In mid-April 2026, the Michael J. Fox Foundation for Parkinson’s Research (MJFF) hosted a webinar titled “What Causes Parkinson’s Disease?”, bringing together a panel of expert researchers to explore what science currently understands about the causes of Parkinson’s — including the roles of genetics, environmental exposures, and aging. The panel featured local legend Caroline Tanner, MD, PhD, Professor of Neurology at the University of California San Francisco and the SF VA. Read our notes.
Key takeaways from the webinar include:
Parkinson’s disease is caused by a combination of factors, not a single trigger. Genetics, environmental exposures, and aging all interact in ways that are unique to each individual. While science can identify risk patterns at the population level, it cannot yet pinpoint what caused any one person’s Parkinson’s.
Genetic risk exists on a spectrum. Very few genetic variants are truly causative — meaning they will definitively lead to disease. Most genetic factors simply increase risk to varying degrees, like a dimmer switch rather than an on/off switch. It was discussed that “every single case is genetic. Every single case is environmental. Every single case is to do with age,” also noting that “the vast majority of genetic risk that’s involved in disease is extremely common in the population,” indicating that these genetic contributors are widespread and not limited to rare genetic mutations.
Environmental exposures are a significant and actionable risk factor. Certain pesticides, solvents, and other chemicals have been linked to increased Parkinson’s risk at the population level. Veterans, farmers, and others with occupational exposure to these substances may face elevated risk. Reducing ongoing exposure — even after diagnosis — may help slow disease progression.
Aging weakens the body’s ability to compensate for genetic and environmental stressors. As we age, the body’s internal defense and repair mechanisms become less effective, making us more vulnerable to the combined effects of genetic risk and environmental exposure. This is why Parkinson’s most commonly develops later in life, though young-onset cases do occur.
Genetics research is directly driving new treatments. By identifying the biochemical pathways disrupted by genetic mutations, researchers have uncovered targets relevant to all Parkinson’s patients — not just those with known genetic links. Clinical trials are now recruiting patients based on specific genetic profiles, including LRRK2 and GBA mutations, while also testing these therapies in people with idiopathic Parkinson’s.
Genetic testing is a personal decision worth discussing with your healthcare provider. Programs like PD GENEration offer free genetic testing and connect participants with relevant clinical trials. Knowing your genetic profile may open doors to emerging targeted therapies and can inform lifestyle decisions to reduce risk.
The recording of this webinar is posted on the MJFF YouTube Channel
A link to the slides used in the webinar is available here
PD GENEration — free genetic testing program for people with Parkinson’s, connecting participants to relevant clinical trials and collecting research samples.
PPMI — recruiting volunteers with and without Parkinson’s to study causes and biomarkers of Parkinson’s
For further reading on environmental toxins and Parkinson’s disease, see this Stanford Parkinson’s Community Outreach blog post featuring Dr. Ray Dorsey
Keep reading for detailed notes,
— Elizabeth
What Causes Parkinson’s Disease?
Panelists:
- Todd Sherer, PhD, chief mission officer, MJFF
- Caroline Tanner, MD, PhD, professor of neurology, University of California San Francisco
- Andrew Singleton, PhD, co-lead, Global Parkinson’s Genetics Program (GP2), Bethesda, Maryland
Moderator: Jimmy Choi, Parkinson’s Advocate, 7-Time American Ninja Warrior, MJFF Patient Council Member
Webinar Host: Michael J. Fox Foundation for Parkinson’s Research (michaeljfox.org)
Webinar Date: April 16, 2026
Summary by: Elizabeth Wong, Stanford Parkinson’s Community Outreach
Jimmy Choi opened the webinar by sharing his personal experience with PD, diagnosed in 2003 at age 27. He reflected on the many possible contributors to his own disease — repeated head trauma from years of playing American football, exposure to agricultural chemicals while driving through farmland in Indiana and Illinois, and drinking well water from those same areas. While science cannot identify the precise cause of any one person’s Parkinson’s, studying large populations has revealed that genetics, lifestyle, environmental exposures, and aging can all increase risk. In most cases, it is not one factor alone but a combination that interacts with an individual’s biology.
Why Understanding the Causes of Parkinson’s Matters
Research into causes points toward prevention. Identifying specific environmental triggers could enable efforts to remove those substances from the environment and prevent future cases. The MJFF is currently active at the state level in Minnesota and Vermont, advocating for the banning of certain pesticides linked to Parkinson’s risk.
