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Phoenix, Arizona • May 2026
Randy L. Thurman, CFP®, CPA/PFS™

I am a retirement planner by profession and a Parkinson’s patient by circumstance. So
when I travel halfway across the country to spend a week surrounded by the world’s
leading Parkinson’s researchers, neurologists, patient advocates, and fellow people with
PD, I pay attention — with both hats on. The 2026 World Parkinson’s Congress in
Phoenix was, without question, one of the most information-dense and emotionally
resonant weeks of my life.
What follows are the twenty things that stuck with me most. Some will give you hope.
Some will keep your expectations in check. And a few might make you laugh. That last
category matters more than you think.

  1. Day Zero: The Blood Test Is the Holy Grail
    The conference technically started on Day Zero, and the opening session set the tone for
    everything that followed. Dr. Laura Parkkinen from Oxford presented on the biology of
    Parkinson’s disease — how the protein alpha-synuclein misfolds into toxic clumps in the
    brain, how the disease spreads through those brain cells over years before any
    symptoms appear, and how a new type of laboratory test called a Seed Amplification
    Assay (SAA) can detect whether the protein is already in its dangerous, spreading form
    — in spinal fluid, skin, and even stool. The field, she said, is now moving toward
    diagnosing Parkinson’s based on what is actually happening inside the body rather than
    waiting for tremors and stiffness to show up.
    Her description of a blood test for Parkinson’s as “a holy grail” stuck with me. The goal
    is a simple, inexpensive blood draw that can detect the disease before a single symptom
    appears — giving doctors years of runway to intervene. We’re not there yet. But we are
    closer than we’ve ever been. As a patient and a planner, I find that combination of
    honesty and optimism exactly right.
  2. Pickleball Was There — and It Belongs
    I will confess that I played pickleball at the conference (because of course I did) and I
    picked up a handout from an exhibit booth called Pickleball for Parkinson’s that is
    developing a program called “Pick It Up.” The mission: train pickleball instructors on
    how to help players with PD play safely, effectively, and confidently. Given that
    pickleball is arguably the fastest-growing sport in America, has relatively low injury risk,
    and demands the exact combination of footwork, hand-eye coordination, and social
    engagement that researchers say is beneficial for Parkinson’s, this program deserves
    more attention than it got.
    Rock Steady Boxing — a non-contact boxing fitness program designed specifically for
    Parkinson’s — had a prominent presence at the conference as well, which reinforced a
    theme I heard all week: exercise is not optional. The specific form it takes matters f
    less than the fact that you enjoy it enough to keep doing it.
  1. Parkinson’s Is Not One Disease — It’s Several
    One of the most intellectually satisfying sessions of the week was actually a back-to-back
    pair: Dr. Sam Fereshtehnejad from the University of British Columbia on clinical
    subtypes, followed by Professor Charalampos Tzoulis from Bergen, Norway on
    biological subtypes. The short version: no two Parkinson’s patients are alike, and the
    differences between them are not just cosmetic — they reflect genuinely distinct
    biological mechanisms that are likely to require different treatments.
    Dr. Fereshtehnejad’s research identified three clinically distinct groups based on
    symptoms beyond the classic movement problems: a Diffuse subtype (early REM sleep
    behavior disorder — the condition where you physically act out dreams — along with
    blood pressure drops when standing and early memory changes — faster progressing), a
    Motor/Slow Progressive subtype (primarily tremor, fewer non-movement symptoms,
    slower decline), and an Intermediate group in between. Most of us have never been told
    which subtype we are. That is about to change.
    Professor Tzoulis added the biological layer: his research group discovered that roughly
    20 to 25 percent of people with Parkinson’s who have no known genetic cause actually
    have a distinct disease driven by failing energy production in their brain cells — a
    subtype he calls MitoPD, for mitochondrial Parkinson’s. These patients are more likely
    to be female and more likely to have the slower-moving, rigid form of the disease rather
    than tremor. His dry comment when asked how we test for this in living patients: “We
    can’t be taking brain samples from living people. Well, we can, but we shouldn’t.” He is
    working on a blood test. Watch this space.
  2. Stem Cells: Japan Is Selling What the Rest of the World Is Still Testing
    Professor Roger Barker from Cambridge delivered what was easily the most carefully
    balanced session on stem cell therapies I have ever heard. The history goes back to the
    1980s: transplanting dopamine-producing cells from donated fetal brain tissue into
    patients in Sweden produced stunning results in a handful of people — two returned to
    near-normal function for 15 years and stopped all medication. But overall, only a third
    of patients showed meaningful benefit, and the supply of fetal tissue is essentially
    impossible to scale.
