Alzheimer's Breaks Through. Parkinson's Plays Catch-Up.

Alzheimer's has finally crossed into the era of disease-modifying treatment. Parkinson's is still waiting for its breakthrough.

The arrival of disease-modifying drugs that can clear amyloid plaques has pushed Alzheimer's into a new phase, where the race is moving toward earlier diagnosis and earlier treatment.

"We can now talk about prevention," Jeffrey Cummings, a leading Alzheimer's researcher, told a brain diseases conference at the World Laureates Forum in Shanghai.

Parkinson's remains on the other side of that divide. Existing drugs largely control symptoms, while researchers are still hunting for reliable biomarkers, better targets and the first treatment that can slow the disease itself. The pressure is rising fast: Nobel laureate Randy Schekman said Parkinson's is growing faster than any other neurodegenerative disease and could affect close to 20 million people over the next 10 to 20 years, with China accounting for more than half of new cases over the coming decade.

For Alzheimer's, the breakthrough was not a cure. But it proved that the course of the disease could be changed.

Anti-amyloid drugs such as lecanemab and donanemab can remove plaques from the brain and slow cognitive decline in some patients with early Alzheimer's. They also come with limits, including modest clinical benefits and the risk of brain swelling or bleeding. Still, their arrival broke a decades-long run of failures and gave drugmakers something the field had lacked: proof that targeting the biology behind the disease could work.

That has pushed the race earlier.

Alzheimer's can begin in the brain about 15 years before symptoms emerge, Cummings said. New blood tests can now help identify signs of the disease without sending every patient for an expensive PET scan, opening the door to much broader screening.

"These tools are something we could not have imagined before," he said.

The impact could reach well beyond diagnosis. Cummings said 20 to 30 percent of participants entering Alzheimer's clinical trials have in the past turned out not to have amyloid in their brains, meaning some patients may have been enrolled in trials for drugs that could never have helped them. Easier blood testing could make trials faster, cheaper and more selective.

Parkinson's does not yet have the same advantage.

One of its hallmark proteins, alpha-synuclein, forms abnormal deposits in the brain, but researchers still lack a widely available way to see those deposits in living patients. Schekman said researchers currently rely heavily on cell models and tissue from patients after death, although new PET tracers under development could eventually change that.

That leaves Parkinson's drug developers fighting on two fronts: finding a treatment that can alter the disease, and building better tools to tell whether it is working.

The problem is not a shortage of ideas.

Researchers at the Shanghai meeting pointed to alpha-synuclein, damaged mitochondria and genetic pathways such as PINK1 and Parkin as possible routes into the disease. But most remain far from producing a medicine that changes the course of Parkinson's.

Some of the most obvious bets have already disappointed. Schekman pointed to an antibody designed to block the spread of alpha-synuclein that failed to slow disease progression in a clinical trial. "The trial was not successful," he said.

That failure also shows why simply copying the Alzheimer's playbook may not work. In Alzheimer's, antibodies that target amyloid outside cells have delivered measurable benefits. Schekman said alpha-synuclein may spread between brain cells in ways that are harder for antibodies to reach, forcing researchers to rethink how, and where, to attack the disease.

For now, much of that work remains upstream of drug development.

Schekman leads the Aligning Science Across Parkinson's initiative, or ASAP, which brings together research teams from around the world to study the basic biology of Parkinson's. Its goal, he said, is not to develop drugs or run clinical trials itself, but to generate findings that biotech and pharmaceutical companies can take forward.

The ambition is less dramatic than a cure, but potentially more realistic.

"Our goal is to make Parkinson's a disease that can be controlled like diabetes," Schekman said.

Getting there will require what Alzheimer's has only recently achieved: turning a growing understanding of disease biology into treatments that can show, in patients, that they actually change what comes next.

China is likely to be central to that effort. If Schekman's projection holds, the country will account for more than half of the world's new Parkinson's cases over the next decade, creating both a growing treatment burden and a much larger base for clinical research.

For drugmakers, that raises the stakes. Alzheimer's has shown that decades of basic science can eventually produce medicines that alter disease. Parkinson's now has to prove it can do the same.