Podcasts

Episode 96: PD Medications and Side Effects

Adverse effects, often called side effects, are a common phenomenon that accompanies the use of many drugs, including ones used to treat the symptoms of Parkinson’s disease (PD). Any treatment is a balance between the desired effects of a drug and undesirable ones, so how to best ease symptoms while making the treatment tolerable. Specific to classes of drugs used for PD, some of the side effects may be drowsiness, insomnia, light headedness, hallucinations, cognitive impairment, swelling of the legs, dry mouth, weight gain, compulsive behavior, and others. These are just possibilities, and a good working relationship with a PD health care team can help avoid many of them. Beyond the PD team, keeping other health care providers informed is advisable since drug interactions can occur, so all practitioners (including dentists) should be aware of all medications that a person is taking, prescription, over-the-counter and even supplements.

In this podcast episode, neurologist Dr. Irene Richard of the University of Rochester Medical Center discusses several of the various drugs and drug classes used to treat the symptoms of PD in relation to the adverse effects that can accompany them. She offers insights into several ways to avoid or minimize adverse effects of drug therapy, what clinicians should tell people starting a new drug, and what people should ask as well as be aware of and report back.

Released: December 29, 2020

Podcasts

Episode 134: Meet the Researcher: Disparities in PD Care

As with many medical conditions, people with Parkinson’s disease (PD) may experience disparities in access to care, in diagnosis, treatments, and ancillary care. These disparities may be based on age, gender, race, financial situation, language barriers, and geographic location, among other factors. Dr. Lynda Nwabuobi, now a movement disorders specialist at New York-Presbyterian/Weill Cornell Parkinson’s Disease and Movement Disorders Institute in New York City, received her specialized training at Columbia University, supported by a Parkinson’s Foundation Movement Disorders Fellowship.

During her training, she noticed that women with PD who were home bound were more likely than men to be alone and to have less access to a neurologist. She also recognized disparities in the care between the majority white population of people with PD seen at the main hospital clinic of New York University (NYU) compared to the more racially diverse, multicultural community of people seen at NYU’s public Bellevue Hospital nearby – even though they were being treated by the same doctor. In this podcast episode, she describes how she acted on her passion of “creating access to better care to marginalized communities and bring more diversity to the clinic.” Rather than waiting for the community to come to the health care setting, she reached out to them on their turf — at a farmers’ market.

Released: August 9, 2022

My PD Story

Donghe Yang headshot
Researchers

Donghe Yang, PhD

2026 Launch Award

Building Stem Cell Models to Study Dopamine Neuron Vulnerability in PD

In Parkinson’s disease (PD), dopamine neurons in the midbrain break down over time, leading to progressively worsening symptoms. However, not all dopamine neurons are affected the same — some remain healthy, while others break down. This selective vulnerability of dopamine neurons has baffled scientists for decades and remains a major unanswered question in the PD field. 

Donghe Yang, PhD, recipient of a Parkinson’s Foundation Launch Award, is determined to investigate what differentiates dopamine neurons that die off in PD and those that seem unaffected. By understanding what makes certain neurons uniquely fragile, we can explore new ways to biologically reinforce them and protect them against PD.

“My research aims to uncover why the neurons most affected in PD are uniquely vulnerable and to use that knowledge to guide better treatments for patients.” – Dr. Yang

In Parkinson’s disease, a specific type of dopamine neuron in the substantia nigra (called A9 neurons) are lost. Meanwhile, closely related dopamine neurons (called A10 neurons), located in the directly neighboring brain region, do not degenerate in the same way. While similar biologically, Dr. Yang has uncovered subtle yet important differences between A9 and A10 neurons that could be the key to their differing fragility.

Donghe Yang working with a pipette in a laboratory.

Within the lab of Dr. Lorenz Studer, at the Memorial Sloan Kettering Cancer Center in New York, Dr. Yang has used these clues to develop a blueprint on how to turn stem cells directly into  A9 or A10 neurons in petri dishes — a remarkable feat for which a provisional patent has been filed. 

Using complex tools, Dr. Yang will validate that this process can create authentic A9 and A10 neurons consistently. Dr. Yang will also transplant these neurons into mice brains to ensure that they integrate properly, ensuring their health and testing their potential to be used for future dopamine neuron transplantation approaches.

With these generated A9 and A10 neurons, Dr. Yang will then use them as a new model of PD, altering them to have PD-related genetic variants. By observing how the different neuron types react to these genetic changes, he can better understand what makes the A9 neurons more vulnerable and the A10 neurons more resilient to PD. 

