The physical chaos of earlier weeks has begun to settle into a calmer rhythm. Here is where the data, the medications, and the daily reality stand at my 35-day mark.

Dialing in the Tacrolimus Window

After tuning my medication dosages downward last week, my latest blood draw clocked my tacrolimus trough level at 5.9 ng/mL.

Seeing that number land squarely inside the 5 to 10 ng/mL safe target range recommended by the hematology team was very encouraging. Calibrating the dosage has noticeably reduced the bilateral, symmetrical shaking tremors that flared up post-op.

That said, it was eye-opening for me just how potent this immunosuppressant is. That 5.9 reading came from a blood draw taken at the tail end of a 12-hour period after my last dose. Managing this drug is a constant tuning process, but keeping it in the target zone is what keeps the neurotoxic side effects in check while protecting the donor cells.

PD Medication Dosages: A Battle for Another Day

On the Parkinson’s front, I am back on my regularly programmed medication schedule as prescribed by my primary neurologist to maintain a baseline quality of life.

I experimented with cutting my dosages to half for a week, but it simply wasn’t working. The drop-off in motor functions was too steep, and I had to return to my original higher dosages. Tapering off pills and getting to a less medication reliant state is my ultimate goal, but that is a battle for another day. For now, the cardinal Parkinson’s symptoms I experience remain persistent:

• The shuffling gait and heavy “cement feet” sensation

• Left-side dominant resting tremors

• Core/trunk instability and spinal stiffness

• Recurring dystonia alongside swelling in my feet, ankle, and heel

Radical Patience Required

At five weeks post-transplant, I am constantly reminded of the need for patient resilience. It is easy to feel anxious, but I am doing my best not to get ahead of myself.

Biologically, the transplanted stem cells are still in the survival and anchoring stage. They haven’t matured into fully functioning dopamine factories yet. Right now, maintaining steady immune suppression is the sole priority to ensure the graft takes root safely.

Looking back at the trial data keeps me grounded. In the initial Phase I/II trial of seven participants at Kyoto University, follow-up brain imaging confirmed that the transplanted iPSC-derived cells survived in all seven patients across the two-year observation period. Furthermore, brain imaging documented an average 44.7% overall increase in putaminal dopamine synthesis. In plain English, that means: the cells successfully integrated in 100% of the trials, and restored nearly half of the missing dopamine production. Although the trial numbers are only a handful, it’s good enough for me to feel hope. It just requires time.

Out-of-Body Brain Sensations and Walk-Before-Run

Inside, the strange out-of-body sensations have continued. I still have a persistent, tingly feeling at the top of my head that gives things an almost out-of-body quality. I jokingly describe what I’ve been feeling as a strange progression from Indiana Jones and the Temple of Doom, where Indy is writhing in hallucinations and pain after drinking the Blood of Kali; to Men in Black where Tommy Lee Jones flashes me with the neuralyzer and something feels really off since my recent memory of an alien encounter has been wiped. Whenever I encounter physical strain or stress, the top of my head feels like an erupting volcano.

The bright spot is that I feel a small spark of energy now that my abdominal strength is coming back. I have started rehabilitating with very slow walk/jog intervals to keep the body moving. Taking things one day at a time, letting the cells anchor, and taking the small wins.

I was not expecting any surprising, immediate breakthroughs at this visit. There were no MRIs or PET scans scheduled this time—just routine blood and urine lab draws, followed by a neurological evaluation to compare my motor symptoms in both “ON” and “OFF” medication states.

Overall, the physical tests with the neurologist showed no major difference compared to my previous numbers. Clinically, that makes sense.

What Neurologists Are Evaluating at 4 Weeks

At one month post-op, neurology was not expecting to see transplanted stem cells producing functional dopamine yet. Instead, this check-in focused on recovery, safety, and establishing an initial post-operative benchmark:

• Surgical Recovery & Safety: Monitoring the incision sites and confirming that local swelling or inflammation around the needle tracts is resolving.

• Distinguishing Surgical Trauma from Parkinson’s State: Stereotactic brain surgery can cause temporary “microlesion effects,” balance issues, or acute symptom flare-ups.

• Immunosuppressant Calibration: Confirming that daily immunosuppression is within a safe therapeutic window without toxicity, while balancing carbidopa-levodopa doses to stay safe and mobile.

• Comparison Points for the Trial: Standardized rating scales (like MDS-UPDRS Part III motor scores during a Levodopa Challenge Test) provide the post-procedure data points that will be compared against future follow-ups at 3, 6, 12, and 24 months.

So… stem cell integration requires time and patience. I am now more informed that implanted dopaminergic progenitor cells take several months to differentiate into mature neurons, extend neurites across the striatum, and form functional synaptic connections with the host neural network before biological dopamine delivery begins. Four weeks is simply too short of a time frame to see the effects of the operation.

Connecting the Symptoms to Tacrolimus

Over the past couple of weeks, I noted an emergence of negative symptoms: more fine-finger motor issues when picking up a fork or typing on my phone, difficulty telling whether I was “ON” or “OFF” my regular carbidopa-levodopa, and pronounced symmetrical tremors across both wrists and hands. These were all new symptoms that did not show up in the same way pre-operation.

Looking further into it, the current theory is that they are largely driven by tacrolimus-induced neurotoxicity.

My tacrolimus trough measurements have mostly been at a higher level than the advised target. My daily dosage started high at 7 mg, stepped down to 5 mg, then 4 mg, and is now sitting around 2 to 3 mg a day to maintain the target range of 5 to 10 ng/mL.

Last week was definitely rough with those side effects. This week, I feel more stable and in control with less of the symmetric tremors as we have fine-tuned the daily dose.

Experiencing this firsthand makes it obvious that long-term immunosuppression is destructive and not gentle to the body. While I worry about staying on it for an extended period, I hope the long-term regenerative benefits of the stem cells will outweigh the temporary downsides, without introducing new complications down the road.

That said, the target trough level for this procedure (5 to 10 ng/mL) is much lower than what is required for solid organ transplants. Because neural transplants benefit from the brain’s relative immune privilege behind the blood-brain barrier—and because this protocol utilizes HLA-homozygous “super donor” lines—immune surveillance is lower. I now have a new sympathy towards organ recipients, who have no choice but to take lifelong immunosuppression maintained at higher trough levels. The regimen for this treatment is a temporary bridge of roughly 12 to 15 months until the cells integrate.

Cell Sourcing Approaches: Autologous vs. Allogeneic

Researching the immunosuppression side of this makes it clear that not all stem cell procedures are structured the same way.

A friend recently shared an article about Aspen Neuroscience’s trial for Sasineprocel (ANPD001). Comparing it to Raguneprocel (CT1-DAP001 / Amchepry) which is the trial I am in, highlights two very different approaches to cell sourcing:

Raguneprocel (Amchepry / CT1-DAP001)

• Cell Sourcing: Allogeneic (”Off-the-shelf”) from healthy donor blood

• Immunosuppression: Required (12–15 months of tacrolimus)

• Donor Matching: HLA-homozygous “super donors” via CiRA (Kyoto Univ.)

• Manufacturing: Batch-produced in advance; scalable inventory (but non-scalable logistics at this point in time)

• Delivery: Fresh, non-frozen delivery (Cryopreserved in DSP-1083)

• Developer: Sumitomo Pharma & Kyoto University

Sasineprocel (ANPD001)

• Cell Sourcing: Autologous (Personalized) from the patient’s own skin biopsy

• Immunosuppression: None required (recognized as self)

• Donor Matching: Patient-specific match (100% self-match)

• Manufacturing: Individualized, multi-month custom run per patient

• Delivery: Cryopreserved (”thaw-and-inject”)

• Developer: Aspen Neuroscience

It is still very early in both clinical trials, but knowing that we may eventually have a menu of different stem cell treatment choices in the coming decade is encouraging. Being part of this research and seeing the field advance is exciting.

For now, the four-week check-in is complete, my daily dosages are stabilizing, and the quiet process of cellular integration and recovery continues.

I mentioned in an earlier post that in several physical ways, I am currently worse off than I was before the operation. Poking around inside the midbrain introduces raw physical trauma, and my body is still processing the triggered aggravation.

