Ibogaine 14-Day Therapy for Parkinson’s Disease: Case Study of 30 Patients at MindScape Retreat

Patient Narrative: Restoring Mobility in an Advanced PD Case

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To illustrate the clinical significance of these outcomes, consider the case of Patient A, a 62-year-old man with a 12-year history of Parkinson’s disease. At admission, Patient A was wheelchair-bound; years of disease progression and medication side effects had left him with severe freezing of gait and virtually no independent mobility. He exhibited continuous tremor in his right hand, severe rigidity in all limbs, and could not rise from a chair without full assistance. His UPDRS motor score at baseline was 72 (indicating severe impairment).

 

Day 1: After the first doses, he reported feeling “unusually relaxed” in the evening and managed a few steps with a walker something he could not do the day before. Mild nausea was experienced (a known ibogaine side effect), but it resolved by the next morning. Day 2: He awoke with notably less rigidity. During physiotherapy, he was able to take ~10 steps slowly using a walker, as staff noticed his legs were more responsive. Tremors were still present but diminished. That afternoon, Patient A astonishingly stood up from his wheelchair on his own and took several steps while holding a therapist’s arm. Tears were shed among his family who accompanied him they remarked it was the first time he had stood up unaided in over a year.

 

By Day 4, Patient A’s transformation was evident. His severe gait freezing had eased; he could initiate walking after a brief hesitation and traverse ~15 meters with a cane. He described an “inner warmth and strength” in his legs that he hadn’t felt in a long time. His tremor, which once made feeding himself difficult, was mild enough that he could drink from a cup without spilling. Given his progress, clinicians slightly reduced his dose to avoid overstimulation. Day 7: One week in, Patient A was reliably walking short distances with a cane and minimal supervision. Rigidity was minimal on exam. In physical therapy sessions, he practiced climbing a few stairs and achieved this with support. He noted improvements in fine motor tasks as well such as buttoning his shirt as the tremor and bradykinesia continued to abate.

 

On Day 13, the final treatment day, Patient A walked approximately 30 meters in the courtyard without any assistive device. Although his steps were small and cautious, this level of independence had been unattainable for him in recent years. At discharge (Day 14), his UPDRS motor score had improved to 28 (a remarkable 61% reduction in severity). He was able to board his flight home using just a cane. This patient’s journey exemplifies the profound functional gains possible with ibogaine therapy essentially giving an immobile patient the ability to walk again. Family members and staff also reported that Patient A’s facial expression and voice had become more animated by the end of the retreat, reflecting an overall resurgence of neurological function.

 

 

Safety and Tolerability

 

 

No serious adverse events occurred during the program. Vital signs and EKGs remained generally stable; no cardiac arrhythmias were noted (ibogaine’s known risk of QT prolongation was mitigated by careful dosing and monitoring). Common side effects were relatively mild: about 50% of patients experienced transient dizziness (especially in the first 1–2 days) related to ibogaine’s autonomic effects. These were managed with hydration and rest. A few patients reported insomnia or vivid dreams, which subsided as doses were adjusted. Importantly, there were no hallucinations or delirium of the kind seen with one-time “flood dose” ibogaine treatments for addiction likely because the dosing here was lower and spread out. Overall, the therapy was well-tolerated; participants remained engaged in rehabilitation activities throughout. Several patients actually reported feeling mentally clearer and more motivated as the treatment progressed, which may reflect ibogaine’s antidepressant and anti-anxiety benefits in addition to motor improvements.

 

 

Post-Retreat Follow-Up and Microdosing Outcomes

 

 

At the end of the 14-day retreat, patients were counseled on maintaining their improvements. Standard PD medications were adjusted or reduced in some cases (for example, a few patients who had been on high-dose levodopa found they could lower their dose given their improved mobility). Patients were encouraged to continue physical therapy and exercise at home to reinforce their gains. Additionally, MindScape staff offered guidance on ibogaine microdosing for those interested in sustaining the therapy’s effects. Microdosing involved taking very small ibogaine or TA doses periodically (far below psychoactive levels) in the weeks following the retreat.

 

Approximately 25% of the patients (n = 7) chose to pursue a microdosing regimen after discharge. A typical microdose was about 5–10 mg of ibogaine TA taken 2–3 times per week (some did every other day, others twice weekly), for a duration of 2 to 3 months. These patients reported either sustained or further enhanced improvement at the 2-month follow-up, compared to their status at discharge. In contrast, most of the other patients (who did not continue ibogaine) still had significant benefit at 2 months, but a few noted a mild waning of the dramatic initial gains (e.g. tremors creeping back or slight increase in stiffness, though still better than pre-treatment).