Dr. Yang will also simulate aging in these neurons, further exploring how aging and PD-related variants result in A9 neuron breakdown while A10 neurons stay functional.

Finally, Dr. Yang will create a simulated midbrain using the A9 neurons and other immune cells. He will induce inflammation in this simulated midbrain, collecting more data on how A9 neurons react to biological stress, which could contribute to their breakdown.

The ability to grow distinct populations of A9 and A10 neurons creates a new, unique, and valuable model in which to study PD. With many advantages over previous approaches, these experiments will establish an important foundation from which PD scientists can explore A9 neuron vulnerabilities, leading to future therapies and treatments that prevent dopamine neuron degeneration. 

“This award gives me strong encouragement to continue my work on Parkinson’s disease and to pursue research that may one day help people living with this condition,” said Dr. Yang. “This work could help identify new ways to protect vulnerable brain cells, as well as develop better disease models and future cell-based therapies.”

Meet more Parkinson’s researchers! Explore our My PD Stories featuring PD researchers.

My PD Story

Per Petersson
Researchers

Per Petersson, PhD

2026 Impact Award

Counteracting Levodopa-Induced Dyskinesias with a New Genetic Therapy

Levodopa is the gold standard medication for most people with Parkinson’s disease (PD), effectively treating movement symptoms. However, routine use of the medication can lead to levodopa-induced dyskinesias (LID), involuntary and erratic movements that are a side effect of the drug and not directly caused by PD. Dyskinesias are often as debilitating as the disease itself, and better treatments for the condition are desperately needed.

Per Petersson, PhD, recipient of a Parkinson’s Foundation Impact Award, is exploring a new way to counteract LID through genetic therapy. This one-time treatment gives the brain the tools to sense and silence overactive neurons the moment an episode begins. 

“This research could lead to a completely new way of treating levodopa-induced dyskinesia, one of the most common and disabling side effects of Parkinson’s disease therapy.” – Dr. Petersson

Research indicates that a small group of neurons in the brain often contribute to LID. As dopamine levels increase following a levodopa dose, these specific neurons can suddenly increase in activity and lead to involuntary movements.

Gabriele Lignani, PhD, coinvestigator for this project, recently developed an experimental genetic therapy for epilepsy in which neurons are given a genetic “pressure release valve” that is activated when neurons become overactive and reduces their activity. By specifically targeting the overactive neurons, the treatment ensures that properly functioning neurons remain unaffected, preserving normal brain function. This therapy is currently advancing towards clinical trials in epilepsy patients. 

Dr. Petersson and his team at Umeå University in Sweden recognized that this therapy could also work on overactive neurons contributing to LID, potentially benefiting those with PD. Excitingly, his initial studies in mice have shown greater reductions in LID-like involuntary movements than the only medication specifically approved to treat dyskinesia in Parkinson’s disease. Now, Dr. Petersson will continue to test this genetic therapy in mice with simulated PD and LID. In addition to carefully checking for side effects, he will observe if the treatment reduces their episodes without otherwise affecting their health and behavior. He will also scan the brain to see in which neurons the pressure release valve is activated most often. This will help confirm which types of brain cells contribute to LID, which will help fine-tune the treatment in the future.

“Receiving a Parkinson’s Foundation Impact Award is both an honor and an important validation of a research direction that we believe has the potential to change how levodopa-induced dyskinesia is treated,” said Dr. Petersson. “If successful, this research could provide the foundation for a long-lasting, potentially one-time treatment that improves quality of life for people living with Parkinson’s disease.”

Meet more Parkinson’s researchers! Explore our My PD Stories featuring PD researchers.

My PD Story

Prayag Murawala headshot
Researchers

Prayag Murawala, PhD

2026 Impact Award

Studying Axolotls to Unlock New Regenerative Therapies for Parkinson’s

In Parkinson’s disease (PD), dopamine neurons in the brain progressively break down, leading to worsening symptoms over time. Unlike other cells in the body, the human brain is unable to regrow replacements for these neurons after they degenerate. Replacing lost dopamine neurons is a major disease-modifying treatment goal for Parkinson’s disease. Prayag Murawala, PhD, recipient of a Parkinson’s Foundation Impact Award, believes that the regenerative properties of the axolotl salamander could hold the key to future restorative PD therapies.