Here is where things stand at the 21-day mark:

• Symmetrical Tremors: The uncontrollable shaking and twitching across both my wrists and hands remain much more pronounced and visible. Pre-surgery, my tremors were heavily asymmetrical, primarily targeting my left side. Now, it is a balanced, symmetrical battle on both sides. Curiously, some past tremors have subsided - I especially remember a wobbly spine and hip feeling pre-op, that feeling is not present.

• Carbidopa-Levodopa: My standard carbidopa-levodopa doses don’t seem to be doing much to quiet the symmetrical tremors. I also feel less of a drastic “crash” between when I am ON my medication versus when I am OFF it. Could this be an early sign that the new cells are beginning to establish a baseline of dopamine? It’s far too early to know, but it’s a notable difference.

• Sluggish Body & Shuffling Gait: Getting out of a chair or simply moving around remains a herculean effort. My balance is definitely off. Right after surgery, I couldn’t even stand up straight, and now I clumsily waddle my way around. Walking was already an inconvenience before the procedure, but the surgical trauma has raised the difficulty, hopefully temporarily. I suspect much of this will simply require time and rehabilitation.

• Degraded Precision: Precision movements have become by far the biggest new challenge. Because of my shaking fingers and wrists, basic daily tasks—like unscrewing a bottle cap, picking up a fork, or holding a knife cleanly—take extra concentration.

• Abdominal Core Weakness: I’ve noticed a marked decrease in my core and abdominal strength. Part of this is likely from extended bed rest and sleeping more during early recovery, but it also feels like the brain-body engine is figuring out how to engage the core properly again.

The Brain Tingle

Beneath the physical clumsiness, there are two notable internal changing:

• The Forehead “Vibration”: The sharp surgical skull pain is gone, replaced by a continuous, tingly, vibrating sensation felt right in my forehead, extending deep into the center of my brain. I know this isn’t scalp tissue or suture pain.

• Unexpected Win (for my wife) — Quiet Nights: Before surgery, my REM sleep was turbulent—I was frequently talking, yelling, or screaming out loud in my sleep, and would not remember a thing the next morning. My wife recently mentioned that since the procedure, I have become remarkably quiet in my sleep.

Dosage Calibrations & Emotional Shifts

• Calibrating Tacrolimus Trough: My hematologist actively fine tunes my immunosuppressant intake. It’s a constant trial-and-error feedback cycle: I get a blood weekly draw, they read the tacrolimus trough level, and if it’s running too high or low, we adjust the dose. Thankfully, the adjustments so far have been downward to date, but this week we had to do two blood draws since I was clocking in higher than expected. Respect to the UCSD pharmacy for their responsiveness to my labs, usually on the same day.

• Emotional Sensitivity: I noted this before, but my emotional volume knob remains turned up. I find myself reacting much more fluidly to everyday moments —cracking up at small jokes around the dinner table, feeling deeply touched by a movie scene, or feeling a swell of pride over my kids’ first day of school. These changes feel odd but welcomed, I don’t mind being the emotional dad.

• A Spark of Energy: Despite the physical slowness, it is very subtle but my overall spirits feel up. I feel a small spark of mental energy. For the first time in a long while, I am actively prospecting for career opportunities just to see what’s out there. Since I’m a technology person at heart, I’ve also started diving into AI to vibe code a few app ideas I’ve been kicking around. Pre-surgery, I had neither the energy nor curiosity to pursue these kinds of activities, a welcome shift.

What’s Next?
Next week marks an important milestone — my 4-week post-op check-in at UC San Diego. It will be a comprehensive milestone: an updated Parkinson’s motor assessment with the lead neurologist, and maybe an MRI or PET scan.

I’m looking forward to getting more objective data to compare against these subjective daily micro-shifts. More to come soon. Thanks for following along.

The primary metric we are tracking is my tacrolimus trough level —measuring the exact concentration of immunosuppressant in my blood to ensure it stays in the therapeutic target zone of 5 to 10 ng/ml. This week, my test clocked in at 8.7 ng/ml. It was a massive relief to see that number land squarely in the sweet spot. It means I don’t have to adjust my medication dosages and can simply stay the course.

Because this is still very early in the recovery process, I want to break down how I am feeling across two distinct dimensions: what I am observing externally on a physical level, and the subtle sensations happening inside.

1. Physical Observations: The Post-Op Reality

Visually, the incisions on my scalp are healing at a solid pace. UC San Diego used dissolvable sutures for the procedure, so I am currently in the mid-stage phase where the knots are softening and melting into my scalp. I am officially allowed to wash my head again, but I have to exercise extreme caution—avoiding any scratching or abrasive rubbing over those exposed knots and delicate incision lines.

I will be the first to admit that I underestimated the raw physical trauma of this procedure. Poking around inside the brain carries unavoidable consequences.

Prior to surgery, despite fighting Parkinson’s symptoms, I maintained a solid baseline of physical fitness and worked out three to four times a week. Two weeks post-op, my physical capacity has taken a noticeable hit. I am tracking two main physical changes:

• Symmetrical Dyskinesia & Fine-Motor Trips: I am experiencing an increase in uncontrollable twitching (dyskinesia) across both arms, wrists, and fingers. What is fascinating is that these twitches are now symmetrical—happening equally on both sides of my body. Pre-surgery, my tremors and involuntary movements were heavily asymmetrical, impacting my left side. Coupled with this, my fine motor skills in my fingertips are degraded. Typing has become a trip hazard; on my phone’s virtual keyboard, I repeatedly hit the “M” key when I am aiming for the adjacent delete key.

• Degraded Balance and Speed: My coordination is noticeably off. The classic Parkinson’s sliding tiptoe and shuffling gait are more pronounced right now, and my overall body speed is slower. If I thought I was a bad aerobics student before surgery, post-surgery you can officially call me a self-paced misfit.

2. Internal Sensations: Brain Chemistry and Emotional Nuance

Inside, the physical and emotional feelings are much harder to put into words, but I want to capture them with as much fidelity as possible while they are fresh.

The Physical “Pull”

The initial dull pain in my skull has completely transitioned into an intense dryness and itchiness as the sutures dissolve. But beneath the itch, there is a constant, distinct physical sensation—it feels as if someone is placing two open hands behind my head, gripping my scalp, and pulling the skin outward and away from the center of my brain. I suspect this is the physical tension of the healing tissue and the scalp stretching over the repair sites.

The Chemical Shift and Heightened Emotions

Beyond the surgical sites, there is a far more subtle, feeling-based shift occurring. It feels as though the fundamental chemistry of my brain is recalibrating. I feel a persistent, tingly sensation deep inside my head that is entirely separate from the scalp sutures—and I like to think it is the new cells beginning their long work of integrating.

Stranger still are the subtle emotional shifts. I am finding myself much more sensitive and unconsciously reactive to emotional cues around me.

Don’t judge me, but I used to think Matthew Perry’s character in FRIENDS wasn’t funny—now, his sarcastic one-liners are making me crack up. I was re-watching The Hunger Games the other night and found myself on the verge of tears during Jennifer Lawrence’s emotional scenes. (Again, please reserve judgment on my take on her acting!)

The point is: my emotional volume knob has been turned up, and I am reacting more fluidly to external inputs. I would like to hope that the emotional reactions to bad acting are coincidental!

Rebalancing the System

Jokes about sitcoms aside, I believe these physical and emotional swings are classic indicators of a body undergoing an abrupt shift in how dopamine is being processed, replaced, and regulated.

When looking into clinical data on dopamine system adjustments, the overlap with what I am experiencing is clear:

• Physical Side Effects: Temporary waves of nausea, dizziness, fatigue, and heightened dyskinesia (twitching).

• Behavioral Side Effects: Subtle shifts in impulse control, mood sensitivity, and sensory changes.

It is too early to draw definitive conclusions, but the observations fit the profile of a brain in transition. I am taking it one day at a time, letting the scalp heal, and tracking every micro-shift as these new donor cells settle in.