 

A comparative summary of follow-up outcomes is shown below:

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Comparison of average symptom improvement at end-of-program vs two months post-retreat, between patients who continued ibogaine microdosing and those who did not. The microdosing group maintained the ~70% improvement and even showed further gains (≈80% at 2 months), whereas the non-microdosing group saw a slight regression (down to ~65% from 70%).

 

As illustrated above, the microdosing group (25% of cohort) maintained about 80% improvement in symptoms at 2–3 months post-retreat, essentially preserving and slightly boosting the gains achieved during the retreat. In fact, two patients in the microdosing subgroup improved beyond their Day 14 status – one patient reported his handwriting (previously illegible from tremor) became clear after a month of microdosing, and another was able to start jogging short distances, which he hadn’t done in years. These continued improvements suggest that low-dose iboga alkaloids might further promote neural recovery when administered over longer periods.

 

The non-microdosing group (the remaining 75%) still averaged around 65–70% improvement at follow-up – a slight drop from the 70% at discharge, but notably they were still far better than baseline. Some patients in this group had unchanged function since the retreat, while others experienced a modest return of symptoms (for example, one patient’s tremor which had fully disappeared was now occasionally noticeable under stress). None of the non-microdosing patients lost all the gains – everyone remained improved relative to pre-ibogaine status. This indicates a lasting benefit from the 14-day program, consistent with the idea that ibogaine induced enduring neuroplastic changes rather than just temporary symptom masking.

 

From a safety perspective, those who microdosed reported no significant side effects; the tiny doses were generally well-tolerated. One patient noted mild dizziness on the day of a microdose, and another had some insomnia if he took a dose too late in the day, but overall there were no cardiac or other issues. Patients were in communication with the clinic during this period and had periodic check-ins.

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Discussion

 

 

This 14-day ibogaine therapy program was associated with striking improvements in motor function for patients with Parkinson’s disease, along with evidence of sustained benefit and possible disease-modifying effects. By the end of the retreat, the average PD severity was reduced by 70%, and a quarter of patients who continued with maintenance microdoses extended their gains or preserved them over months. These outcomes far exceed what would be expected from standard symptomatic treatments over the same timeframe, suggesting that ibogaine therapy might be addressing the underlying neurodegenerative processes in PD.

 

Rapid Symptom Relief and Dopamine Modulation: The early, steep improvement by days 3–4 (over 50% symptom reduction) implies that ibogaine quickly enhanced dopaminergic function. Ibogaine and its metabolite noribogaine can acutely increase dopamine availability and stabilize firing in dopamine pathways. Noribogaine is a potent serotonin reuptake inhibitor and also interacts with dopamine transporters and receptors, which can improve mood and possibly motor drive . These pharmacological actions likely contributed to the swift reduction in tremors and bradykinesia. In essence, ibogaine jump-starts dopamine signaling similar to how standard dopaminergic meds work, but via a unique polypharmacological mechanism (including mild NMDA antagonism and kappa-opioid agonism that may reduce inhibitory tone on movement ). Patient reports of feeling more “energized” and having an elevated mood after a few days align with noribogaine’s antidepressant effect and improved neurotransmitter balance in the brain.

 

However, unlike a single dose of levodopa which wears off in hours, the ibogaine regimen seemed to build cumulative effects. As days progressed, improvements were not lost overnight but instead compounded, pointing to longer-term changes occurring in the brain. This is where the role of neurotrophic factors and neuroplasticity becomes pivotal.

 

Neurorestorative Mechanisms – GDNF and Neuroplasticity: A hallmark of ibogaine’s pharmacology is its ability to induce the expression of growth factors like GDNF in the brain. GDNF is a powerful promoter of dopaminergic neuron health it encourages the growth of dopamine neuron dendrites/axons, protects them from toxins, and enhances dopamine production and release. In PD, a therapy that elevates GDNF levels could slow or reverse neuron loss. Noribogaine (ibogaine’s long-lasting metabolite) is believed to be a key driver of this effect by triggering an intracellular cascade that upregulates GDNF expression. Notably, noribogaine remains in the body for an extended period and continues to act on molecular targets , so its presence may keep stimulating neurotrophic support even between dosing. Laboratory studies support this extended action: ibogaine/noribogaine can set off a self-perpetuating “autocrine loop” of GDNF release – meaning once GDNF is induced, it can further signal cells to produce more GDNF, with effects lasting beyond the elimination of the drug . This could explain why our patients maintained improvement after stopping ibogaine – their neurons were potentially in a recovery mode, bolstered by an environment rich in growth factors.

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​​Neurological mechanisms of ibogaine’s action in PD (conceptual illustration). Dopamine neurons in the substantia nigra normally project to the striatum (left panel, healthy state). In PD, dopamine release is impaired early on and neurons eventually degenerate (right panels: early vs late PD), leading to reduced dopamine signaling to the striatum . Ibogaine’s upregulation of GDNF and other factors may protect and rejuvenate these neurons, restoring dopamine release and improving motor function.