“This research could provide a blueprint for developing therapies that stimulate the human brain to regenerate dopamine neurons, offering a path toward treatments that restore brain function rather than simply managing symptoms.” – Dr. Murawala

Pale axolotl in an aquarium.
Axolotl

Axolotls are vertebrate animals that can uniquely regrow body parts like limbs, heart tissue and even brain tissue after injury. They also share biological similarities to humans that are important for research, including having dopamine neurons in the brain that govern movement. 

Dr. Murawala and his team at the Mount Desert Island Biological Laboratory in Bar Harbor, Maine, have developed a sophisticated research environment to study the healing abilities of axolotls. 

For this study, they will induce an injury in the axolotl brain that simulates PD dopamine neuron degeneration. As regeneration begins, Dr. Murawala will track the activity of stem-cell-like ependymoglial cells (EGCs) in the brain, which give rise to the restored neurons. Through this process, his team hopes to discover the molecular clues that underlie their regenerative ability.

Fluorescent axolotls under a microscope.
Photo from Dr. Murawala’s lab

Additionally, Dr. Murawala will perform whole-brain scans of the axolotls at the start and end of the experiment to see if the regenerated neurons properly rewire across the brain. He will also observe the axolotls’ behavior during recovery to see if the regeneration restores any movement impairments caused by the injury.

This study will reveal the biological processes that trigger and guide the axolotl EGCs to create new and effective dopamine neurons in the brain after injury. Understanding the cellular mechanisms behind neuron regeneration in axolotls could unlock new PD therapies centered on restoring lost dopamine neurons in the brain.

“This award recognizes the potential of regenerative biology to contribute new ideas to a disease that urgently needs therapies capable of restoring lost neurons rather than only treating symptoms,” said Dr. Murawala. “I hope this project will serve as the foundation for a long-term research program focused on developing regenerative approaches that could ultimately benefit people living with Parkinson’s disease.”

Meet more Parkinson’s researchers! Explore our My PD Stories featuring PD researchers.

My PD Story

Helen Bronte-Stewart headshot
Researchers

Helen Bronte-Stewart, MD, MS

2026 Impact Award

Creating a New Brain Model of Good Gait to Improve Deep Brain Stimulation

Most people with Parkinson’s disease (PD) experience gait impairment, a symptom impacting their ability to walk. Some also experience freezing of gait, moments when they are temporarily and involuntarily unable to move. Together, these movement symptoms make simple activities like crossing a room or navigating a hallway difficult and dangerous due to the increased risk of falling. 

Deep brain stimulation (DBS) can help address movement symptoms and may help to reduce falls, but for some people it loses its effectiveness over time or does not help at all. Helen Bronte-Stewart, MD, MS, recipient of a Parkinson’s Foundation Impact Award, will dive deep into complex brain circuitry data to find why DBS may not help walking for some people. She also seeks to find new signal patterns that could be leveraged to improve DBS treatments for people with PD in the future.

“This research could transform deep brain stimulation treatment for Parkinson’s disease by making it a smart therapy that adapts to the needs and symptoms of the patient.” - Dr. Bronte-Stewart

As director of the Human Motor Control and Neuromodulation Laboratory at Stanford University, a Parkinson’s Foundation Center of Excellence, Dr. Bronte-Stewart has built a research team focused on analyzing how brain signals translate into movement. They are interested in how those signals are compromised by PD, and how treatments like DBS can be used to restore them.

For this study, Dr. Bronte-Stewart and her colleagues will analyze data from previous DBS clinical trials, which collected brain signaling and movement data from people performing a variety of tasks that triggered freezing of gait. Running this unique data through their advanced machine-learning programs, her team hopes to reveal new insights into how different brain signals—specifically, different types of brain waves—coordinate during effective movement and go awry during freezing.

This analysis will help Dr. Bronte-Stewart create a brain signal model of “good gait,” which could improve DBS treatments for walking by providing a better brain reference point. Finally, Dr. Bronte-Stewart and her team will apply this framework to understand and improve adaptive DBS treatments. The goal is when gait impairment occurs, the DBS implant could sense that the person is no longer within the “good gait” threshold and provide real-time stimulation to counteract the signals that are out of order. 

As a world-renowned leader in the development of adaptive DBS technology, Dr. Bronte-Stewart is excited about this support to help her team continue their pioneering work to improve walking in people with PD. 

“It is wonderful to be able to continue to use our DBS data to investigate the brain signals and circuits that contribute to gait impairment and freezing of gait in PD,” she said. “This award will enable us to continue our research into this complex cognitive-motor disorder that is one of the most debilitating features of PD, and I hope my lab can contribute to finding new therapies to address it.”

Meet more Parkinson’s researchers! Explore our My PD Stories featuring PD researchers.

