2026 Parkinson’s Breakthroughs: Stopping Progression with LRRK2, Stem Cells, and the New Biomarker Revolution

Is 2026 the year we finally stop Parkinson’s in its tracks? In this high-energy,  episode of Live Parkinson’s – Live an Exceptional Life, I’m pulling back the curtain on the most historic year in Parkinson’s clinical research. We are moving beyond just managing symptoms with Levodopa and stepping into the era of Precision Medicine.

For decades, we’ve been fighting the "smoke" of Parkinson’s, but today, we talk about how science is finally putting out the fire.

In this episode, you’ll discover:

• The LRRK2 Milestone: Everything you need to know about the LUMA study results and how these new inhibitors are targeting the biological "switch" of PD.
• The Biomarker Revolution: How the α-Synuclein Seed Amplification Assay (αSyn-SAA) is allowing doctors to diagnose Parkinson’s years before a tremor even starts.
• Stem Cell Replacement: A deep dive into BlueRock and Aspen Neuroscience—are we finally ready to replace the neurons we’ve lost?
• AI & Wearables: How 2026 technology is giving you and your neurologist a 24/7 "biological fingerprint" of your symptoms.

The rules of Parkinson’s are being rewritten. The future isn't coming—it’s already here. Tune in to learn how you can benefit from these breakthroughs and continue to live your most exceptional life.

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 #ParkinsonsResearch2026 #LRRK2 #StemCellTherapy #ParkinsonsCure #AlphaSynuclein #PrecisionMedicine #LiveParkinsons #NeurologyBreakthroughs #Cl

Chapters

• 0:10 Mission And Bold Roadmap
• 2:20 Why 2026 Is A Turning Point
• 3:37 Biomarker Revolution Explained
• 7:18 Genetics Target: LRRK2 And LUMA
• 15:24 GLP-1 Drugs And LixiPark Results
• 18:47 Trials Reimagined: EJS ACT-PD MAMS
• 23:52 Regenerative Medicine: BlueRock Phase 3
• 27:53 Personalized Cells: Aspen ANPD001
• 31:48 Daily Life Now: Tavapadone And AI Wearables
• 36:46 Momentum, Optimism, And Community Resources

Transcript

SPEAKER_00: 0:10

Hello and welcome to Live Parkinson's Live an Exceptional Life. I'm your host, Chris Kustembotter, and I've been living an exceptional life with Parkinson's for the past 15 years. The mission of this podcast is to help as many people as possible to lead a great quality of life with Parkinson's. Now get ready because the rules of Parkinson's are being rewritten as we speak. Imagine a world where we can spot this disease a full decade before a single tremor even shows up. But we aren't just talking about spotting Parkinsons, we're talking about potentially reversing it. Today, I'm taking you deep inside the 2026 biomarker revolution and the mind-blowing world of stem cell transplants that are actually replacing lost neurons in human trials right now. We're pulling back the curtain on technology that makes the invisible visible, an irreversible, hopefully a thing of the past. Now, if you believe that the cure is a lifetime away, think again. The future is here and we're diving into it today. Wow, that sounds fascinating. I can't wait to see what we'll uncover on our journey. So let's lay out a roadmap of where we're going and where that's going to be taking us. So we're going to lead it off with why 2026 is a turning point and discuss a shift in philosophy and the power of data. Then we'll join the biomarker revolution and talk about detecting Parkinson's before the tremors even start. Then we'll explore disease modifying therapies designed to help us slow the clock, and as we know, the holy grail is a treatment that stops Parkinson's progression. Here we'll look at targeting genetics, the GLP1 story. Yes, the diabetes drugs that helps with weight loss as well, and accelerating clinical trials. Then we'll follow the twists and turns into regenerative medicine and look at replacing what is lost, and we'll focus on stem cell breakthroughs, and then in the final leg of our journey, we'll be focused on improving daily life, and we'll look at new symptom management drugs and AI wearables. Then we'll tie it all together. So if you're ready to take this journey, hop on and let's get the train rolling. Alright, let's start off with why 2026 can be viewed as a turning point in Parkinson's research. And we'll start off with the shift in philosophy and how Parkinson's is managed. Now Parkinson's was typically viewed as just a dopamine deficiency, so therapies were really just designed to help replace lost dopamine to help manage our motor symptoms. That's why Levadopa has been the gold standard since the late 1960s. Now researchers and clinicians are treating Parkinson's as a complex, multisystem, protein folding disorder. Now this is why areas like the gut brain access are being researched. So this change in philosophy is helping researchers target new areas in the search for a Parkinson's cure. Now the next key piece in the puzzle is using the power of data to drive research. The integration of artificial intelligence and large-scale genetic databases, like the