely to die of ALS than the general population. Similar clusters have been found among soccer players in Italy and the UK, and very recent studies have pointed to a possible connection between highly vigorous exercise and MND.

One of the most intriguing clusters of ALS occurred on the island of Guam in the 1950s and '60s, when the disease was at least 50 times more common than in the mainland US. A possible culprit is a toxin called BMAA, found in unwashed cycad seeds. The locals devoured the seeds when food was scarce during World War II, only succumbing to the disease one or two decades later.

The same neurotoxic amino acid, BMAA, has been found in the blue-green algae caused by agricultural run-off from pesticides and fertilisers, known to kill livestock. For the past six years Rowe and his team have been studying a cluster of MND sufferers in the Riverina area of south-west NSW, where blooms of blue-green algae have frequently popped up along the Murray and Murrumbidgee Rivers, and in the state's Hunter Valley. "Studies in the US have shown that those who live near rivers and lakes, with frequent algal blooms, are more susceptible to MND," he says.

ALS isn't a new disease – it's been killing people at least since the late 19th century, when, in 1874, the French neurologist Jean-Martin Charcot coined the name. Some scientists believe these MND clusters represent a veritable Rosetta Stone of clues pointing to the possible environmental contributors to the disease, something that's becoming increasingly important given MND's unexplained increase.

The news flashes across screens large and small over the globe. The world's most famous and longest living sufferer of ALS, the man they called Einstein's heir, Stephen Hawking, has died at 76. He passes away on the night before my second meeting with Peteris. "What I took from Hawking is that you can maintain a quality of life with ALS, although it's a very different quality of life," Peteris says.

Meaning that it leaves your personality intact and your intellect free to roam? "Yes. I'm grateful this isn't a cognitive disease. Mind you, I may change my position on all this if it gets to the point where I need assisted breathing. I'm hoping that will be a long time off because the drug is slowing everything down…"

ALS has a few well-known faces in Australia, including Neale Daniher, the former AFL Essendon player and Melbourne coach, who was diagnosed in 2013; scientist Justin Yerbury, who recently featured on ABC TV's Australian Story; and former Balmain Tigers star halfback Scott Gale, who died at 39 in 2004.

Diseases like ALS are a crucible, not just for the sufferers, but for their close friends and family. Caroline and the children, now 15 and 13, have been a boundless support; you can feel the love as soon as you enter the family's apartment. A couple of good friends have fled, while some former acquaintances have become much closer. "Some of the people you think are most reliable and supportive are not necessarily so," Peteris reflects. "And then other friends really step up to the plate, without you even asking for it."

His former colleague, barrister Robert Reitano, has organised a couple of lunches that have raised more than $60,000 for MND research. He has also booked a table at the MND gala dinner, to be held at Sydney's Doltone House a week before MND/ALS Global Day on June 21. Reitano regales me with hilarious stories of Peteris, including the time the pair were punked by The Footy Show's Beau Ryan while walking in Pitt Street Mall.

Peteris knows he's in a more fortunate position than many sufferers of MND, both emotionally and financially. "I'm grateful to be now in a position where I can see my kids set off for school and come home at night." He's optimistic about the capacity of Cu-ATSM to slow the progress of this unforgiving disease. "Turning in bed has become a little more difficult in the past few months, but if I was to sum up my decline in percentage terms since I've been on the trial, I'd say my arms might be 5 per cent weaker – nothing compared to what I was losing before – and my lung capacity has dropped less than 10 per cent."

When he was a teenager, Peteris was a soccer goalie – and a good one, according to his old mates, able to execute deft little pivots and nimble dashes. Does he miss his days running and cycling? "I miss it desperately," he says wistfully. "But do I worry about it? No, because life has just moved on to a different phase. I can't run or ride anymore, but I can enjoy an enormous amount of quality time with my family, and I can read a lot, which is a passion of mine."

He's just finished a biography of Leonardo Da Vinci. "I'm arrogant enough to say I've got a pretty good brain," Peteris says. "The one thing I can still do is to keep it active."

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