My PD Story

Nora Bengoa-Vergniory
Researchers

Nora Bengoa-Vergniory, PhD

2026 Impact Award

Trying to Slow Parkinson’s by Targeting a New Type of Cell in the Brain

In Parkinson’s disease (PD), dopamine neurons in the brain break down over time, leading to progressively worsening symptoms. Most of these neurons affected by PD are found in the substantia nigra pars compacta (SNc) region of the brain. However, neurons are not the only type of brain cell in this region, leading researchers to wonder if other types of brain cells may play a role in PD progression.

Nora Bengoa-Vergniory, PhD, recipient of a Parkinson’s Foundation Impact Award, will investigate if oligodendrocyte progenitor cells (OPCs) could be an important go-between of PD progression in the brain. Previous research in her lab has shown that these OPCs become impaired by alpha-synuclein tangles, much like the surrounding dopamine neurons. Data suggest that OPCs could be functioning like a bridge for PD, helping to spread the tangles from one neuron to the next. If so, targeting them in new therapies could help slow PD progression.

Dr. Bengoa-Vergniory, from her lab at the Achucarro Basque Center for Neuroscience in Biscay, Spain, will test if a type of drug called PDGFRα inhibitors, which targets and shuts down cells like OPCs, can reduce the spread of alpha-synuclein tangles. By using OPCs and lab-grown neurons, she can quickly and efficiently observe how such treatment could be effective in the human brain.

“By defining the role of oligodendrocyte precursor cells (OPCs) in Parkinson's and evaluating PDGFRα as a potential therapeutic target, this research has the potential to reveal new avenues for intervention.” – Dr. Bengoa-Vergniory

After finding which PDGFRα inhibitor is most effective at blocking OPCs, Dr. Bengoa-Vergniory will then see if such a treatment is able to reduce the spread of alpha-synuclein in mouse brains. This experiment will be performed alongside similar mice tests to confirm if OPCs play a causal role in alpha-synuclein spread from neuron to neuron.

Nora seated at a computer workstation in a research lab.

Through this work, Dr. Bengoa-Vergniory will uncover how an understudied group of cells contribute to disease progression, with the hope of advancing PDGFRα as a druggable treatment target for PD.

“Despite Parkinson's being first described over two centuries ago, the contribution of OPCs has remained largely unexplored,” said Dr. Bengoa-Vergniory. “This funding will be crucial to enable my laboratory to address this critical gap in knowledge, contributing to the development of disease-modifying therapies that slow or halt disease progression.”

Meet more Parkinson’s researchers! Explore our My PD Stories featuring PD researchers.

My PD Story

Zachary Freyberg headshot
Researchers

Zachary Freyberg, MD, PhD

2026 Environmental Trigger Award

Using Toxin Exposures to Find Genes that Protect Neurons from Parkinson’s

In Parkinson’s disease (PD), dopamine neurons in the brain break down over time. This leads to the progressive and worsening symptoms seen in people with PD. However, scientists have observed that some dopamine neurons in the brain are naturally more resilient than others, staying functional while other similar neurons fall apart.

Zachary Freyberg, MD, PhD, a recipient of a Parkinson’s Foundation Environmental Trigger Award, is looking for the genetic reasons why some neurons are more resistant to PD than others. In doing so, he hopes to discover new ways to spread such resilience throughout the brain and protect against the disease.

From his research lab at the University of Pittsburgh, Dr. Freyberg is tackling this question from a highly relevant angle: by observing which dopamine neurons survive following exposure to PD-related toxins. His team has already found two genes in animal models that seem to be associated with neuron resilience: NDUFB1 and ULK1. These genes were more active in neurons that stayed healthy when exposed to pesticides linked to PD. When Dr. Freyberg and his research team turned off those genes, the neurons became vulnerable again, signaling their protective importance.

“By identifying and testing the genes and cellular structures that protect human dopamine neurons, this work may uncover new therapeutic targets and biomarkers for neuroprotection.” – Dr. Freyberg

Now, Dr. Freyberg will determine if NDUFB1 and ULK1 are also important for neuron protection against PD in humans. First, he will grow human dopamine neuron cells in a lab, modifying some samples to overexpress these two genes. After exposing these neurons to PD-related toxins, Dr. Freyberg will observe whether the neurons with more active NDUFB1 and ULK1 resist degeneration better than the unchanged neurons. 

Zachary sitting beside a microscope in a research lab.