Looking at causes illuminates disease mechanisms. Understanding what is happening at the cellular level — what goes wrong inside affected brain cells — opens pathways to developing diagnostic tests and new treatments that target the underlying cause of disease rather than just managing symptoms. Both genetic and environmental research have converged on the same biochemical pathways, strengthening confidence that these are meaningful therapeutic targets.
The Three Major Risk Factors
Genetics
There has been two decades of progress in understanding the genetic basis of Parkinson’s. Early research focused on rare families where disease occurred far more frequently than expected, identifying causative genes. Over the past 15 years, genome-wide studies comparing hundreds of thousands of people with and without Parkinson’s have identified approximately 100 regions of the genome containing variants that each contribute a small amount of risk individually but collectively push a person toward the threshold of disease.
Genetic risk as a spectrum. The analogy of a light switch versus a dimmer switch was used. A causative variant — rare in Parkinson’s — functions like an on/off switch: carrying it means a very high likelihood of developing disease. Most genetic variants, however, function more like dimmer switches: they don’t cause disease on their own, but they move a person closer to the threshold. The vast majority of genetic risk variants are extremely common in the general population. This means that in a meaningful sense, every case of Parkinson’s has a genetic component — it is not accurate to think of Parkinson’s as either “genetic” or “not genetic.”
The GBA mutation as an example. Community member Sheryl Lowenhar, diagnosed in 2016, shared in a pre-recorded video that she carries the GBA1 mutation, identified through the PPMI program (www.ppmi-info.org). She noted that only about 6% of people with this mutation develop Parkinson’s, and asked why. It was explained that other genetic risk variants — the collective “load” of common low-risk variants — also modulate whether a GBA carrier develops disease. Environmental factors play a role as well. Genetics alone does not determine outcome.
Family history and genetic testing. Having a family member with Parkinson’s does not mean you will develop the disease. People with a family history are encouraged to consult their healthcare provider and a genetic counselor about whether genetic testing is appropriate. Knowing one’s genetic profile may provide insight into eligibility for targeted clinical trials and can support informed lifestyle choices. Jimmy Choi noted that he personally tested negative for known genetic markers and is the first in his family to be diagnosed — pointing out that family members may share not only genes but also environments, which may be the more relevant shared factor.
How genetics informs treatment. Each gene linked to Parkinson’s provides a tangible biological target. Researchers have identified overlapping biochemical pathways — including processes related to how cells manage misfolded proteins and respond to cellular damage — that are disrupted both by genetic mutations and by environmental exposures. This convergence has generated high confidence that these pathways are central to the disease. Clinical trials are now enrolling patients specifically with LRRK2 or GBA mutations, while also testing the same therapies in people with idiopathic Parkinson’s, based on the hypothesis that shared pathways mean shared benefit.
Environmental Exposures
Environmental risk is studied by comparing the life histories of large numbers of people with and without Parkinson’s and identifying which exposures are more common among those who developed the disease. Most people cannot recall or document their past exposures, but occupational settings such as farms with pesticide records provide more tractable study populations.
Known risk factors include:
- Exposure to Agent Orange (a combination of herbicides used in Vietnam and Korean War era service), recognized as a service-related disability risk for veterans
- Traumatic brain injury, which is more common in military and certain occupational settings, and which may initiate protein aggregation and inflammatory processes in the brain — and also disrupt the blood-brain barrier, potentially compounding the effects of chemical exposure
- Contaminated water supplies, as documented at Camp Lejeune, where residents exposed to the solvents trichloroethylene and perchloroethylene had significantly higher rates of Parkinson’s compared to residents of Camp Pendleton
- Paraquat, an herbicide linked to Parkinson’s risk in farming populations, which acts on the body through mechanisms similar to other known Parkinson’s-causing chemicals; people with certain genetic variants that impair their ability to break down toxic exposures are at especially elevated risk when also exposed to paraquat
- Pesticide exposure more broadly, particularly for farmers and pesticide applicators
The elevated rates of Parkinson’s among veterans likely reflect occupational exposure — not something inherent to military service — including chemical exposures, blast injuries, and traumatic brain injury. Similar patterns are seen in other high-exposure occupations such as farming.
Gene-environment interaction. People exposed to paraquat who also carry certain genetic variants that impair detoxification pathways face significantly higher risk than those with either factor alone. This illustrates how genetic and environmental risks compound each other.