    The current era uses stem cells grown in a lab and converted into dopamine-producing
    neurons. Four published trials covering 33 patients have shown the cells are safe and
    produce some clinical benefit at higher doses. The BlueRock Therapeutics Phase 3 trial
    is now enrolling 102 patients and represents the most rigorous test to date.
    Then there is Japan. Thanks to its approval process, a commercial stem cell therapy is
    already available there — at a reported cost of $350,000. Professor Barker received a
    LinkedIn message informing him of this price. His point to the audience was direct:
    “You should never have to pay for a stem cell therapy. If you are, you need to seriously
    look into that.” He was not subtle about it, and he shouldn’t be.
  1. Cannabis: Good for Sleep, Modest for Everything Else
    A palliative care physician who has practiced in both Colorado and Rochester delivered
    one of the more refreshingly honest sessions of the conference on cannabis and
    Parkinson’s. His opening made the parameters clear: he hasn’t inhaled, and no one is
    paying him to sell marijuana. What followed was a fair-minded tour through the
    evidence.
    For the core motor symptoms of Parkinson’s — tremor, stiffness, and slowness — the
    human trial evidence is either negative or too small to draw conclusions. Cannabis
    affects the brain in ways that are biologically interesting for Parkinson’s, and animal
    studies look mostly positive, but the human trials have been too small to tell us much.
    There is a Czech survey showing 31 percent of cannabis users reported tremor
    improvement, but the speaker noted that has not matched his experience with US
    patients.
    For non-motor symptoms — the ones that don’t involve movement — the picture is more
    encouraging. From his palliative care practice, he reported consistent benefit for sleep,
    appetite, nausea, pain, and anxiety. He recommends CBD over THC for most patients
    because THC risks worsening apathy and can trigger anxiety or even hallucinations.
    Start low, go slow, stay with the same dispensary (product consistency matters
    enormously), and — critically — tell your neurologist. He described colleagues who
    could not figure out why a patient’s motivation and energy were getting progressively
    worse, only to eventually learn the patient had been using a lot of cannabis to treat their
    symptoms. When cannabis directly stimulates certain brain receptors, it suppresses
    dopamine — the last thing a Parkinson’s patient needs more of.
  2. Diet: The Mediterranean Diet Has Two Clinical Trials. Two.
    Dr. Fiona Lithander from the University of Auckland gave what was probably the most
    clarifying talk of the conference on nutrition. She came with a strict rule: she would only
    discuss gold-standard clinical trials — studies where participants were randomly
    assigned to a treatment or a control group — conducted in people with Parkinson’s. No
    animal studies, no population data, no extrapolation from other diseases.
    The Mediterranean diet — which is the dietary pattern with the most evidence for
    Parkinson’s — has exactly two such trials globally. Two. One showed improved cognitive
    scores and a better disease progression measure over ten weeks. One showed reduced
    constipation and lower gut inflammation over eight weeks. Both are promising. Both are
    tiny. There is no officially recommended diet for Parkinson’s disease, and anyone who
    tells you otherwise is running ahead of the evidence.
    What this means practically: eat across all food groups, maintain a healthy weight, eat
    fiber for gut health, and nudge toward Mediterranean patterns — more olive oil, more
    fish, more vegetables, more nuts — without treating it as a rigid prescription. You do not
    need to live in the Mediterranean to eat this way.
  1. Combining Diets: Promising But Hard to Stick To
    The most innovative dietary research presented was a Canadian trial from the
    University of British Columbia that combined the Mediterranean diet with a ketogenic
    approach. The Mediterranean diet is high in fiber and anti-inflammatory foods. The
    ketogenic diet forces the body to burn fat instead of carbohydrates, producing an
    alternative fuel called ketone bodies that may help brain cells that are struggling to use
    their normal energy source. The idea was to get the benefits of both at once.
    The results were encouraging on safety: no serious adverse events, no worsened blood
    lipids in the combination arm. But adherence — meaning whether people could actually
    stick to the diet — was a genuine problem. Participants found the ketogenic restriction
    extremely difficult to maintain, and the dropout rate was high. Dr. Lithander noted —
    with some humor — that even at the conference itself, you could not easily find
    ketogenic-compliant food. The results on whether it actually helped are still
    forthcoming; what has been published so far is only the safety and feasibility data.