He will also use a technology called cryo-electron tomography to perform microscopic CT scans of the neurons. This will let his team visualize how the biological machinery in the cells like mitochondria are affected by toxins with and without the protection of NDUFB1 and ULK1.

Lastly, Dr. Freyberg will analyze donated brain tissue from people with and without PD to see how NDUFB1 and ULK1 levels associate with healthy and disease-affected neurons. He hypothesizes that they will see higher levels of activity from those genes in the remaining dopamine neurons of PD-affected brains.

If Dr. Freyberg and his team find that NDUFB1 and ULK1 help protect dopamine neurons in humans, this research could open the door for new treatments that fight PD progression. 

“To be chosen and supported by the Parkinson's Foundation is deeply meaningful to me,” said Dr. Freyberg. “This award could lay the groundwork for therapies designed to slow, or even halt, the loss of dopamine neurons that drives Parkinson's disease.”

Meet more Parkinson’s researchers! Explore our My PD Stories featuring PD researchers.

Advancing Research

The "Golden Year" in Parkinson’s: Why Early Clinical Trial Participation Matters

🧠 What will you learn in this article?

This article highlights how the first year after a Parkinson’s diagnosis can be a valuable window for clinical trial participation.

  • The “golden year” refers to the first 12 months after a Parkinson’s diagnosis, when symptoms may be mild and medication may not yet be needed.
  • Before beginning PD medications, researchers can observe a person’s natural baseline and test treatments that may slow or stop PD progression.
  • Greater awareness and early conversations with care team members can help newly diagnosed people join clinical trials sooner.
A female patient talking with her doctor who is holding a tablet.

After a Parkinson’s diagnosis, many people start their journey by learning about treatments to help ensure their best quality of life. But according to experts like Robert Hauser, MD, from the University of South Florida, a Parkinson’s Foundation Center of Excellence, the initial months after a diagnosis also hold a unique window of opportunity that may go unnoticed by people newly diagnosed with Parkinson’s and their care team. 

In Episode 108 of the Parkinson’s Foundation podcast Substantial Matters: Life & Science of Parkinson's, Dr. Hauser discusses the "golden year," a time prior to starting Parkinson’s medications. This window may hold a key to finding therapies that could change the course of PD. 

What is the “Golden Year”?

The "golden year" refers to the period of about 12 months after diagnosis when a person is more likely to have mild movement symptoms and may not yet need Parkinson’s medications to manage activities of daily life. 

Before starting medications to manage Parkinson’s symptoms, the brain is at its natural baseline. People who have not started medications are sometimes called treatment naïve. Being treatment naïve gives researchers a window to test disease-modifying therapies — treatments designed to slow, halt or possibly reverse Parkinson's progression. 

Timing Matters

Current Parkinson's medications manage movement symptoms such as stiffness and slowness of movement. However, they do not treat symptoms that may appear after many years, such as cognitive changes or serious balance issues. An important need in Parkinson's research is finding a way to diagnose the disease as early as possible and halt its progression before these long-term symptoms arise. 

For a clinical trial to test how a new treatment works, researchers must track changes in a person’s PD over time. Entering a trial before daily medication becomes necessary gives researchers the clearest picture of how well the new treatment works. This makes the "golden year" a unique opportunity for both researchers and people with PD.

Despite the importance of trials in the first year after a Parkinson’s diagnosis, finding eligible participants is a hurdle. It remains a challenge because of these factors: 

  • Starting medication: Neurologists often start people with PD on medications right away, making treatment-free baseline observations unavailable.
  • Wait times: Delays in scheduling appointments with movement disorder specialists can cause newly diagnosed people to miss early trial eligibility. 
  • Awareness: Many health care professionals are unaware of clinical trials for newly diagnosed and treatment naïve people — or how important the golden year is to Parkinson’s research — and do not share trial information with people with PD.

What can we do?

To make the most of this critical time, collaboration is needed between people with Parkinson’s and their care teams:

  • People with Parkinson’s and families: If you or a loved one is newly diagnosed and do not feel an immediate need for medication to manage daily activities, ask your PD doctor about clinical trial opportunities for treatment-naïve individuals.
  • Healthcare providers: Doctors and care teams should discuss clinical trials with their newly diagnosed patients before prescribing PD medications. If symptoms are mild and manageable, allowing time to consider a trial can open doors to groundbreaking research. 
  • Improving access: Some medical centers are working to improve systems to get newly diagnosed people into appointments quickly, so they can explore trial options before starting standard treatment. 