PPMI study by the Michael J. Fox Foundation, helps researchers analyze data faster and identify links or commonalities. Now, of course, the data is all blinded, so there's no personal information being shared. Now, the use of large databases and the AI has helped accelerate the drug discovery by years. Now that we understand why 2026 is a turning point in Parkinson's research, let's begin our journey by looking at the biomarker revolution and how biomarkers were used in developing technology to identify people with Parkinson's before any initial signs of tremor occur. Now, for the past several decades, we waited for symptoms to appear. And still, oftentimes it took multiple doctor visits to get a diagnosis. As we all know, a lot of times we go with symptoms and they couldn't figure out what was going on until finally enough of the symptoms showed up that they said, Oh, you have Parkinson's disease. Now we're looking at what I'll call the seeds of the disease, specifically the alpha senuclein seed amplification assay. Now, this is a biological test that can detect abnormal alpha senuclein proteins in spinal fluid and increasingly in skin and blood years before tremors start. Now there were several studies that were evaluated not only how well could the assay predict results, but also if they could determine the progression rate of Parkinson's for that individual. Now the first study was a systematic review and analysis 2025 titled Alpha Sinuclean Seed Amplification Assay in Parkinson's Disease. It was a systematic review and network meta-analysis that was published in Clinics and Practices. Now this study looked at the assay's accuracy in distinguishing Parkinson's disease from controls using cerebrospinal fluid, blood, skin, extracellular vesicles, saliva olfactory, which is nose mucosa, GI tract, and submandibular glands. Now the assays showed strong diagnostic performance in distinguishing Parkinson's from controls across various tissue types. Overall, the assays demonstrated high sensitivity 86% and specificity 92%. Now, spinal fluid, skin, blood, and the ECU yielded the highest diagnostic accuracy with sensitivity and specificity approaching or exceeding 90%. What do the alpha senuclein seed assessment assays actually measure? The assays detect misfolded alpha-sinuclein seeds, the pathological form that drives Lewy body formation. So the way it works is it works by amplifying tiny amounts of misfolded protein until they become detectable. Now, besides accuracy, there was another study that looked at the rate of disease progression. And that study was titled Diagnostic and Prognostic Value of Alpha Sinuclein Seed Amplification Assay, Kinetic Measures in Parkinson's Disease, a longitudinal cohort study. Now that was a mouthful. And that was published in the journal Lancet in 2025 in July. And it found that the seed amplification assay, kinetic parameters, especially lag time and growth rate, correlates with the rate of motor progression, rate of cognitive decline, and likelihood of developing freezing of gait. They also found faster seeding kinetics correlated with more aggressive disease biology and slower kinetics related to slower clinical progression. So this is the first time that the seed amplification assay is not just diagnostic, but also prognostic. So the data is nice, but what does that mean for the Parkinson's community? Well, the seed amplification assay is the first biomarker that directly detects the core pathology of Parkinson's. It's becoming central to early diagnosis, clinical trial enrollment, and helping to track disease progression and understanding the biological subtypes of Parkinson's. And it may soon help us identify who will benefit most from disease modifying therapies. Alright, let's move into our next area of research, and that's disease modifying therapies. As I mentioned earlier, this is the holy grail of Parkinson's research, being able to identify therapies that stop the progression of Parkinson's. Now there are three major pathways that are being explored. Targeting genetics, and they're looking at the LRRK2 and GBA genes. Then we'll look at the GLP1, which is a class of diabetes drugs, which has also helped people with weight loss because it suppresses appetite, so you eat less. And then finally, accelerating clinical trials. And let's start with the first pathology, which is targeting genetics. There currently is a study called the LUMA study, L U M A, which is testing a molecule designed to inhibit the LRRK2 enzyme, which is overactive in many patients with Parkinson's. Now before we get into the study, let's talk about what LRRK2 is. LRRK2 stands for leucine-rich repeat kinase 2. Now you can use that for trivia if you want, but I'm not going to remember that. And it's arguably the most talked-about biological target for Parkinson's. LRRK2 is not just a Parkinson's gene, but think of it as a high-stakes biological switch that controls trash clearance and energy production systems within your brain cells. So