The last few days have been a complete haze. When you sign up for stereotactic brain surgery to have stem cells implanted into your midbrain, you intellectually know it is going to be difficult. But the physical reality of the recovery is an entirely different beast.

I am currently eight days post-surgery, and the transition from the operating room back to daily life has been a daunting, humbling process. Here is an unfiltered look at what this week has actually entailed from the medication mountain to the surprising realities of my Parkinson's symptoms.

The Medication Mountain

Right out of the gate, UCSD sent me home with an overwhelming post-surgery cocktail. This wasn't just about managing the surgical site; it was about managing the fallout of the surgery itself. My daily intake suddenly included:

• Opioid painkillers (oxycodone and acetaminophen) for brain pain and numbness.

• Zofran and Pepcid to manage intense nausea and stomach discomfort.

• Stool softeners to counteract the opioids and promote bowel movements.

• My standard, daily Parkinson's disease medications.

• Tacrolimus, the aggressive immunosuppressant required to keep my body from rejecting the donor cells.

For the first five days, my body drifted in a suspended state between pain and nausea. I was taking painkillers to numb the skull pain, and then taking anti-nausea meds and antacids to handle the stomach wrecking caused by the painkillers and the tacrolimus.

Add in a persistent, rattling cough and phlegm from the general anesthesia breathing tube that had been shoved down my throat during surgery, and the severe dehydration that led to zero bowel movements until Day 6. It was a brutal physical loop.

The "Hallucination" and the Reality of Day 7

In the immediate days following the surgery, I noticed a positive flex in my legs and feet. For a brief moment, I wondered if the cells were already working. But the pragmatic reality soon set in: that initial relief was likely a "hallucination" brought on by the heavy painkillers, not the miraculous, instantaneous effect of the stem cell implants.

By Day 7, the painkillers had cleared enough for reality to hit, and my feet felt like they were made of cement, a cardinal symptom of Parkinson’s disease. In fact, it feels like my condition has gotten completely worse before getting better.

• Pre-operation, my shaking was predominantly on my left side; now, I am experiencing shaking in both hands.

• Standing up and managing my shuffling gait has become an immense challenge.

• My overall physical response time is noticeably slower than it was before the procedure.

Part of this regression is undoubtedly trauma. Drilling into the skull and injecting fluid into the brain has obvious, immediate negative consequences that will take months to heal. However, part of this is also self-inflicted: I have intentionally been taking half-doses of my standard PD medications. It is a personal experiment to see if the stem cells will start showing their effects, even though I know it is far too early to tell. For now, I have to accept that things are going to be worse before they get better.

Day 8: The UCSD Lab Check-In and The Itchy Skull

Today was my first official post-op check-in at UCSD, involving routine blood and urine draws. I have to give massive credit to the clinical staff. They were incredibly fast in assessing my lab results, specifically measuring my "tacrolimus trough" to ensure the immunosuppressant was staying at safe, non-toxic levels in my blood.

By the evening, the doctor and pharmacy had already adjusted my tacrolimus dosage down from 7 mg a day to 4 mg a day. This drop immediately provided some much-needed relief for my stomach.

As for the surgical sites on my head, the team used dissolvable sutures. The sharp pain in my skull has slowly transitioned into intense dryness and itchiness as the soft sutures begin to dissolve and absorb into my body (a process that should take about two weeks). Resisting the urge to scratch my own head is currently requiring monumental willpower.

On the Logistics and the Global Trial

While I heal, i have been keeping my ear to the ground regarding the broader scope of this trial, and the logistical realities are staggering.

I recently heard that Japan is moving forward with a Phase 4 trial involving 30+ people, directly related to the fast-track commercial approval of this therapy (Amchepry) over there. My concern is that this massive ramp-up in Japan might affect the priority and speed of our American Phase I/II trial.

I am patient #3 out of the 7 slated for the U.S. cohort. From what I am hearing about the pipeline, the next candidate's surgery date might be a full year out.

When you look at the supply chain, the delay makes sense. I had it confirmed that the live, non-frozen cells for my surgery were shipped same-day from Japan and literally hand-carried from LAX down to San Diego just in time for the operation. That is an incredible logistical feat, but it is in no way scalable. If this treatment is ever going to reach the millions of people who need it, they are going to have to figure out a local distribution method or a far more predictable sourcing pipeline.

For now, I am simply focusing on healing the holes in my head, managing my half-dosed symptoms, and waiting for the dust to settle. The cells are in. The waiting game continues.

The day started in the dark at a nearby hotel. I kissed my two sleeping kids and said my prayers, just in case I didn’t return. Heading to the Medical Center felt like an entirely surreal experience. By 5:20 AM, I was checked in, changed into a standard hospital gown, and hooked up to an IV. I took my first 4 mg dose of the immunosuppressant tacrolimus, anticipating we were just an hour away from the procedure. 

The Agonizing Wait

At 7:20 AM, we were standing by. Surgeons dropped in, mentioning they were ready to roll me in between 7:20 and 8:30 AM. We had to do a retake of a CT scan because the first angle wasn't quite right, but after 8:30 AM, an agonizing silence fell over the room. 

The surgery was delayed. While UCSD never gave me a direct answer, it became pretty clear that the "package" of fresh stem cells hadn't arrived that morning. The logistics were bottlenecked somewhere between the international transit shipment, the UCSD lab prep, and the pharmacy's release process

For a therapy like this to scale in the future, they will have to figure out a smoother delivery method. Otherwise, these cells will likely have to be frozen. It gave me a near heart attack just thinking about the absolute village of highly specialized professionals—the head neurosurgeon, the general anesthesiologist, hematologists, pharmacists, and nurses—sitting idle for hours while waiting for the cells to arrive. 

11:15 AM: Into the Spotlight

The surgery finally started around 11:15 AM, and from that point on, everything became a blur. I was moved from my pre-op bed to a very narrow surgery table equipped with armrests. I honestly expected the operating room to be dark and subdued, but it was unexpectedly, intensely bright. It felt like a massive spotlight with nowhere to hide. The room was freezing, but the team warmed it up with heavy blankets. 

The 5+ surgeons in the room were cordial and professional, letting me know more people would be joining the room once I was under. They connected my health monitors and started feeding me oxygen through a mask. The mask made me feel deeply claustrophobic, but soon a tingling sensation from the anesthesia kicked in, and everything faded to black.

Post-Op: Hallucinations and Fight-or-Flight

When I regained consciousness in the post-op ward, my awareness was fleeting. The procedural checks—pupil responses, name, date of birth, vital signs—felt frantic, triggering intense fight-or-flight responses. 

I was hallucinating heavily. I drifted into a lucid dream where the hospital was under attack by an unknown army, and I was actively defending the floor alongside the nurses. The physical reality was just as intense. My brain and skull throbbed with a sharp, acute pain (hitting a 9 or 10 on a scale of 10) right at the incision sites and the center of my brain. I repeatedly asked for Tylenol and was managed on timed dosages of acetaminophen and a fentanyl IV to withstand the agony.

Time completely unraveled. One moment I was undergoing medical checks, the next my wife and kids were visiting. I was , incredibly loopy, complaining to my kids about the deeply uncomfortable urinary catheter, all while somehow managing to eat vanilla pudding, strawberry yogurt, and chocolate pudding. At 3 AM, I hallucinated again that my son was visiting at the door, asked the nurse for two Jell-Os, and collapsed back into a pain-filled sleep. 

The Morning After: The First Glimmers of Change

By 7 AM the next morning, the sharp pain had downgraded to a dull, lingering ache—similar to the feeling after a dentist fixes a cavity (about a 3 or 4 out of 10). I still felt numb, but my coherent self was returning. Taking out the catheter ended up being the most painful part of the morning, but I was relieved to have my normal urinary functions back. 

Because the pain was localized to the back of my head, looking at my phone or watching TV was out of the question; I could only lay down and close my eyes. After some rest, a CT scan, and an MRI, I was back to eating breakfast like a champion.

