A record number of today’s clinical trials are advancing therapies to slow Parkinson’s progression or to stop symptoms from getting worse. By targeting the biology that causes Parkinson’s, these drugs — called disease-modifying therapies — have the potential to do something none of the currently approved treatments Parkinson’s disease (PD) can yet do: halt or slow the disease process itself, and perhaps even prevent it from ever taking hold.
Disease-modifying therapies remain the greatest unmet need for people with Parkinson’s, but there are reasons to feel optimistic that we’re moving closer to them. Here are five key things to know.
Disease-modifying Therapies Work Differently Than Symptom-improving Therapies.
The ultimate treatment goal for Parkinson’s is to protect existing brain cells and prevent dopamine neurons from dying — something today’s symptom-improving drugs cannot do. It’s the loss of dopamine neurons that leads to dopamine depletion and subsequent motor impairments, such as tremors and difficulty walking, as well as other PD symptoms.
So rather than focusing on easing the symptoms that result from neurodegeneration, disease-modifying therapies are designed to interrupt the biological processes causing the symptoms, preventing the neurodegeneration from happening in the first place.
Disease-modifying Therapies Won’t Replace Symptom-improving Therapies.
Parkinson’s is a complex disease, so achieving a world without it will likely take more than a single cure. Instead, many solutions may be needed, including treatments that lessen PD symptoms and treatments that target underlying biology to slow or stop the disease.
Today’s therapeutic pipeline of potential treatments is rich with both, with about half of PD clinical trials testing new formulations that give individuals more options for managing the varying symptoms associated with Parkinson’s — including motor symptoms, thinking and memory challenges, and sleep and digestion difficulties — and the other half testing therapies focused on the biology that underpins the disease.
Disease-modifying Therapies Are the Path Forward for Precision Medicine.
The biology that leads to PD isn’t the same in everyone with the disease. So no single disease-modifying therapy is likely to fully target the biology in everyone with the disease. Much like cancer care today, researchers foresee a precision medicine approach to PD, tailoring treatment to a person’s specific cellular dysfunction at the level of genes and proteins.
For instance, researchers believe that some people's PD may be linked to problems in how cells handle, recycle and get rid of old proteins. Mutations in certain genes or exposure to other nongenetic factors may disrupt this system. A disease-modifying therapy could be designed to precisely treat the disease by specifically targeting that disrupted biology
Scientists still have more to learn about the biological processes that underpin Parkinson’s, and their findings will guide emerging precision medicine approaches involving disease-modifying therapies.
Disease-modifying Therapies for Parkinson’s Are Closer Than Ever.
While there are likely still years of work ahead before the first disease-modifying therapies become available, signs of progress indicate that we are on the right path to achieving them and give us reason to feel optimistic.
In June 2025, Swiss pharmaceutical company Roche announced that its disease-modifying therapy to stop the buildup of alpha-synuclein would move into Phase III clinical trials. Earlier trials of the drug, called prasinezumab, showed some signs that it slowed disease progression in people with PD. Over the next several years, researchers will gather more data to better understand how prasizenumab affects disease progression. If these trials are successful and lead to FDA approval, prasizenumab would be among the first disease-modifying Parkinson’s therapies to reach the marketplace.
Prasizenumab isn’t the only hope for disease-modifying therapies in Parkinson’s. Other closely watched drugs in Phase II or III trials target biology associated with genetic changes in LRRK2 and GBA1. Research into the biology behind these genetic differences linked with PD development has fueled a robust clinical pipeline of potentially promising treatments.
The list of clinical trials testing drugs to reduce inflammation also is growing: Researchers believe that inflammation may contribute to the loss of dopamine neurons in Parkinson’s disease. Several of these drugs target proteins that drive chronic inflammation in brains of people with PD.
The Michael J. Fox Foundation Plays a Vital Role in Speeding the Path to Disease-modifying Therapies.
Our research team is taking a strategic approach to accelerate the development of disease-modifying therapies, including wide-ranging, urgent efforts to improve our understanding of Parkinson’s and optimize clinical trials to produce better results more quickly. This work happens alongside equally urgent efforts to develop treatments to alleviate PD symptoms, since people with the disease need both types of medicines.
We’re leveraging funding, tools, education, leadership and advocacy to encourage the field — including industry and regulatory partners, patients and families — to work together to create a future free of Parkinson’s with therapies capable of stopping the disease in its tracks.