technically, LRRK2 is a large complex protein that's found throughout the body, but it's most active in the brain and the immune system. It acts as a kinase, which is a type of enzyme that acts like a biological formin, proteins to form their activity either in the on or off position. It's involved in autophagy, and that's the cell's internal recycling system that breaks down old or toxic proteins and helps make your mitochondria healthier. So it helps to ensure that the power plants, which are the mitochondria, the power plants of the cell, of your neurons are producing energy efficiently. Okay, that's great, Chris, but why is this so important in Parkinson's? Well, the problem starts when the switch gets stuck in the on position. In certain people, a mutation in the LRRK2 gene causes the enzyme to become hyperactive. Now, when it's hyperactive, it's like the Foreman yelling too many things at one time. Now, I don't know about you, but if somebody starts yelling too many things at me at one time, I get confused and I kind of freeze up and don't do anything. So this causes several catastrophic roadblocks in the neuron. First, it can cause protein traffic jams. Toxic proteins like alpha-sinuclein clump together because the recycling system can't keep up. Second, energy failure. The mitochondria or the powerhouse of the cell becomes damaged, leaving the cells exhausted and vulnerable. And then next is neuroinflammation. An overactive LRRK2 enzyme triggers the brain's immune cells, also known as microglia, to overact, causing chronic inflammation, which further damages the neurons. Okay, this brings us to some exciting new research in 2026. Now let's talk about the LUMA study. What is it and why it matters for LRRK2 and Parkinson's? Now the LUMA study is one of the most important ongoing clinical trials testing whether targeting LRRK2, a major genetic contributor to Parkinson's, can also slow Parkinson's progression. It's part of a broader program by Denali Therapeutics and Biogen to evaluate a compound called BIIB22, and that will be on the quiz, also known as DNL 151, and it's a selective LRRK2 inhibitor. Alright, so let's take a look at the Luma study. According to Clinicaltrials.gov, this is a study to learn about the safety of BIIB122 tablets and whether they can slow the worsening of early stage Parkinson's disease in adults between the ages of 30 and 80. Now Biogen is the sponsor as well as denali therapeutics. Now this study includes both LRRK2 positive and LRRK2 negative participants, making it a broad early Parkinson study. Now this matters because LRRK2 mutations are one of the most common genetic causes of Parkinson's, because they increase LRRK2 kinase activity, which disrupts lysomal function, which is a key pathway in Parkinson's. So by inhibiting this LRRK2, they may restore lysomal health and potentially slow neurodegeneration. So this compound or this tablet they're taking, BIIB122, is designed specifically to do that. So the study design, according to clinicaltrials.gov and Neurology Live, includes 640 adults between the ages of 30 to 80 that have been diagnosed with PD within the last two years. The patients have early stage PD and only both with or without LRRK2 mutations. And then the patients are randomized to take either daily BIIB122, 225 milligrams, or placebo. Now the study duration is 48 to 144 weeks, so one to three years. And the primary outcome measures is time to worsening of PD symptoms, measured by the UPDRS scale. And secondary outcomes include activities of daily living, safety and tolerability, and biomarker changes. And that includes lysomal markers, LRRK2 activity. Now the results are expected, at least major readouts in 2026. And there's also another study called the Beacon Study, B E A C O N study, which is a phase 2A trial specifically for LRRK2 positive people with PD. And the purpose of this study is safety and biomarker effects of the BIIB122. So together, these trials will help determine whether LRRK2 inhibition is safe and whether it slows Parkinson's progression and whether LRRK2 positive patients benefit more than others. So this is really a major step forward for patients and to see if it benefits them. And so it's a major step forward in precision medicine and Parkinson's. So why does this matter for the Parkinson's community? Well, if BIIB122, and again that's going to be on the quiz, works, it could, and that's the keyword, could become the first disease modifying therapy targeting at genetic pathway, a treatment that slows PD progression and a therapy tailored to people with LRRK2 mutation, but possibly for all early stage people with Parkinson's. All right, now let's look at another potential disease modifying therapy, GLP1 drugs, which are used in the treatment of diabetes. And you've probably seen these advertised on TV and heard them talked about because they're often used as weight loss drugs as well. Now, one of the first phase three trials involved in a GLP1 known as xenotide, and the results published