Despite the hazy painkillers, I immediately felt a curious, positive shift post op. The curling dystonia in my feet, a cardinal symptom of Parkinson’s had noticeably improved. I had greater flexibility, particularly in my left foot, and I was able to flex my toes far more naturally than before. The weight and cramps were much lighter than before. Perhaps most notably, the heavy, foggy sensation that has plagued me as part of Parkinson’s felt lifted. My body felt refreshed, and it was pretty clear that the fundamental chemistry of my brain had already changed. It’s amazing to see that positive changes are already taking effect when I’m sure the cells haven’t integrated into my body yet. It will be exciting to see more positive changes in the weeks and months to come.

Thursday, July 23, 2 PM: The Early Discharge

I requested discharge from the hospital on Thursday, July 23, at 2 PM. To be honest, it was probably too early. I was going through a bunch of pain and nausea, but I desperately wanted out because the various monitor beeps were driving me crazy. 

Armed with a bag full of meds—including docusate sodium, Tylenol, Senokot, Pepcid, OxyContin, and tacrolimus—my family picked me up and we checked out. Because our house is in Nevada, I laid down in a local hotel room for the next few days

Friday, 8 PM: The Current State

It is Friday at 8 PM, and I am still going through a ton of painkillers, and my bowels still have not moved yet post-surgery. I am still taking my Rytary and dealing with shaking in my left wrist. I still have the Parkinson's gait when I walk, but my feet feel remarkably less stiff, which makes a huge difference. More updates to come.

Tomorrow morning, I will be wheeled into an operating room at the UC San Diego Sanford Stem Cell Institute. When the surgical team begins, they won’t just be performing a routine medical procedure; they will be implanting the culmination of a 24-hour global logistical feat, decades of Nobel Prize-winning science, and the unique biology of a few anonymous "super donors."

It is incredibly humbling—and entirely wild—to think about what is actually inside the operation room waiting for me. As I sit here prepping for tomorrow, I wanted to step back and share where these new dopamine-producing cells came from, and the astonishing journey they took to get to California.

The "Super Donors"

You might assume that a cell transplant requires an agonizing wait for a perfect 1-to-1 match (like an organ transplant) or taking my own tissue and modifying it. But this clinical trial uses an "off-the-shelf" approach, beginning with adult blood cells donated by a very select group of healthy people in Japan.

These individuals are banked by the CiRA Foundation at Kyoto University, and they are essentially biological unicorns. They were explicitly chosen because they are HLA-homozygous—meaning they possess highly common immune profiles. Because their immune genetics are so frequently shared, a single donor line can match a massive cross-section of the population.

They act as an immunological "master key." By using these specific profiles, the scientists drastically lower the chance that my body will view the new cells as foreign invaders. However, I’ll still be taking immunosuppressants for the next 15 months to ensure everything integrates safely.

Sourcing & Reprogramming Cells

Once the CiRA Foundation collected those donor blood cells, they were handed over to Sumitomo Pharma's commercial-scale manufacturing facility in Osaka. This is where the Nobel Prize-winning Yamanaka method comes into play.

Instead of being stuck as blood cells forever, scientists introduced specific genetic instructions (using clean, non-integrating vectors rather than risky viruses) that completely rewound the cells' biological clocks. The adult blood cells reverted into a blank-slate, embryonic-like state—becoming induced pluripotent stem cells (iPSCs).

From there, the lab biochemically coaxed these blank-slate cells to grow into dopaminergic neural progenitor cells—the exact type of dopamine-producing brain cells I have lost to Parkinson's. Before leaving the facility, they went through a proprietary purification process to filter out any unprogrammed cells, ensuring the final treatment is pure and safe to enter my brain.

The Rapid Global Logistics

The most stressful part of this entire endeavor might actually be the shipping.

The cell therapy I am receiving tomorrow (CT1-DAP001) is delivered fresh and non-frozen to prevent the cell death that occurs during thawing. In future trials I believe there will be frozen attempts of this treatment, but for tomorrow it is non-frozen.

This requirement triggered an international sprint. The moment the live cells were ready in Osaka, they were handed off to a highly coordinated logistics web involving Sumitomo Pharma, Mitsubishi Logistics, and Japan Airlines (JAL Cargo). Using specialized temperature-controlled pharmaceutical freight, JAL staff physically accompanied the live cells, flying them across the Pacific Ocean and delivering them directly to the clinical teams at UC San Diego in under 24 hours.

It’s encouraging to see what’s under review in this clinical trial is not only the surgery and stem cell product, but also the safety of the logistics behind the treatment.

The Final Step

Everything—from the healthy donor in Kyoto, to the reprogramming lab in Osaka, to the cargo hold of a 787 jet over the Pacific—has perfectly aligned to bring these living cells to San Diego.

Tomorrow morning, the science moves from the laboratory into the operating room, and those freshly delivered cells will finally go to work. See you on the other side!

Before diving into the medical weeds, I have to call out the team at the Sanford Stem Cell Clinical Center. The support from the doctors, coordinators, and staff has been phenomenal. Their relentless professionalism and absolute thoroughness haven’t just prepared me physically—they have given me genuine hope that this procedure will pave a safe, definitive path for thousands of others to benefit from in the future.

Here is the blueprint of what happens next.

The Study & The Sponsor

• Official Study Title: A Phase 1 Investigator-Initiated Clinical Trial of Safety and Efficacy of Transplantation of Human-Induced Pluripotent Stem Cell-Derived Dopaminergic Progenitors (CT1-DAP001) for Parkinson’s Disease

• Study Sponsor: Sumitomo Pharma America, Inc.

• The Mission: The purpose of this research is to evaluate an investigational cell product called CT1-DAP001 as a targeted treatment to halt and potentially reverse Parkinson’s disease. Because this is an “investigational” biological product, it means it has not yet been approved by the FDA for routine clinical use.

The Long Road to Eligibility

Getting to the starting line of a phase 1 trial is not for the faint-hearted. It is an exhausting marathon of data collection and radical patience.

My journey began way back in January. First, you undergo an intense battery of screening procedures to determine basic eligibility. Once you clear that initial hurdle, you enter a mandatory three-month observation waiting period. The doctors use this time to carefully track how your symptoms change and progress under standard conditions.

After those three months, the entire gauntlet of screening tests is repeated at a baseline visit, augmented by an F-DOPA PET scan to map the functional dopamine systems in the brain. Fast-forward through a mountain of logistics, and it has taken me into July to officially verify my eligibility, lock in my baseline metrics, and clear me for the operating room. From start to finish, my planned involvement in this study will span approximately 30 months.

The Cohort and the Data So Far

I am one of only seven participants in the United States selected for this study.

UCSD is currently the only medical center outside of Japan conducting a trial using the CT1-DAP001 line. A sister study was previously conducted by Sumitomo at Kyoto University Hospital in Japan, where seven Parkinson’s patients were treated. The 24-month follow-up safety data from that Japanese cohort revealed zero serious adverse events. Furthermore, the four participants in that trial who received the highest doses of the cells showed varying degrees of clear motor system improvement.

Crucially, this U.S. study modifies the approach: rather than testing escalating doses, all seven U.S. participants will receive the same high-dose concentration. This uniform testing environment gives us a much cleaner, standardized look at the therapeutic maximum potential of the cells.

The Surgical Protocol: High-Fidelity Details

The objective of the surgery is to bypass the blood-brain barrier and deliver the regenerative cells directly to the damage zone. The protocol is highly precise:

• Immunosuppression: Because these cells come from a donor line, my immune system’s natural instinct will be to treat them as foreign invaders and reject them. To counteract this, I will start an aggressive immunosuppressant medication called tacrolimus on the morning of my surgery. This drug requires hyper-vigilant monitoring—frequent blood tests to check drug toxicity and therapeutic levels, alongside regular dosage adjustments to keep my blood chemistry in the ideal zone. I anticipate remaining on tacrolimus for approximately 15 months post-surgery.

• Incisions & Access: Under general anesthesia, the surgical team will shave some or all of the hair from my head. The neurosurgeon will make up to three 1.5-inch incisions on each side of my scalp. From there, up to three small holes (1 to 2 centimeters in diameter) will be drilled into each side of my skull.