    Her caution on the ketogenic diet alone bears repeating: six trials have been completed,
    with documented concerns including vitamin and mineral deficiencies, raised blood
    cholesterol, weight loss from reduced appetite, and — in one New Zealand trial —
    worsened tremor and rigidity in the first four weeks. If you want to try ketogenic, do it
    with a dietitian watching your numbers.
  2. Exercise Is Not Negotiable — and 80 Percent Is the Magic Number
    This message was delivered in multiple sessions by multiple researchers, and by the end
    of the week it had hardened into something close to dogma: regular aerobic exercise at
    moderate-to-vigorous intensity is the single most powerful non-drug treatment for
    Parkinson’s disease. Dr. Daniel Corcos from Northwestern presented data from four
    studies showing that people with Parkinson’s who exercised at 80 to 85 percent of their
    maximum heart rate showed zero disease progression on brain scans that measure the
    health of dopamine-producing cells — over the entire study period. Not slowed
    progression. Zero.
    JB Choi — a patient advocate who was diagnosed in 2003, hit rock bottom by 2011, and
    then discovered a forced exercise program — was one of the more powerful voices of the
    week. By 2018 he was completing ultramarathons. His primary workout: 45 minutes at
    80 percent of maximum heart rate, five days a week. His backup session: resistance
    training. His philosophy: “We don’t rise to motivation. We fall to preparation.”
    The American College of Sports Medicine guidelines for Parkinson’s call for at least
    three days a week of aerobic exercise at moderate-to-vigorous intensity, plus strength,
    flexibility, and balance work. People with Parkinson’s are currently 30 percent less
    active than healthy adults of the same age. That gap is costing people years of quality
    life.
  1. The Science Behind Why Behavior Change Is So Hard
    Dr. Matt Buman from Arizona State University delivered the behavioral framework
    session that preceded the exercise and nutrition talks, and it was arguably more
    important than either of them. His thesis: behavior change is a design problem, not a
    willpower problem. And for people with Parkinson’s, it is also a brain chemistry
    problem.
    Parkinson’s depletes dopamine not just in the motor areas of the brain but also in the
    reward and motivation circuitry — the part of the brain that evaluates whether
    something is worth the effort. When this system is impaired, the brain overestimates the
    effort required to start a task and underestimates the anticipated reward. The result is
    clinical apathy — not laziness, not lack of discipline, but a chemical disconnection of the
    brain’s start button. Telling a patient with Parkinson’s-related apathy to just try harder
    is about as useful as telling someone with a broken leg to walk it off.
    His solution was a diagnostic framework called COM-B (Capability, Opportunity,
    Motivation) for identifying exactly which barrier is preventing a behavior, and a
    Stanford-developed system called the Fogg Behavioral Model for designing around the
    problem. The alarm clock story captured the approach perfectly: put the alarm clock
    across the room so that stopping it forces you to get up, and you have engineered the
    desired behavior without needing any motivation at all.
  2. Habit Stacking: The Small Change That Compounds
    Directly connected to the behavioral science session was the concept of habit stacking,
    which several speakers referenced in both the exercise and nutrition talks. The principle
    is simple: attach a new behavior to an existing automatic routine, using the old habit as
    the trigger for the new one.
    After I take my morning medication, I will do two minutes of hand exercises. After my
    morning coffee, I will drink a full glass of water. After my morning walk, I will take a
    smoothie. These are not ambitious lifestyle overhauls. They are tiny bets that compound
    over time. Author James Clear puts it this way: a one percent improvement every day
    yields a 37-fold improvement over the year. For someone managing Parkinson’s on top
    of everything else in life, this framing is not just motivational — it is actually liberating.
    You do not have to fix everything at once. Fix one small thing and let time do the math.
    The celebration piece is important and gets skipped too often. When you complete a tiny
    habit, celebrate it immediately and explicitly — a fist bump, a quiet “good job,” anything
    that provides an immediate emotional reward. You are manually triggering a dopamine
    response in a brain that is low on dopamine. This is not touchy-feely advice. It is
    biochemistry.
  3. Making Exercise Stick Requires a Plan B
    Professor Sandy Brauer from the University of Queensland made an argument that I
    found more useful than any specific exercise prescription: if you don’t have a coping
    plan — a pre-planned response to the specific obstacles you know will arise — your
    exercise program will not survive contact with real life.