in February 2025 were disappointing. So the focus has shifted to another GLP1 compound called lixycinatide. Now, this is a once-daily injectable GLP1 receptor agonist originally approved for type 2 diabetes. Now, because GLP1s reduce inflammation, improve mitochondrial function, and they can cross the blood-brain barrier, they are being repurposed as neuroprotective therapies for Parkinson's. Now, the major clinical program evaluating lexicenoide in PD is the LixiPark trial. Now, this trial was published in the International Parkinson's and Movement Disorder Society moving along issue in September of 2024. Now, it was the trial of lixisenoide in early Parkinson's disease, also called the LexiPark study. Now, this was a double-blind placebo-controlled trial found in 21 centers in France by the Toulouse University Hospital. And the primary objective of the LexiPark study was to assess the effect of lixyenoti on the progression of motor disability in people with early Parkinson's. There were 150 participants within three years of PD diagnosis on stable symptomatic medications and without motor complications, and they were randomized to eat one-to-one to either lixisenoide or placebo once daily for 12 months, followed by a two-month washout. Now the results at 12 months they looked at the MS MDS UPDRS part 3 scale on state scores, that was a primary endpoint, had worsened by 3.04 points in the placebo group and remained at baseline. There was actually a slight negative change of 0.04 points in the elixotide group. So the difference between the groups was significant. So the mean UPDRS motor scores in the practically defined off state following washout were lower on the lixosenotide than they were on the placebo, supporting a potentially neuroprotective mechanism. Now the safety profile was similar to that of diabetes patients. Now the author summarized the study by saying lixisenotide reduced motor disability progression in patients with early PD, suggesting a disease modifying effect that warrants further investigation in larger trials. Now, in the meantime, they say we don't recommend the use of this GLP1 agonist for PD until large trials have confirmed our results. And one of the keynotes is that Sanafir removed lexisanotide from the market for diabetes mellitus in 2023, and the drug currently only exists in a fixed combination which is bound to insulin, which isn't suitable for PD patients. Alright, let's move into the next segment is disease modifying therapies, and that is accelerating clinical trials. And let's discuss a new era in Parkinson's clinical trials. Now in 2025, researchers in the UK launched what may be the most ambitious Parkinson's trial ever attempted. It's called the Edmund J. SAN for Accelerating Clinical Trials on Parkinson's Disease, also called the EJS Act-PD trial. Now, this isn't your traditional clinical trial. It uses a multi-arm, multi-stage design, which is a revolutionary approach that allows scientists to test multiple potential disease-modifying drugs at the same time, all compared against a single shared placebo group. Now, the nice thing about doing the clinical study this way is this design dramatically reduces time, cost, and participant burden while speeding up the discovery of therapies that might actually slow Parkinson's progression. So then that begs the question what makes the MAM design revolutionary? Well, I'm glad you asked. Instead of running one trial per drug, which can take five to seven years each, this new multi arm platform allows them to test several. Drugs simultaneously. It uses one placebo group for all the arms and it performs interim analysis to quickly identify winners and drop the losers and allow new drugs to be added without restarting the entire trial. So this means that the trial can run continuously for years, cycling through new therapies as evidence emerges. Now it's the fastest way we've ever had to find a disease modifying therapy for Parkinson's. And let's look at the first drugs being tested in 2025 and 26. This is based on treatment selection research published in Movement Disorders with the study Treatment Selection and Prioritization for the EJS ACT PD MAMS Trial Platform. Now the first three drugs chosen for the platform are telemosartan, which is a blood pressure medication which showed strong evidence for mitochondrial protection and anti-inflammatory effects. Preclinical data suggests it may protect dopaminergic neurons. The next is herozosin, and that's a prostate medication which activates PGK1, boosting cellular energy metabolism. And multiple studies showed lower PD risk in users of that particular drug. And the third, urosodioxycholic acid, or UDCA. Now that's a mouthful. It's a bioacid drug used for liver disease. It improves mitochondrial function and has been previously shown to rescue dopaminergic neurons in lab models. Now these were selected from 293 candidate compounds that they narrowed down through a rigorous scoring system evaluating mechanistic rationale, safety, and