• Targeting & Delivery: To deliver the cells safely, the surgeon will use an investigational device called a Sunovion needle. The needle guide will be anchored to a stereotactic frame attached to my head. Using an O-arm (an intraoperative CT scanner), the team will align my skull to the needle in real-time, verifying its coordinates with absolute millimeter precision before depositing the cells.

• The Dosage: Once positioned, the surgeon will inject between 7.1 and 7.75 million viable cells at various depths within the corpus striatum on one side of my brain, followed by another 7.1 to 7.75 million viable cells into the opposite side.

• The Grid: All told, the cells will be implanted across a total of six distinct injection sites—up to three structural tracts on each side of the brain—all completed in a single, highly coordinated surgical session.

• Closure & Recovery: Once the cells are delivered, the guide needles will be carefully extracted, the small holes in my skull will be repaired, and the scalp incisions will be closed using surgical sutures and/or staples.

Following the procedure, I will be moved to the inpatient ward, where I will stay in the hospital for approximately three days overnight for close observation, neuro-monitoring, and initial recovery.

Final Thoughts

This is the moment where science fiction becomes an operating room schedule. It is intense, it is deeply technical, and it carries the inherent risks of pioneering medicine. But looking at the safety data behind me and the elite team in front of me at UCSD, I am stepping forward onto this frontier with clear eyes and an incredibly grateful heart.

The reality? While the science of Induced Pluripotent Stem Cell (iPSC) therapy is incredibly encouraging, we are still a long way from this procedure being widely available. It is not an overnight miracle; it is a highly selective, deeply rigorous, and slow-moving scientific process.

Here is a pragmatic look at where the global trials actually stand, the incredibly narrow needle patients must thread to qualify, and where I personally am on this journey.

The Blueprint: What Happened in Japan?

To understand where we are today, we have to look at the groundbreaking Phase I/II trial recently concluded at Kyoto University Hospital in Japan. This was the trial that set off the global wave of excitement, and the data was undeniably powerful.

The trial evaluated 7 mild-to-moderate Parkinson’s patients over a 24-month period using allogeneic (donor) iPSC-derived cells. The results showed:

• Zero Serious Safety Concerns: No tumor formations or severe adverse events requiring hospitalization.

• Restored Dopamine Production: Brain imaging showed an average 44.7% overall increase in dopamine levels.

• Symptom Reduction: Motor scores during “OFF” periods improved by an average of 20.4%.

However, a closer look at the data highlights why we must manage expectations. You might read in the news that only “4 out of 7 patients showed improved clinical staging scores,” which can sound discouraging. But the pragmatics tell a different story:

1. Safety vs. Efficacy: The very first patient was only evaluated for safety, not efficacy, due to a completely different surgical approach (unilateral surgeries spaced 8 months apart). They were entirely omitted from the final symptom pool.

2. The Dosage Divide: The remaining 6 patients were split into low-dose and high-dose cohorts. The variance in symptom tracking was stark: the high-dose group experienced a massive 63.5% increase in dopamine production, while the low-dose group saw just a 7.0% increase.

Because of these strong high-dose indicators, Japan’s regulatory body fast-tracked the therapy under a conditional approval branded as Amchepry. While it is technically the world’s first commercially available iPSC therapy for Parkinson’s, it is heavily restricted, and Sumitomo Pharma has to collect data for the next seven years to prove its long-term viability.

Threading the Needle: The Strict Reality of Qualifying

When these trials transitioned to the United States—specifically the Phase I/II trial evaluating CT1-DAP001 at the University of California, San Diego (UCSD)—the eligibility gate became remarkably narrow.

The trial is designed to isolate variables so scientists can clearly map a “before and after” efficacy baseline. To do that, the inclusion and exclusion criteria are razor-thin.

To give you an idea of how few people actually qualify, a candidate must match a precise medical profile:

• The Right Window of Time: You must be between 40 and 75 years old and have been diagnosed for at least 5 years.

• The “Goldilocks” Stage of Severity: Your disease must be advanced enough to cause definitive “ON” and “OFF” medication fluctuations, but it cannot be in the late stages. You must be a Stage 2 or higher on the Hoehn and Yahr scale when off medication (motor issues on both sides, mild balance changes), but Stage 3 or lower when the medication is active (still functionally independent). Late-stage patients (Stages 4 and 5) who are severely disabled or wheelchair-bound are entirely excluded.

• Levodopa Responsiveness: Your brain must still prove it can respond to dopamine. Candidates must show a 30% or better improvement in motor symptoms when carbidopa-levodopa is active.

• No Prior Surgeries: If you have already undergone Deep Brain Stimulation (DBS), a pallidotomy, or a thalamotomy, you are instantly disqualified.

• Impeccable General Health: Any sign of atypical parkinsonism (like MSA or PSP), abnormal brain MRIs, cognitive impairments/dementia, major psychiatric illnesses, or compromised organ function (liver, kidneys, immune system) will leave you on the outside looking in.

When you multiply all these constraints, the vast majority of the millions of people fighting Parkinson’s today simply would not qualify. The target cohort is minuscule.

My Journey: 7 Months for a Single Baseline

This brings me to my own story. I am currently one of only seven clinical trialists in the United States accepted into this groundbreaking UCSD trial.

Qualifying was a monumental feat on its own. I was first accepted as a potential candidate back in January. It took 7 grueling months of waiting, traveling, undergoing multiple high-resolution brain MRIs, rigorous physical exams, and intensive lab work just to cross the final threshold. All of this was done to establish my precise pre-surgery “baseline.”

If there are separate dosage cohorts in this U.S. trial like there were in Japan, I have been informed that I am in the high-dosage group—the very group that saw the 63.5% dopamine surge in the Kyoto trial.

My surgery date is officially set for July 21st, and it is coming up incredibly fast.

The Calculated Risk

Am I excited? Yes. But I am also pragmatic, and honestly, quite nervous about the risks involved.

Because this iteration of the procedure uses master stem cells derived from a healthy donor in Japan, these cells are foreign bodies. My immune system’s natural instinct will be to attack and reject them. To fight this, my post-surgery reality involves 12 full months of aggressive immunosuppression medication (tacrolimus).

Living with a intentionally suppressed immune system for a year carries its own heavy bag of risks, infections, and unknowns. But it is a calculated risk I am entirely willing to take. For the last 7 years, since my diagnosis at age 41 in 2019, I have watched this disease slowly chip away at my fine motor skills and physical abilities, particularly on my left side. If a year of immunosuppression is the toll required to potentially halt or reverse structural damage in my brain, I will gladly hand over the passport.

The Takeaway

I share my story not to feed into the media hype, but to anchor it in truth. We are standing on the edge of a magnificent medical frontier, but we are still in the territory of early-phase testing with single-digit patient sizes.

If you are a patient or a caretaker reading about iPSC therapy, please do not feel discouraged if the timeline seems long or if the requirements feel impossible. The dominoes are falling. The science is shifting away from masking symptoms with heavy carbidopa-levodopa cocktails and moving toward active, structural cellular regeneration.

The medical frontier is moving right beneath our feet. I am stepping onto it on July 21st, and I look forward to documenting every high-fidelity detail of what happens next for all of us.

On one hand, you have the “miracle drug” carbidopa-levodopa. While it is highly effective, you quickly find yourself trapped in a strict cycle of dependence, forced to manage a heavy cocktail of secondary medications just to mitigate its side effects or smooth out the physical limitations when the oral doses wear off. On the other hand, you have Deep Brain Stimulation (DBS). By all patient accounts, DBS is incredibly successful, but it is a massive mental hurdle to clear. Having a neurosurgeon install permanent electrodes into your brain and a pacemaker-like battery in your chest is highly invasive—making it feel, for many of us, like a last resort.

And underlying all of this is the heavy, undeniable truth: there is no cure for Parkinson’s Disease. When you are diagnosed with Early Onset Parkinson’s (EOPD) at 41, you realize you are looking at a decades-long horizon of managing degeneration. You have to think differently. As I weighed the options, I wanted something that felt less physically destructive and relatively low risk. That was when I heard about a game-changing advancement happening across the globe: Induced Pluripotent Stem Cell (iPSC) therapy.