    She described coping planning as working out your “if-then” responses in advance. If it’s
    raining, I will walk inside in ten-minute loops. If I am traveling, I will find a hotel gym
    or do the workout from my room. If I have had the flu and fallen off for two weeks, I will
    restart at half the intensity. If I have been hospitalized, I will see my physiotherapist for
    a reassessment before resuming. These are not afterthoughts. They are the reason a
    program survives a year rather than collapsing after the first disruption.
    She also made the social case for exercise more forcefully than anyone else at the
    conference: the most frequently cited motivator among Parkinson’s patients who are not
    currently exercising is not information, not equipment, and not physician
    encouragement. It is other people. Group classes, exercise buddies, Dance for
    Parkinson’s programs — anything with social accountability — consistently outperforms
    solo training in long-term follow-through. And yes, she confirmed: the dog is an
    excellent exercise partner. “There is no decision in that.”
  1. Supplements: Probiotics Look Real, But Don’t Ask Which One
    Dr. Lithander’s supplement review applied the same strict evidence standard as her
    dietary pattern review: gold-standard clinical trials in people with Parkinson’s only.
    Under that filter, the most promising supplement is probiotics — five rigorous, well-
    designed trials showing benefit for gut health, primarily constipation. One Malaysian
    trial published in the journal Neurology showed a significant improvement in bowel
    regularity over four weeks. More recent data suggests probiotics may also reduce
    inflammation markers in the blood.
    The caveats matter enormously. Probiotics are not interchangeable. Different bacterial
    strains have different effects. Some strains may interfere with how the body absorbs
    levodopa. There is no standard recommended dose, no standard duration, and no
    clinical guidance on which specific product to use. When audience members asked
    which probiotic they should take, Dr. Lithander’s honest answer was: she cannot say.
    Neither can I. What she can say is this: about two-thirds of people with Parkinson’s are
    already taking some form of dietary supplement, and most of them have not told their
    neurologist. Tell your neurologist.
    For the record, I use a probiotic, so this news is great. The BiotiQuest Sugar Shift
    Probiotic. I feel it makes a positive difference for me.
    Other supplements showing early promise: omega-3 fatty acids combined with vitamin
    E (showed reduced inflammation in trials), and nicotinamide riboside (a form of
    vitamin B3 with some early evidence for slowing disease progression and reducing
    inflammation). Neither is ready for a firm recommendation — but both are worth
    watching.
  1. DBS Has Come a Long Way in 40 Years
    Professor Elena Moro from Grenoble gave a session on deep brain stimulation — DBS —
    that covered 40 years of history in 45 minutes, which is an impressive compression
    ratio. The basics: thin wire electrodes are implanted deep in the brain and connected to
    a small battery-powered device placed under the skin in the chest, much like a
    pacemaker. The device delivers electrical pulses that interrupt the abnormal brain
    signals causing motor symptoms. DBS does not slow the disease. But for the right
    patient, it can dramatically reduce tremor, stiffness, and the wearing-off periods
    between medication doses.
    The most exciting development in DBS is adaptive DBS — systems that listen to the
    brain’s own electrical activity and automatically adjust the stimulation in real time
    rather than delivering a fixed, constant signal. Standard DBS is a light switch. Adaptive
    DBS is a thermostat. The next generation goes further still: feeding in movement data
    from wearable sensors so the device can respond to what you are actually doing —
    walking, sleeping, standing up — rather than just to what your brain is signaling at rest.
    Professor Moro also addressed one of the most common patient questions: does having
    the GBA1 gene mutation — a genetic variant that increases Parkinson’s risk and tends to
    speed up cognitive decline — change the decision about DBS? The answer is nuanced.
    GBA1 carriers’ tendency toward faster cognitive decline affects the risk-benefit
    calculation, but DBS remains a viable option for carefully selected GBA1 patients.
  2. Focused Ultrasound: Non-Invasive Brain Surgery Is Now Available
    Dr. Michele Matarazzo from Spain presented on MR-guided focused ultrasound — a
    technology that uses hundreds of precisely aimed sound wave beams, focused to a single
    point deep in the brain, to eliminate a tiny targeted area of tissue without any incision,
    anesthesia, or implanted hardware. The patient sits in an MRI scanner while the
    treatment is delivered, awake and able to provide real-time feedback about their
    symptoms.
    The procedure has been available for tremor-dominant Parkinson’s for several years.