prior clinical evidence. Now there was a total of 14 top-ranked compounds, and they're starting with these three. So let's look at how the trial works. According to the official trial registry and the and Cure Parkinson's materials called Edmund J. Safra Accelerating Clinical Trials and Parkinson's, a multi-arm, multi-stage platform test that was updated in October 2025 in the Good Clinical Practices Network and the U.S. Clinical Trial Registry. Now the participants are going to be randomized assigned to telemasartan, pterozosin, or placebo. A third active arm with the UDCA is added after year one. Participants are going to be followed for 36 months or three years. And the nice thing is that most visits can be done remotely, making participation for the patients a lot easier. Now, if a drug shows strong benefit at interim analysis, it's moved forward. If it shows no benefit, it's dropped and it's going to be replaced with a new candidate. So this helps create a continuous pipeline of therapies that are going to be tested. Something that Parkinson's research has never done before. So here's why this trial really matters. This is the largest Parkinson's research trial ever launched in the UK, according to Parkinson's.uk.org. It represents a shift toward repurposed drugs with strong biological rationale. Now, what I mean by repurposed drugs is that it's a drug that's been approved for use in another disease state, in this case, blood pressure for the prostate and for bioacid for liver disease. A patient-centered design with remote visits and broad eligibility, and it's global it's a global model for future neurodegenerative disease trials. So for the Parkinson's community, this is a major step towards finally identifying a therapy that slows or stops progression. All right, let's move into our next category, which is regenerative medicine, and we're going to be looking at replacing what's lost. So the question they're trying to answer is if we can't stop cells from dying, can we grow new ones? So let's look at stem cell breakthroughs. And we'll start with Blue Rock's Therapeutics Phase 3 cell therapy breakthrough. Now, this is a new frontier and it's replacing lost dopamine cells. It's one of the most exciting developments in Parkinson's research right now, and it's coming from Blue Rock Therapeutics, a bear-owned cell therapy company. Now their investigational therapy called BEMDane Procel is designed to replace the dopamine-producing neurons that are lost in Parkinson's disease. Now, this is not a drug, it's not a gene therapy, it's actual dopamine neurons grown from pluripotent stem cells surgically implanted into the petumen, the brain region most affected by PD. Now, as of 2025, this therapy has officially moved into a pivotal phase three trial, making one of the biggest milestones ever for regenerative medicine and Parkinson's. Now Blue Rock completed a phase one study with 12 participants, and the results were extremely encouraging. It was well tolerated with no serious adverse events related to the therapy at 24 months. It showed encouraging trends toward improvement in motor symptoms, and the participants showed signals of healthier movement scores compared to baseline. The findings were strong enough for the FDA to grant the therapy RMAT designation, a special pathway reserved for highly promising regenerative treatments. Now, the phase three trial that Blue Rock Therapeutics is now launching, called the Expedite EXPD ITE 2, is the first ever registrational phase 3 trial for an allogenic pluripotent stem cell-derived therapy. Now, pluripotent stem cells are master cells. They can turn into almost any cell type in the human body. And really they have two abilities that they can become like any cell type, like they can be a dopamine neuron, they can be a heart cell, they can change into anything. And the second characteristic of these is that they can self-renew, meaning that they can divide over and over and still stay in their stem state. Okay, back to the expedite study. The key features of this trial drug is it's a randomized double blind sham surgery controlled with 102 participants with moderate Parkinson's. The primary endpoint is change in on time without troublesome dyskinesias over 78 weeks. The secondary endpoints are objective movement measures, activities of daily living, safety and tolerability. Now the first patient was treated in September 2025, marking the official start of this pivotal study. So why does this matter for Parkinson's community? Well, if BEMDANE Procel succeeds, it could become the first therapy to replace lost neurons. It could be a treatment that restores function rather than compensating for loss, which typically the drugs that we take now, Carbodopa Levadopa, do. And it's a major step towards true disease reversal, not just symptom management. This is the closest the field has ever come to cell replacement therapy that could fundamentally change the trajectory of Parkinson's disease. Alright, now let's look