Explore current clinical trials

What’s Next

Every approved Parkinson’s treatment exists today because people chose to voluntarily participate in clinical research in the past. Raising awareness about research options helps to ensure newly diagnosed people know what's available and to decide if research participation is the right choice for them. 

Whether you are newly diagnosed or familiar with Parkinson’s, explore opportunities to get involved with PD research today. Explore current studies now.

My PD Story

Edwin Castillo headshot
People with PD

Edwin Castillo

How Genetic Testing Gave Me Confidence to Move Forward with Deep Brain Stimulation

When you live with Parkinson's disease (PD), every treatment decision feels significant. You weigh the benefits, risks and uncertainty of what the future may hold. For me, one of the biggest decisions was whether to pursue Deep Brain Stimulation (DBS), specifically targeting the subthalamic nucleus (STN).

Like many people considering DBS, I spent countless hours researching. One topic that kept appearing was the relationship between the gene mutation linked to PD called GBA1 and cognitive decline after DBS. What I learned through genetic testing ultimately gave me greater confidence in moving forward with surgery.

What Is the GBA1 Gene?

Certain mutations of the GBA1 gene are the most common genetic risk factor for Parkinson's. Research has shown that people with Parkinson's who carry a GBA1 mutation may experience a faster progression of cognitive symptoms and may have a higher risk of developing dementia over time. 

In recent years, researchers have also explored how GBA1 mutations might influence outcomes after DBS. Studies have found that while people with GBA-associated Parkinson's generally experience excellent motor improvement from DBS, some may face a higher risk of cognitive and neuropsychiatric decline compared with non-carriers. 

The Value of Knowing More

One of the challenges of living with Parkinson's is uncertainty. We often hear statistics and probabilities, but those numbers can feel very impersonal.

Edwin and his wife

Deep Brain Stimulation is a surgical treatment used to help control PD movement symptoms, including tremor, stiffness, slowness of movement and medication fluctuations. For many, DBS can significantly improve quality of life and reduce dependence on medications. However, like any treatment, I had to weigh the potential risks and benefits of DBS. 

When I learned about the possible relationship between GBA1 mutations and cognitive outcomes after DBS, I naturally wondered: Do I have this genetic risk factor?

That question led me to PD GENEration.

How PD GENEration Helped Me

PD GENEration is a Parkinson's Foundation study that offers genetic testing and genetic counseling for people living with Parkinson's. The program helps people understand whether they carry genetic variants associated with Parkinson's. As a participant I underwent genetic testing and learned that I do not carry a GBA1 mutation.

That single piece of information did not eliminate all risks associated with DBS. No medical procedure is risk-free, and every person's Parkinson's journey is unique.

However, knowing that I was not a GBA1 carrier removed a significant concern that had been weighing on my mind. Based on current research, the increased cognitive risk observed in GBA1 mutation carriers was not a factor in my personal situation. 

Rather than making the decision for me, the genetic information helped me make a more informed decision.

Knowledge Replaces Fear

One of the most powerful aspects of genetic testing is that it can replace uncertainty with knowledge. Before receiving my results, I found myself asking:

  • Am I at higher risk for cognitive decline after DBS?
  • Should I reconsider surgery?
  • Am I missing important information that could affect my future?

After receiving my PD GENEration results, I had greater clarity. While I still needed to evaluate all the other factors involved in DBS, I felt more confident discussing treatment options with my neurologist and DBS team.

The information didn't guarantee a particular outcome. But it did provide something equally valuable: peace of mind.

Personalized Medicine in Action

One of the exciting developments in Parkinson's care is the move toward personalized medicine. Instead of treating every patient exactly the same, clinicians can increasingly use genetic, clinical and cognitive information to help guide treatment decisions.

Research suggests that genetic information, including GBA1 status, may help patients and physicians have more informed conversations about DBS, expectations, and long-term planning. 

For me, PD GENEration was an example of personalized medicine at work.

My Advice to Others Living with Parkinson's

If you are considering DBS, learn as much as possible, ask questions and have open conversations with your healthcare team.

Genetic testing may not be necessary for everyone, and it may not change every treatment decision. But for me, understanding my genetic profile helped remove some uncertainty from a major life decision.

Today, I view my PD GENEration results as one of the factors that helped me move forward with confidence. I did not learn that I was "risk-free." What I learned was that one important genetic concern, the GBA1 mutation, was not part of my Parkinson's story.

Sometimes knowledge doesn't change the destination. It simply makes the path forward a little clearer.

And when you're facing a decision as significant as DBS, that clarity can make all the difference.

Read Edwin's story in Spanish

Back to Top