    The significant news from this conference was that in 2025 the FDA approved using
    focused ultrasound on both sides of the brain in a single session — targeting the specific
    brain pathways that cause tremors and movement problems on both left and right sides
    at once. Previously, only one side could be treated, which left the other half of the body’s
    symptoms unaddressed.
    Dr. Matarazzo was honest about the limitations: the procedure works best for patients
    whose Parkinson’s is primarily tremor-driven, and roughly 15 to 20 percent of patients
    have skull anatomy that makes it difficult or impossible for the sound waves to
    penetrate effectively. But for the right patient, it offers a real alternative to surgical DBS
    with far less procedural burden.
  3. Disease-Modifying Therapy: Closer Than Ever, But Not Here Yet
    Simon Stock from Cure Parkinson’s delivered the conference’s comprehensive report on
    disease-modifying therapies — meaning drugs aimed not at managing symptoms but at
    actually slowing or stopping the disease from progressing. His ten-year analysis covered
    444 trials. The headline: we do not yet have a single proven disease-modifying
    treatment for Parkinson’s disease. Not one.
    That said, several trials are generating genuine optimism. Creselevirumab, an
    experimental antibody drug that targets chronic brain inflammation, has reached Phase
    3 trials — the final stage before potential approval. A drug called ambroxol (yes, the
    same ingredient in some cough medicines) is in Phase 3 for a genetically defined group
    of Parkinson’s patients. Nicotinamide riboside, the vitamin B3 derivative mentioned in
    the supplements section, has shown some signal for slowing progression. And a
    program targeting a specific gene mutation called LRRK2 — which causes some
    inherited cases of Parkinson’s — is still active despite recent setbacks.
    Professor Tom Foltynie from University College London described the EJS Act PD study
    as the world’s largest Parkinson’s trial — simultaneously testing three existing drugs (a
    blood pressure medication, a diabetes and weight-loss drug, and a liver bile acid drug)
    in thousands of patients at once. His most quotable line on what a cure would look like:
    “A cure is multiple drugs that together make the progression curve close to flat. That is
    the target. We are building toward it.”
  1. Early Financial Planning Is a Medical Recommendation
    This one does not come from a scientific session — it comes from John Poma, a patient
    advocate and healthcare professional who was diagnosed with REM sleep behavior
    disorder in 2018 and Parkinson’s in 2022. He described sitting in a neurology
    appointment when a nurse asked him — out of nowhere, at his second visit — whether
    he had good disability insurance.
    He did not see it coming. He went home shaken. But looking back, he called it exactly
    the right question at exactly the right time. The ability to detect Parkinson’s earlier —
    through biological staging, which means categorizing where someone is in the disease
    based on measurable biology rather than just waiting for symptoms — gives patients
    something they desperately need: a longer runway. If the disease can be detected years
    before motor symptoms appear — during the REM sleep behavior disorder phase, or
    even earlier through blood tests — that is years of additional time to make financial
    decisions, plan for care, adjust insurance coverage, and have honest conversations with
    family.
    As a CFP and CPA who has spent 40 years helping people retire, I cannot agree more
    with John’s framing. Parkinson’s is a long disease. The earlier you plan around it, the
    more choices you preserve. The disability insurance question is not morbid. It is
    practical. And your financial advisor should be asking it.
  2. The Patient Advocates Were Some of the Best Speakers of the Week
    Three patient advocates in particular stood out in ways that the scientific sessions could
    not. JB Choi, the ultramarathoner, reframed what is possible for a person diagnosed
    with Parkinson’s. His session was not inspirational theater — it was a training manual,
    complete with specific heart rate targets, session structures, and a philosophy built on
    preparation rather than motivation.
    Astrid Liv Garshol from Norway gave the most uncomfortable and most necessary talk
    of the conference. She described her relationship with her medication as being like an
    abusive relationship — it made her feel good sometimes but was unreliable and
    sometimes hurt her. She described a neurologist who looked into her eyes and conveyed
    such hopelessness that it “extinguished her own.” And she delivered the most
    memorable line of the week: “Hope is not an infinite resource.” But she followed it with
    the most important one: “A plan is also hope.”
    Paul Mayhew-Archer, who co-wrote the British sitcom The Vicar of Dibley and co-hosts
    the Movers and Shakers podcast, gave a humor keynote that should be required viewing
    for every newly diagnosed patient and every clinician who treats them. His thesis:
    “Every laugh is like Sinemet and Ropinirole all squeezed into a pill of joy.” The illness is
    bad enough as it is. Do not deny patients the chance to laugh at it.