at another cell therapy from Aspen Neuroscience and discuss the rise of autologous cell therapy and a personalized approach. And what this is is using your own cells to restore dopamine. While companies like Blue Rock Therapeutics are implanting donor-derived dopamine neurons, Aspen Neuroscience is taking a completely different and incredibly promising approach. Their therapy, ANPD001, is made from your own skin cells. Those cells are reprogrammed to induce pluripotent stem cells, remember those are the master cells that can turn into anything, and then they're turned into dopaminergic neuronal precursor cells, the exact type of cells that are lost in Parkinson's. Now, because the cells come from you, the body recognizes them. This means no immunosuppression, no anti-rejection drugs, and therapy, and it's a therapy that is truly personalized to you. This is the first multi-patient, multi-center, autogalous cell replacement trial ever conducted in Parkinson's. And what we know from the Aspiro phase 1 and 2A trial in terms of safety and tolerability, the first three treatment patients in the aspiro trial showed no major safety issues, no hemorrhages, or serious surgical complications, no severe graft-induced dyskinesia, only mild procedure-related side effects such as back pain, incision site discomfort. Now, this data comes from the publication by Aspen Neuroscience titled Aspen Neuroscience announces six-month aspiro phase one and two A clinical trial results of personalized cell therapy for Parkinson's disease. And this is dated May 7th, 2025. It was also published in Neurology Live on the same date. Now the Aspira study showed early signs of clinical improvement. At six months, patients demonstrated improvement in motor symptoms, better off time, and good on time. Clinicians reported and patient reported improvements. These gains were seen without immunosuppression, which is a major differentiator from donor-derived cell therapies. So, how far is this therapy towards advancing toward commercial readiness? Well, in 2025, Aspen Neuroscience announced the initiation of Cohort 3 using a commercial ready formulation of ANPD001, a new cryo-preserved thaw and inject product simplifying surgic workflow, scalable manufacturing platform using machine learning guided cell production, and a precise delivery system with MR1 guided submillimeter accuracy. And this announcement comes from Aspen Neuroscience titled Aspen Neuroscience Initiates Cohort 3 in a Spiro Phase 1 slash 2 trial, highlighting commercial formulation of ANPD001 and its transformative potential for Parkinson's disease. And this was dated in September 25th, 2025. So this marks a major step toward late stage trial and eventual real world usage. Now, here's why autoanalogous therapy matters for the Parkinson's community. Autologous therapy could become a game changer because no immune rejection, there is no lifelong immunosuppressive drugs that are needed, cells are genetically matched to the patient, potential safer long-term integration, and a truly personalized regenerative medicine. Now, if successful, ANPD001 could offer a future where a person's own cells are used to rebuild the dopamine system. A deeply intuitive and elegant solution. Alright, now we've covered a lot of new research. Now let's round it out with what's new that can help us improve our daily life and look at new symptom management and AI. Now, I want you to keep in mind that research isn't just about the cure. Now, well that's the ultimate goal. It's also about the now. What can we do now? So let's look at what's on the front burner that can help us in 2026 live better. And let's lead it off with Tava Padone. And that's a D1 slash D5 agonist. Now, Tavapadone is an investigational selective dopamine D1 slash D5 receptor, partial agonist, and has a new twist on the classic dopamine agonist approach. Unlike current dopamine agonists like Framopexol and Ropenerol that broadly stimulate D2 family receptors, Tavapadone targets D1 and D5 receptors, which play a key role in motor control circuits. Now, according to the Michael J. Fox Foundation, a new drug application or NDA has been submitted for Tavopadone, which is a once-daily oral treatment for the tremors, slowness, and stiffness, which are the motor symptoms that occur in Parkinson's. And the article notes, unlike the other dopamine agonist, tavapedone selectively stimulates only two of the five dopamine receptors in the brain. This more focused action may ease Parkinson's motor symptoms, potentially, and that's the key word, without adverse effects that some other dopamine agonist can cause, such as impulse control disorders like gambling, spending, or overeating, leg swelling, or excessive daytime sleepiness. In clinical trials, Tevapadone improved motor symptoms in people in early Parkinson's and increased on time for people already taking Levadopa. Researchers hope its targeted approach may offer stronger symptom control with fewer side effects, although that still needs to be