Instead of just masking symptoms, this therapy aims to do what was once thought impossible: actually replace the dopamine-producing neurons that the disease has destroyed.

Breaking Down the Procedure

To understand why I felt comfortable pursuing this, you have to look at how the surgery actually works. The procedure involves drilling two dime-sized incisions into the skull—one on the left, one on the right. Using a specialized, ultra-fine needle, surgeons target the substantia nigra—a crescent-shaped structure in the midbrain that acts as the critical control center for movement, reward, and motivation. They then inject the stem cells into multiple precise points.

For an EOPD patient, the risk-to-reward ratio here felt entirely logical. The disease has already taken my dopamine-producing cells; I literally do not have them anymore. Implanting new ones to do the job felt like a natural fix.

Furthermore, while the cells themselves are cutting-edge, the delivery mechanism is not a shot in the dark. The surgical technique is highly similar to DBS, minus the permanent hardware installation of an electrode and pacemaker. This stereotactic brain surgery framework has been refined, proven repeatable, and utilized for over 35 years—with the first U.S. clinical trials for Parkinson’s utilizing similar surgical paths taking place as far back as 1991.

The Hunt for a U.S. Trial

When I first learned about this research, it was in its earliest stages, primarily concluding early clinical trials in Japan. But the moment I realized the science was real, I became hyper-focused. I didn’t wait for a doctor to bring it to me; I actively started hunting for any sign of a U.S.-based trial.

If you or a loved one is navigating Parkinson’s, you need to know about clinicaltrials.gov. It is an absolute treasure trove of data, though it isn’t exactly advertised or packaged for light bedtime reading. If you go there right now and search for “Parkinson’s Disease,” you will find over 3,800 entries of active trials, testing everything from new delivery methods to revolutionary compounds. It proves that behind the scenes, an immense amount of scientific momentum is building.

My vigilance paid off. I caught a brand-new entry on the site: a Phase I/II trial titled Transplantation of Human iPS Cell-derived Dopaminergic Progenitors (CT1-DAP001) for Parkinson’s Disease.

Even though this trial was strictly limited to just seven participants in the United States, I didn’t get in because of a special privilege or medical insider connection. I got in simply because I stayed informed. I had been tracking Kyoto University’s breakthrough successes in Japan, and with absolute conviction that a U.S. counterpart would eventually emerge, I kept searching.

When I saw the entry, the pieces clicked. The trial listed a powerful alliance of sponsors and collaborators: the University of California, San Diego (UCSD), Sumitomo Pharma, Kyoto University, and the CIRA Foundation. I knew instantly that this was the exact procedure I had been searching for. (They are actually still actively recruiting, though the eligibility criteria are incredibly narrow—a checklist I will break down in a future post).

Why We Should Have Radical Hope

To understand why this is a massive milestone for the entire Parkinson’s community, look at what just happened internationally. In March 2026, Japan’s health ministry made history by granting conditional approval to this exact therapy under the brand name Amchepry (developed by Sumitomo Pharma and Dr. Jun Takahashi at Kyoto University).

The science behind Amchepry is fascinating. It starts with adult cells taken from healthy donors. Scientists then “reprogram” them into iPS cells, which essentially act like embryonic stem cells—meaning they have the unique ability to rewrite their identity into almost any cell type in the body. Researchers guide these cells to become fully functioning dopamine neurons, which are then transplanted into the patient’s brain.

In the initial Japanese trial of seven patients, the results were incredibly encouraging. Over a two-year observation period, the implanted cells survived safely, caused zero serious safety concerns or tumor formations, and led to clear symptom improvements in the majority of the patients evaluated. Because Japan has created an accelerated regulatory pathway for regenerative medicine, they fast-tracked it for limited commercial rollout.

While Amchepry isn’t commercially available in the U.S. yet—and navigating insurance, international cross-over, and wide-scale manufacturing will take years—the dominoes are officially falling. Right now, UCSD is running the U.S. trial for CT1-DAP001 (the exact product underlying Amchepry), and Sumitomo Pharma America is concurrently recruiting for a sister trial across the U.S. using a similar iPSC concept called DSP-1083.

The Takeaway

I am sharing this not to promise an overnight cure, but to give you a tangible, data-driven reason to hold onto hope.

For decades, treating Parkinson’s has felt like managing a slow, invisible retreat. But the science is shifting. We are moving away from simply masking the decay and moving toward active, structural regeneration.

If you have this disease, do not tune out. Watch the trial registries, ask questions, and recognize that the medical frontier is moving forward right beneath our feet. We can’t control the hand we were dealt, but we can choose to look forward, stay informed, and believe in the advancements being written into medical history right now.

When I was first diagnosed with Parkinson’s disease in December 2019 at the age of 41, my doctor started me out with this introductory prescription: Sinemet (carbidopa-levodopa) Instant Release 25/100 mg, one dose three times a day. Fast forward seven years to July 2026, my medications have evolved into a complex cocktail through many years of trial and error. Currently, my daily regimen includes:

• Rytary (Carbidopa-levodopa Extended-Release): 36.25/145 mg — Two doses, three times a day

• Amantadine: 100 mg — Two times a day

• Propranolol: 10 mg — As needed for performance anxiety

• Mirtazapine: 10 mg — One dose at bedtime

• Sertraline: 50 mg — One dose daytime

Before getting into the specifics of these medications, I want to emphasize that my general approach has always been to minimize my dependency on them. Yet, even with that cautious approach, I have become increasingly dependent on this routine just to maintain my quality of life. For many years, working as a tech executive in Silicon Valley, I had no choice but to rely on these medications to avoid showing the weaknesses of my disability or letting it interfere with my job.

If my upcoming stem cell procedures work out and dramatically improve my situation, my goal is to stop using medications completely and remove this dependency. It is simply not a good long-term state to be balancing all these drugs. In the long run, I believe they can cause more harm than good due to the side effects they introduce.

The Reality of Carbidopa-Levodopa and Dyskinesia

The necessity for this medical cocktail begins and ends with the benefits and side effects of carbidopa-levodopa. On one hand, it helps restore your ability to walk, talk, and handle daily tasks with less stiffness and fewer tremors—which is a massive benefit. On the other hand, it comes with a trade-off of common side effects ranging from dizziness and stomach upset to nausea and uncontrolled movements, also known as dyskinesia.

In my case, I have had continuous trouble every time I take a dose. It frequently makes me feel sick enough that I have to lie down for hours. It also causes unnatural, involuntary movements—specifically an uncomfortable, sideways twisting type of motion.

If you have ever watched the movie *Awakenings* from a few decades ago with Robin Williams and Robert De Niro, it does a very good job of portraying what happens after many years and higher dosages of carbidopa-levodopa. The involuntary shaking is entirely real. Finding the right balance—an amount that helps with daily routines without interrupting life or causing other issues—is a constantly moving target that is very difficult to pinpoint.

Over the seven years I’ve been using carbidopa-levodopa, my dependency has close to tripled. At times I have tried higher doses to find a sweet spot, but tripling my intake over time is a trend I view with concern. Because the dyskinesia and nausea are highly distracting, I eventually transitioned to the extended-release formula. ER provides a smoother transition between on-and-off periods and feels a bit milder on my stomach.

Counteracting Side Effects: Amantadine

Strangely enough, Amantadine is a medication I have to take primarily to mitigate the negative side effects of my main medication. Because I experience extreme muscle stiffness and pronounced dyskinesia after taking carbidopa-levodopa, these symptoms can flare up to a large degree.

Amantadine during the daytime is a necessity for me to cope and stay balanced. It is an odd challenge of medication management to take a second drug just to counteract the first one, but that is the reality. If I get too much carbidopa-levodopa, the dyskinesia flares up to the point where the movement can feel unstoppable, much like the scenes in *Awakenings*. Amantadine does a great deal to mitigate that and keep things manageable, though like levodopa, it carries its own ongoing struggles with nausea, dizziness, and insomnia.

A Tool for High-Stress Situations: Propranolol

Of all the medications I take, Propranol is the mildest and most useful, with the fewest side effects. While it is a beta-blocker traditionally used to treat high blood pressure, heart rhythm issues, and migraines, it acts as an excellent tool for managing the physical symptoms of anxiety.