  1. 25 Million People Will Have Parkinson’s by 2050
    Dr. Sirwan Darweesh from Radboud University in the Netherlands opened his session
    with a graph that quieted the room. In 1990, there were three million people with
    Parkinson’s disease worldwide. Today there are more than 12 million. By 2050,
    scientific projections put the number at 25 million.
    This is not an abstract statistic. It is a planning crisis. Fewer than 10 percent of
    American Parkinson’s patients currently see a movement disorder specialist — a
    neurologist with specific expertise in Parkinson’s. Some US states have no movement
    disorder specialists at all. Every biomarker, every subtype, every exercise protocol, every
    behavioral intervention discussed at this conference is currently reaching a small
    fraction of the people who need it. The access gap is not a footnote to the Parkinson’s
    story. It is one of its defining chapters.
    The closing panel session returned to this theme repeatedly. Community health
    workers, online education, peer support programs, the University of Tasmania’s free 12-
    week online course on Parkinson’s disease, the Parkinson’s Foundation’s rural provider
    training program — these are the tools the field has for reaching the 90 percent that
    specialist medicine is not currently reaching. They are not glamorous. They matter
    enormously.
  2. AI in Medicine: Useful, Dangerous, and Here
    The closing panel produced a candid and somewhat entertaining exchange on artificial
    intelligence in clinical medicine. Dr. Rajesh Pahwa, the moderator, shared that AI built
    into his electronic health record system drafts responses to patient messages that are
    “eight out of ten times” better than what he would have written under time pressure. Dr.
    Benzi Kluger noted that AI responses have been rated as more compassionate than
    physician responses in some studies — which is either fascinating or sobering depending
    on your perspective.
    Dr. Indu Subramanian and Dr. Fiona Lithander offered the necessary counterweights.
    AI systems trained primarily on data from white, Western, higher-income populations
    will reproduce the biases already baked into that data. Women’s symptoms that tend to
    be underreported in clinical notes will continue to be underrepresented in AI outputs.
    And Dr. Lithander cited studies showing significant AI errors in clinical documentation
    — patients documented as having conditions they don’t have, and conditions they do
    have going unrecorded.
    The consensus was cautious optimism: AI is a useful tool that must not replace clinical
    judgment, must be watched for bias, and should remain subject to human review. The
    concern I left with is this: the clinicians most likely to lean on AI without checking it are
    the ones who are the most overextended and seeing the most patients — which is exactly
    where errors will do the most damage.
  1. We Are on the Same Team — We Just Don’t Always Act Like It
    The session I keep returning to is not any of the scientific ones. It is the closing panel,
    where Dr. Subramanian from UCLA described what good Parkinson’s care actually looks
    like: not reactive, not episode-based, not putting out fires after the fact, but proactive,
    continuous, and built around the patient at the center of a team that includes their
    family, their community, their primary care physician, and their specialist.
    Becca Miller, a care partner and advocate, put it more sharply: the entire healthcare
    model needs to shift from appointment-based to plan-based. Instead of a series of
    disconnected fifteen-minute visits where everyone tries to cram everything in, there
    should be a shared, documented, living care plan accessible to everyone on the team —
    one that survives provider changes and stays current as the disease evolves. She is right
    about this, and not just for Parkinson’s.
    Professor Barker ended the week’s proceedings with a reflection on how to counsel
    patients being pulled toward stem cell clinics charging $25,000 and up for procedures
    with no peer-reviewed evidence. His framework was simple and exactly right: don’t
    dismiss. Don’t judge. Educate. Ask the right questions together. Be honest about what
    you know and what you don’t. And never, ever make the patient feel foolish for hoping.
    Because hope — as Astrid reminded us — is not infinite. Our job as clinicians, advocates,
    researchers, and fellow patients is to make sure it is well-directed.
    I left Phoenix more informed, encouraged, humbled, and genuinely grateful. I hope to
    see you at the next World Parkinson Congress, 2029, in Quebec City.

About the Author
Randy L. Thurman, CFP®, CPA/PFS™ is CEO and Managing Partner of Retirement
Investment Advisors, Inc. (TheRetirementPath.com), a fee-only fiduciary retirement
planning firm with offices in Oklahoma City and Frisco, Texas, managing approximately
$1.5 billion in assets under management. He is also a person living with Parkinson’s
disease, a runner, a pickleball player, and a white belt in Brazilian jiu-jitsu. He attended
the 2026 World Parkinson’s Congress in Phoenix, Arizona.