proven. Now, if approved, Tevapadone can become a new option across the Parkinson's journey from early treatment to managing motor fluctuations, giving people another tool to help you stay active, independent, and in control. All right, now let's round out this segment talking about AI wearables. And I want to talk about one called stat on. And one of the biggest challenges in Parkinson's care is that your symptoms just don't happen in the doctor's office. They happen at home, at work, and throughout your day. And for decades, neurologists have had to make major medication decisions based on, you know, a 20-minute snapshot with you sitting in the office every six to nine months. And if you think about it, that's like trying to understand a whole movie by just watching a single frame. Now, here's where AI wearables like Sat On are changing that Saton is a small, waste-worn medical device that uses artificial intelligence to track your real-world symptoms 24 hours a day. Now, it doesn't just guess, it measures. It captures your on time, your off time, gate changes, freezing episodes, and even medication patterns with remarkable accuracy. Now, what makes staton so powerful is that it gives your doctor an objective, continuous report, how you're really doing, not how you're remembering what you did, just how you felt this morning, but how you actually behaved across an entire week. So this means your neurologist can fine-tune your medication timing with near perfection. Now the research backs this up. A 2025 study in PLOS1 found that continuous monitoring with STAT on can improve your symptom assessment, optimize your therapy adjustments, and even reduce healthcare costs by catching problems earlier and preventing complications. Now, if you're interested, this comes from the journal PLOS 1 titled Improving Parkinson's Disease Management Through Wearable Technology, a cost-benefit perspective. So this is a moment where wearable technology stops being cool and actually starts becoming standard care. Now, for people with living with Parkinson's, StatOn offers something we've never had before: a clear, objective picture of your day-to-day life and a chance to build a treatment plan that truly fits your real world. Not what you remember, but actually real world data that the doctor can use. Now, StatOn is commercially available, but not in the same way as a consumer device would be. It's marketed as a medical grade Parkinson's Holter monitor through Sense4Care and partner services like Life Neurotech. And Life Neurotech offers Staton directly to patients as part of a home monitoring prescription service delivery to the device to users at home. Staton is configured and used by neurologists or healthcare professionals, and the device must be set up by a clinician who enters your patient-specific parameters like your age, your home and yard, stage of Parkinson's, leg length, etc. Now, if you have an Apple Watch and you want to track your tremors and dyskinesias to share with your doctor, I use and recommend the Strive PD app. It also provides medication reminders, tracks your physical activity, and asks how you're doing on a daily basis. It's a free app that I use every day. Now to learn more, listen to my podcast with Dr. Amanda Hare from Rune Labs titled Transforming Parkinson's Care with Real Time Data. Listen, if there's one thing that you take away from today's episode, let it be this. The momentum has shifted. We're no longer just reacting to Parkinson's in 2026. We're finally playing offense. The science we discussed today, from the biomarker breakthroughs to the neurons being grown in labs, isn't a someday dream. It's the reality on the ground and we're gaining right now. But remember, while researchers are working in labs, your job is to keep moving on the ground. So keep exercising, keep advocating, and keep demanding the precision care that you deserve. Now the future is bright, the research is historic, and you have the every reason to be optimistic. So continue to learn more on your Parkinson's journey. Join the Live Parkinson's community by visiting LiveParkinsons.com and subscribing to the free monthly newsletter, which is filled with the latest research and upcoming educational events. And you can also get other free resources like the free nine balance exercises to help you improve your balance, as well as a number of articles. Now, if you want to support my mission of helping people to deliver a great quality of life, consider supporting the show by clicking the support the show link in the description or by donating on my Kofi page, kofi.com slash libparkinsons. Your help allows me to continue doing research and providing free resources to the Parkinson's community. Also, check out my new 30-day tip challenge on my YouTube channel, where for 30 days I'm posting a daily tip based on research to help you live your best life. So until next time, stay healthy, stay strong, and live your best life with Parkinson's. See you soon and thanks for listening.