Whether it is a racing heart or a high-adrenaline situation where you feel nervous or need to perform under pressure, Propranolol mitigates those symptoms. This was an incredibly valuable tool for me during my career in leadership and management. Without it, I would have been lost. High tension and stress naturally trigger the involuntary movements and uncontrollable conditions that come with Parkinson’s. While I take my Rytary and Amantadine on a regular schedule, I save Propranolol for high-stakes moments—like giving a speech or handling a difficult interaction—to steady myself and get through the situation. It has been a true lifeline.

Managing Mood: Mirtazapine and Sertraline

The remaining two medications are focused on managing the mood swings, depression, and anxiety that have become more prominent the longer I have lived with Parkinson’s.

• Mirtazapine (10 mg, bedtime): This is an atypical tetracyclic antidepressant primarily prescribed for major depressive disorder, but used off-label for insomnia, anxiety, and nausea. I use it as a nighttime sedative to help me get to sleep when anxiety takes over before bed. Because I take it in a small amount, I haven’t experienced concerning side effects, with one exception: it definitely triggers a strong desire for midnight snacks, which isn’t ideal for long-term weight management.

• Sertraline (50 mg, daytime): Widely known by the brand name Zoloft, this antidepressant takes a few weeks to feel the full effect. Its impact is very subtle; once you are on a regular cycle and schedule, you simply feel a distinct shift toward a more stable brain chemistry.

The Takeaway

In summary, this unwieldy cocktail is the result of managing the side effects of carbidopa-levodopa while trying to sustain a reasonably good quality of life. Honestly, if I didn’t have daily routines to fulfill and a life where I need to function and show up, I would live without the medications entirely. I would choose to embrace the body slowness, the tremors, and the irregular gait over the side effects. But realistically, to function day-to-day, that isn’t an option.

For any other Parkinson’s patient looking at a complex regimen like this, please do not feel discouraged. You do not face all of this on day one. It is a gradual process of trial and error that you will explore and work out over time with the help of your neurologist and behavioral health specialist.

It is manageable, but it will often feel like a zero-sum game where you are trading one benefit for another. Knowing that this condition-by-condition trade-off will evolve over time is incredibly useful going in. The most important things you can do are to remain patient and stay completely clear on what you uniquely need to maintain your daily stability.

To get real answers, they have to peer inside your brain. For most of us, that means two specific tests: a DaTscan and an MRI.

The Science of Seeing Parkinson’s

A DaTscan (Dopamine Transporter scan) is a specialized nuclear imaging test designed to visualize your brain’s dopamine system. It’s the tool physicians use to clearly confirm Parkinson’s and rule out other conditions like essential tremors or certain types of dementia.

During the scan, a safe radioactive contrast agent called Ioflupane I-123 is injected into your arm. It travels through your bloodstream and binds to the dopamine transporters in the basal ganglia of your brain.

• A healthy brain shows beautiful, symmetrical, comma-shaped patterns on the screen.

• A Parkinson’s brain shows a loss of dopamine cells, which visually morphs those commas into asymmetrical shapes, tiny periods, or fades away entirely.

An MRI (Magnetic Resonance Imaging), on the other hand, uses powerful magnets and radio waves to create detailed cross-sectional images of your tissue. It’s completely painless, but it is incredibly loud (hello, earplugs!) and requires you to lie perfectly still inside a giant tube.

In my case, back in December 2019—about three months after a whirlwind of intense doctor visits and tests—my results came back with a classic Parkinson’s twist: My DaTscan showed clear signs of the disease, but my MRI was completely normal.

Enter the “Miracle Drug” (And the Dicey Reality)

The second my DaTscan results were confirmed, my neurologist immediately recommended medication. For Parkinson’s, the gold standard—often called the “miracle drug”—is Sinemet, the brand name for carbidopa-levodopa.

I started on a standard introductory dose:

Carbidopa-levodopa Instant Release (IR) 25/100 mg — 1 tablet, 2 to 3 times per day.

This is where the journey gets a little dicey. As a patient, it is incredibly hard to tell early on if a medication is doing more harm than good.

Don’t get me wrong: the medicine is undeniably effective. It does exactly what it’s supposed to do by replacing the missing dopamine in your brain, which restores your ability to walk, talk, and handle everyday tasks. But the trade-off is brutal.

Because raw levodopa causes severe nausea, it has to be paired with carbidopa. Think of carbidopa as a protective shield; it stops the levodopa from breaking down prematurely in your bloodstream, allowing a smaller, safer dose to successfully cross the blood-brain barrier.

Even with that shield, my body did not tolerate it well at first. Every single dose triggered intense dizziness and waves of nausea. I had to lie down constantly just to cope—a reality I still have to manage today.

The Name Game and the Pharma Cash Cow

As you navigate this disease, you will hear a dozen different names for the exact same chemical compound. Carbidopa-levodopa is simply the generic name. You will hear it called Sinemet, which was the original brand name manufactured by Merck before the rights were acquired by Organon.

Today, the pharmaceutical industry has found a way to make a killing (and I mean a huge amount of money) by repackaging this exact same drug into proprietary variants. You’ll hear names like:

• Crexont or Rytary (Extended-release formulations)

• Dhivy (Fractionated tablets)

• Parcopa (Orally disintegrating tablets)

• Stalevo (Carbidopa-levodopa combined with entacapone)

• Vyalev (Continuous subcutaneous infusion)

Here is what fires me up: the standard generic carbidopa-levodopa pill is dirt cheap and widely covered by insurance. Yet, pharmaceutical companies rake in thousands of dollars out-of-pocket from patients by introducing these branded variations.

Are some of these variants innovative? Yes. For instance, I personally find significant relief from the controlled, steady release of Crexont. But at the end of the day, it is all just carbidopa-levodopa. As patients, we have to take control of our care, look past the marketing, and tread carefully so we don’t get financially drained by the industry.

The Bottom Line

If your DaTscan comes back positive for Parkinson’s, you should fully expect your neurologist to write a prescription for carbidopa-levodopa right out of the gate. It is the cardinal first option for a reason—it gives you your movement and your quality of life back.

But while it is immensely helpful for symptom control today, it also introduces long-term side effects and unique complications down the road. We will dive into those challenges in another post.

However, I’ve learned that the absolute best treatment for Parkinson’s—before any prescription or cocktail of medications—is exercise.

The Battle Against the “Stuck” Sensation

With Parkinson’s, the mandate is simple but physically demanding: you have to keep moving your arms and legs as much as possible to slow down the progression of the disease.

Living it is a daily mental battle. You will experience moments of high stress when you realize you can’t move the way you used to. You will be slower. You will feel self-conscious because your movements feel completely “stuck” at times, trapped behind a wall your brain chemistry built. But pushing through that resistance is exactly how you fight back.

Redefining My Workout: Gym Weights vs. Cardio

While staying active is crucial, I had to completely reinvent how I look at physical fitness.

• Weight Training: Resistance training is a vital piece of my weekly ritual, but the goals have changed. If you were someone who loved lifting heavy or trying to bulk up at the gym in your pre-diagnosis life, you have to adjust. In my experience, carrying extra bulk or overdoing heavy weights only serves to slow you down. Keep weight training to a moderate, functional level.

• Cardio is King: The most effective exercises I have integrated into my routine are high-intensity cardio activities. Running, walking, and spin biking are fantastic for keeping the neural pathways firing.

• Shadow Boxing: Air boxing is incredible for coordination, speed, and forcing your arms out of their guarded, rigid posture.

Personally, I rely heavily on a spin cycle multiple times a week. Spinning gives me a high-intensity cardio workout without the harsh joint impact issues that come with outdoor running as my balance shifts.

The Takeaway: Treatment isn’t just about what a doctor prescribes you; it’s about the conscious choice to keep moving your body every single day, even when it feels stuck. This is easier said than done, as moving will become increasingly difficult as the medication dosages increase over time.

But general documentation entirely misses the point. It completely fails to capture the agonizingly slow, subtle deterioration that chips away at your body, your confidence, and your identity over years of steady progression.

