Parkinson’s disease (PD) is not a single disease but a diverse syndrome with varied biological mechanisms, symptoms, and trajectories. Outdated stereotypes and one-size-fits-all approaches to disease-modifying therapies have stymied progress in research, and public understanding. Emerging efforts in biomarker-based subtyping and precision medicine emphasize personalized methods tailored to an individual’s biology. Progress requires research includes all segments of the patient population and the understanding that the cure is personalized.
How we got to where we are
There’s a stigma associated with people with Parkinson’s (PwP) - assumptions made by others when they see someone with what they believe to be Parkinson’s Disease (PD) symptoms. These assumptions are generally based on an outdated, singular image of a hunched-over, elderly man, clearly lacking energy and cognitive rigor. It’s a stereotype rooted in a fundamental misunderstanding that PD is scripted and predictably staged, invariably leading to debilitation1. With no ill intent, it is a widely-held view by those whose lives have not been touched by PD and thus have not been educated about Parkinson’s otherwise.
Breaking from the past to greet the future
There has been a long-held belief that PD is a single disease stemming primarily from a loss in dopamine. This notion ignores research that demonstrates biological differences among individuals and a variety of molecular mechanisms behind PD neurodegeneration, including neuroinflammation, lysosomal dysfunction, and disruption of mitochondrial pathways2. Environmental exposures to products, including pesticides and heavy metals are also believed to contribute to PD3.
There is, in fact, not one PD. It is as varied as the people who live with it. Symptoms range broadly among people. Some may have a few symptoms, others may have a complex mix. There is a growing consensus that PD is a syndrome - a variety of diseases that together make up an individual’s “brand,” so to speak, of the disease.
The clinicopathologic model has defined neurodegenerative disorders for over a century. The model is based on the belief that clinical features result from a pathology identified as abnormally aggregated proteins in autopsy studies. It is assumed that the pathology must therefore be causal to the disease. While this clinicopathologic approach has been helpful in the development of therapies aimed at correcting common neurotransmitter deficiencies and in providing symptomatic relief, it has not been successful over the last four-plus decades in the study of neuroprotection. This one-size-fits-all approach is incongruent with the individual biological nature of Parkinson’s and impacts the lives of millions and limits innovation in basic, translational, and clinical research. Moreover, it leaves many people, in the end, lacking the personalization they require for their specific illness (syndrome).
When I look around the country and globe at individuals I know with PD, they are holding positions of authority and leading volunteer initiatives that would exhaust your most seasoned Fortune 500 professional. With young-onset PD on the rise, you have a group of individuals who may not only be juggling a job but also raising children or caring for elderly parents. They do what they need to do to lead a productive life, and at the same time, they are often making significant contributions as advocates for Parkinson’s research and those living with PD. These examples demonstrate the lack of understanding of the disease, its image, and how together they impact PwP’s lives.
The path forward: personalized medicine
Because PD can be as different as the people who live with it, there cannot be a single cure. Just as we must replace the image of the elderly man, we must also update our perspective that we are not looking for “a” cure. We are looking for cures and as many ways to prevent it as possible. Why? Because, as we have learned, there is no pill or combination thereof, or exercise routine or lifestyle intervention that should be expected to work the same for everyone. Each PwP requires his/her/their own personalized solution or cure4.
PD is a collection of conditions without one cause or trajectory5. What scientists learn in the laboratory may not apply to all individuals, given that each is unique within the broad spectrum of PwP. Consequently, it is critical that the requirements for a personalized approach be kept top of mind and that research design and protocol be challenged as necessary.
We have learned much about PD as a concept, but our understanding of how to apply that knowledge and to whom is still limited.
For research and clinical trials to truly make a difference, research institutions, funding agencies, clinicians, and advocacy organizations must support efforts that include diversity, the voice of people with PD, underrepresented populations such as women and young-onset PwP, and atypical presentations. The differences among the individual populations must be identified in the results. That is to say that if research includes a diverse cohort but results are presented with global conclusions, there is limited added value.
Current leading efforts
Many leading research institutions and funders recognize that PD is not a single disease, but the transition is slow, and the diversity of approaches and study populations that may be included in the laboratory is not always reflected in clinical trials6. The need for better standardized biomarkers continues, especially for early-stage or prodromal PD that can help identify those at highest risk for progression to advanced stages. Widespread clinical application of subtyping is still a few years away7.
Currently, efforts that stand out among others are those that acknowledge the existence of individual differences between people affected by PD and focus on the identification of biological and cellular markers to stratify people with neurodegenerative diseases into their proper biological subtypes. The Cincinnati Cohort Biomarker Program (CCBP - ccbpstudy.com)8 is notable in this regard. In this program, once assigned to a subtype, each individual is offered a therapy that has a high likelihood to alter disease progression based on their specific syndrome.
Other initiatives that focus on biomarker-based subtyping include:
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The Parkinson’s Progression Markers Initiative (PPMI) – Led by the Michael J. Fox Foundation, this international study is collecting bio samples, imaging, genetics, and digital health data to define subtypes based on biomarkers and progression rates.
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The University of Pennsylvania MIND Initiative Cohort - An “all-comers” cohort focused on capturing the full biological and genetic diversity of PD patients. DNA and biomarker samples are collected from every patient participating in the initiative. This inclusive database supports precision-matching individuals with Parkinson’s to targeted therapies; and
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The DIG-PD (Developing Imaging Genetics Biomarkers for Parkinson’s Disease) – The objective of which is to classify people into biologically and genetically distinct Parkinson’s subgroups.
In sum, the overarching goal is to move toward precision medicine, where therapies are based on individual biological profiles. At present, there has been limited progress in recruiting and treating based on subtypes in clinical trials. Current trials are beginning to stratify patients, yet most treatments are still not personalized to tailored to the underlying disease biology of the individual patient. There’s much work to be done for patients with PD to realize the benefits of personalized medicine, but I hold a positive outlook for the future.
Data availability
No datasets were generated or analysed during the current study.
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Bowen, S.J. There is not one Parkinson’s disease, nor is there one cure. npj Parkinsons Dis. 11, 339 (2025). https://doi.org/10.1038/s41531-025-01183-w
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DOI: https://doi.org/10.1038/s41531-025-01183-w