Aging
Aging is a major risk factor because the body’s internal protective and repair mechanisms become less effective over time. Stresses that a younger body compensates for well — whether genetic or environmental — become more difficult to manage as we age. This makes older individuals more vulnerable to the combined effects of accumulated risk.
Young-onset Parkinson’s. Jimmy Choi, diagnosed at 27, raised the question of why younger people are diagnosed if aging is a primary contributor. Several hypotheses include: increased awareness and diagnosis, possible increases in actual incidence, and the likelihood that younger-onset cases carry a higher genetic load. Even with a young-onset diagnosis, aging plays a role — the accumulated impact of genetic changes on the nervous system builds over time before symptoms emerge. In the Camp Lejeune cohort, the average age of onset was in the 50s — younger than typical — possibly reflecting the compounding effects of chemical exposure with genetic risk.
Questions and Answers
Q: I’ve been living with Parkinson’s for 23 years. If you’re already diagnosed, should you continue to reduce environmental exposures, or is it too late?
A: Research from PPMI and other studies suggests that changing behavior, maintaining healthy lifestyles, and reducing environmental exposures can help change the trajectory of disease — making a person less likely to experience rapid progression or develop cognitive changes. Dr. Tanner recommended that patients look under their kitchen cabinets and in their garages to identify toxic chemicals, some of which may be specifically associated with Parkinson’s risk. She also noted evidence that air pollution increases Parkinson’s risk and suggested practical steps: using air filters, wearing a mask when appropriate, and avoiding heavy exercise on heavily polluted days. A plant-based, low-animal-fat diet and regular exercise are also important. Jimmy Choi added that he personally makes a conscious effort to minimize his own environmental risk.
Q: Are Alzheimer’s and Parkinson’s caused by the same things? Is there overlapping research?
A: There is significant overlap in the cellular mechanisms involved in both diseases — particularly around how cells handle protein and how the immune system interacts with the nervous system — and this is an active area of study within PPMI. Dr. Singleton added that while some genes involved in inflammation appear in both diseases, the genetic overlap is surprisingly minimal, and the two diseases have largely distinct genetic origins. He noted that the differences are as informative as the similarities. Dr. Tanner emphasized that PPMI research is revealing more of a continuum between neurodegenerative diseases than a clear dividing line, with misfolded protein markers seen in both conditions. She expressed hope that this work will ultimately support highly personalized therapies matched to each individual’s biomarkers and clinical trajectory.
Q: Should people with Parkinson’s get genetically tested? And how?
A: Genetic testing is a very personal decision, and people are encouraged to explore it with their physician or a genetic counselor. There are two key upsides to testing: first, knowing your genetic profile may make you eligible for therapeutic trials targeted to specific genetic forms of disease, which is increasingly actionable as more such trials come online; second, participating in studies like PPMI or PD GENEration allows participants to contribute samples for research while also receiving their own results. PD GENEration provides free genetic testing services, and MJFF will be working with PPMI to expand testing access in the near future. Jimmy Choi acknowledged that many people are reluctant to know their genetic risk, but framed testing as an opportunity rather than a burden given the growing number of targeted therapies in development.
Q: What are you most hopeful for in the next few years?
A: Dr. Tanner expressed hope that the field is close to having therapeutics that can target the mechanisms of disease — not only for people with genetic forms of Parkinson’s, but for all people living with the disease — with treatments that can meaningfully slow progression.
Dr. Sherer reflected that 25 to 30 years ago, most Parkinson’s was called idiopathic — a word he noted translates from Greek as “we have no idea what the cause is.” Thanks to the work of researchers like Dr. Tanner and Dr. Singleton, the field now has a vast understanding of both the genetic and environmental causes of Parkinson’s. That understanding has moved from theoretical to actionable, with treatments now being tested in people today. Dr. Sherer called the current moment an important inflection point, with the potential for truly transformative and innovative therapies on the horizon.
Dr. Singleton agreed, expressing hope that the field continues to accelerate in discovery, adding that if it does, a treatment is inevitable. He credited the Michael J. Fox Foundation with transforming the field over the past two decades by driving research forward — not only toward therapies, but toward earlier diagnosis before people even know they have the disease. He said the work is bearing fruit and progress is remarkable.
Jimmy Choi closed by sharing his personal sense of hope. When he was first diagnosed with Parkinson’s, he recalled looking at the research pipeline and finding almost nothing in terms of disease-modifying treatments. Today, multiple clinical trials are moving into Phase 2 and 3 and are listed as disease-modifying.