Before my diagnosis, I was a highly confident, fiercely ambitious Silicon Valley executive. I was living the high-pressure tech dream—running a large-scale global team and hustling in a fast-paced media and entertainment role. Slowly but surely, that confidence began to deteriorate.

It is incredibly difficult to put into words how exhausting it is when your self-esteem is punched day after day, year after year.

The Evolution of the "Fiend"

At first, the thief shows up as a tiny thing—a slight trembling in a finger or two. You adapt. You become extra meticulous, constantly finding clever ways to conceal or hide your symptoms from colleagues and friends.

Then come the heavier losses:

• The Medication Fatigue: A constant, heavy lethargy brought on by a cocktail of daily prescriptions, leaving you needing a nap just to function.

• The Emotional Flattening: A strange, persistent brain fog that desensitizes you. You realize you can’t fully feel happiness or appreciate the good times—like a daughter's birthday—the way you used to. You feel a crushing sense of apathy and indifference.

• The Mental Slowing: Realizing you are no longer as sharp, witty, or quick on your feet as you were in the past.

• The Social Withdrawal: As physical symptoms worsen, you stop wanting to be around people. You avoid big crowds and public spaces, doing everything you can to remain invisible out of a painful mix of embarrassment and indifference.

For me, the most heartbreaking loss has been music. I used to be an avid musician, playing the piano, cello, guitar, drums, and singing. As Parkinson’s has taken its course, I have slowly lost my coordination and my ability to keep time and tempo. Lacking the fundamental motor skills and limited by dexterity, what used to be my most enjoyable hobby has been warped into moments of sheer anger and disaster.

And that really messes with your head. Because it’s never just about the music. It’s everything. Every chore, every exercise, every interaction with your family, every high-pressure moment at work—everything is altered by this slow and steady fiend.

The Chemistry of Apathy

I want to be clear about the mood aspect of this disease, because it is an invisible battleground. Long before my official diagnosis, I felt a heavy shroud of apathy, indifference, and fogginess. It required monumental effort just to reach out to friends, say hello, or meet someone for lunch. It created a painful rift between me and the people I cared about. Performance anxiety became my daily norm, forcing me to lean on beta-blockers (propranolol) just to steady my nerves and compensate for the shakiness born from a shattered self-image.

When my physical symptoms became visible, a new layer of frustration emerged: pity.

It is deeply irritating when people notice your struggles and ask if they can help. It enrages me, because I don't *need* to be helped. I am okay. I just need a little more time to do things. I am capable, and I want to remain capable.

But the sad reality is a losing battle. I have lost my balance and can no longer stand on one leg. I have a shuffling gait. Getting up from sitting or laying down is a monumental chore. It is both embarrassing and enraging to know exactly what you want to do in your brain, only to have your body refuse because a chemical dopamine deficiency simply won't allow the signal to go through. It feels like a slow, excruciating war of attrition.

To be clear: I have never felt suicidal or hopeless to the point of wanting to end my life. But what is truly terrifying is the apathy. It is a numbing indifference where you simply stop caring about things you *know* you should care about. This isn't an intentional emotional choice; it is literally the shifting chemistry of the brain dulling your range of emotions and your response to the world around you. That fogginess is a physical weight you feel right in your forehead, all day long.

A Jolt of Reality

I don’t write this to make you feel depressed. I write this to give high-fidelity language to an internal experience that is nearly impossible to convey to someone who hasn't lived it.

Facing an Early Onset diagnosis at a younger age brings a painful, yet profound, revelation. Suddenly, you find yourself empathizing with people 20 or 30 years older than you. You are forced to become incredibly wise, astute, and intensely aware of the delicate, limited nature of human life.

At that point, the noise and trivia of the world evaporate. For me, all the corporate formalities have dropped away, and I’ve taken radical ownership of what actually matters. I stop spending time on social media like Facebook or Instagram. I focus strictly on eating well, exercising, and spending precious time with the family and friends who are closest to me.

When your time feels highly limited, you are forced to cut through the nonsense and value yourself. It is a brutal jolt of reality, but it teaches you to make the absolute most of the precious, limited time you have left.

Then came the pinky.

It was a tiny, rhythmic betrayal. It showed up at dinner tables during a “cheers” or when I reached for something in public. In the cold, it became a visible tremor that felt like a neon sign of my own discomfort. I spent years dismissing it as nerves or fatigue, even though, deep down, I knew I wasn’t actually nervous.

The Imposter Inside

By the time I was an executive at a leading tech company, leading a global team, the stakes had changed. In high-pressure meetings, the shaking intensified. I didn’t think “neurology”; I thought “Imposter Syndrome”. I worked with professional coaches, convinced this was a confidence gap I could bridge with enough willpower.

It took an outside perspective to see what I was hiding in plain sight. Eric, my coach at the time didn’t talk about my leadership style; he pointed at my left shoulder. “You’re shielding yourself,” he noted. He urged me to see a doctor.

The Gauntlet of “No”

The path to the truth was paved with false starts. I was misdiagnosed with herniated discs and neck issues, spending months in physical therapy and chiropractic sessions that did nothing for my tremors.

The healthcare system isn’t always designed to find the truth; it’s often designed to find the easiest answer to avoid liability. My first neurologist dismissed me entirely, suggesting I was overthinking it. The second was stumped. It wasn’t until I broke through the “healthcare politics” and demanded a specialist with deep Parkinson’s experience that the fog cleared.

Five minutes. That’s all it took for the third doctor to see what the others missed. “Early Onset Parkinson’s,” she said with conviction.

The Anatomy of an “Aha” Moment

People expect a diagnosis like this to be a moment of devastation. For me, it was a moment of profound demystification.

The mystery that had haunted me for over a decade finally had a root cause. It wasn’t a lack of confidence, a bad back, or “all in my head.” It was a biological reality. There is a strange, refreshing peace that comes when your internal hypothesis is finally validated by data.

Lessons from the Shaky Path

Through this journey, I’ve realized that while we cannot control the cards we are dealt, we are the only ones responsible for how they are played.

• You are your own Chief Medical Officer: Doctors and specialists are often not incentivized to hunt for the truth; they are incentivized to process the patient in front of them. If an answer doesn’t feel right, question everything. Exhaust every question until you are satisfied.

• Trust Your Intuition over the “Expert”: The first neurologist ignored my data; I had to contest that ignorance to get to the bottom of my condition.

• Radical Acceptance is Freedom: The hardest part of this process was accepting the reality of the diagnosis. But once I accepted it, I could finally prioritize what actually matters in life and work.

• The Power of Observation: Sometimes we are too close to our own “shielding” to see it. Listen to the “Erics” in your life—the people who see the things you’ve subconsciously learned to hide.

As a naturally private person, I have spent years guarding my journey, keeping the vulnerabilities and the “odd” sensations to myself. However, I’ve decided to step forward and share my story for two vital reasons.

1. Capturing the “Now” While the Signal is Clear

Parkinson’s is a progressive thief. Year after year, the symptoms have gradually deepened.

• Current State (2026): I can still stand and walk independently.

• The Impairment: My fine motor skills and physical abilities—specifically on my left side—are now quite impaired.

• The Motivation: I am acutely aware that later stages of this disease can impact cognitive ability or even lead to dementia.

I feel a sense of urgency to document my experiences with high-fidelity detail right now, while my mind remains sharp and my voice is still my own. If these reflections can help others navigating their own diagnosis, then every word is worth the effort.

2. Standing on the Edge of a Medical Frontier

The second reason is perhaps the most profound. I am currently one of only seven clinical trialists in the United States undergoing a groundbreaking new treatment: Induced Pluripotent Stem Cell (iPSC) therapy.

This procedure involves:

• Reprogramming: Converting adult donor cells into dopamine-producing neurons.

• Transplantation: Surgically placing these new neurons directly into my brain to replace what the disease has taken.

Being part of this small cohort is both a heavy responsibility and a beacon of hope.

More to Come

I hope this information serves as a companion for those on their own Parkinson’s journey and as a resource for the caretakers who support us. While I cannot control the cards I’ve been dealt, I am taking full responsibility for how I play them.