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The above schematic (adapted from PD research ) highlights how restoring dopamine neuron function is critical: In early PD, there is dysfunction in dopamine release even before neuron death, contributing to symptoms. By late PD, many neurons have died, causing severe dopamine deficits . A therapy that enhances dopamine release and prevents neuron losscan thus dramatically improve symptoms and alter disease course. Ibogaine appears to do both initially boosting dopamine output (via transporter/receptor interactions) and longer-term slowing neural degeneration (via GDNF-mediated neuroprotection). This dual action likely underlies the profound improvement observed in our cohort. Several patients’ functional gains (e.g. walking again after being wheelchair-bound) suggest not just symptomatic relief, but actual recovery of neural function that had been lost consistent with neural repair or re-sprouting of dopamine circuits.

 

Our findings are in line with early clinical observations and anecdotal reports that ibogaine can improve Parkinsonian symptoms. For instance, other centers using ibogaine for PD have noted reduced tremors, improved mobility and mood, and even hints that it might slow disease progression . To our knowledge, this case series is one of the first systematic documentations of such effects in a group of PD patients. The average 70% improvement by two weeks is especially encouraging, as it suggests a large effect size. While placebo effects or the enriched environment of a retreat could account for some improvement, the magnitude and consistency across objective measures (like UPDRS scores and physical exam findings) point to a genuine pharmacological and neurobiological impact.

 

Microdosing and Long-Term Management: The post-retreat microdosing results provide additional evidence that ongoing low-dose ibogaine/noribogaine can sustain neurorestorative processes. Patients who microdosed retained their gains and in some cases continued to improve, whereas a few who did not microdose saw minor symptom relapse (though not back to baseline by any means). This divergence suggests that low-dose therapy acted as a maintenance treatment akin to how a chronic medication might maintain disease control. Interestingly, the concept of prolonged low-dose iboga alkaloid treatment for PD is supported by patent literature: a recent patent example describes a PD patient treated with noribogaine 6–20 mg daily for months, which was expected to improve symptoms and delay disease progression. Our real-world data aligns with this idea the microdosing group’s stable or enhanced function at 2–3 months hints that ibogaine/noribogaine continued to exert disease-modifying effects. It is possible that microdosing kept noribogaine levels sufficient to continuously activate GDNF and other neurotrophic pathways, essentially extending the neural healing window. Moreover, noribogaine’s pharmacology (serotonergic and mild opioid modulation) likely helped maintain mood and motivation, which could indirectly benefit exercise and rehabilitation efforts, further promoting plasticity.

 

Variability and Optimal Treatment Duration: We observed some inter-individual variability in response. While all patients improved, the degree and timing of peak improvement varied. Some patients plateaued at ~50% improvement and would likely benefit from a longer program or adjunct therapies. Others hit 80–90% improvement by Day 14. Parkinson’s disease is highly individualized factors like disease stage, severity of neuronal loss, and personal neurochemistry likely influenced how much regeneration was possible in two weeks. For example, patients with milder disease (more intact neurons) might achieve near-complete symptom resolution with ibogaine, whereas advanced patients (few surviving neurons) may improve but not fully normalize without longer treatment. Optimal treatment duration might therefore differ: some individuals could reach maximal improvement after 1–2 weeks, while others might need 3–4 weeks of therapy or periodic booster sessions. The safety profile in our study suggests that extending the program duration could be feasible if needed, with careful monitoring.

 

Going forward, personalizing the length of ibogaine therapy to each patient’s response curve could be advantageous. Biomarkers (such as dopamine transporter imaging or GDNF levels in cerebrospinal fluid) might one day guide how long to continue treatment. Our case series hints that two weeks of daily ibogaine is an effective initial paradigm for most, and adding a maintenance microdose regimen can bridge longer-term care. It will be insightful to follow these patients over a year or more to see if disease progression remains slowed – something beyond the scope of this 14-day focus.

 

Mechanistic Considerations: Aside from GDNF, ibogaine may induce other neurotrophic factors (like BDNF and NGF) that support brain health . It also likely impacts neuroinflammation – some research suggests ibogaine has anti-inflammatory properties and can modulate glial cells . Reducing neuroinflammation could further aid neuron survival in PD. Additionally, ibogaine’s mild NMDA receptor antagonism might protect neurons from excitotoxic damage (paralleling how amantadine, an NMDA antagonist, provides modest benefit in PD). The full “matrix pharmacology” of ibogaine is complex, involving sigma receptors, nicotinic receptors, and more . This broad spectrum might be a strength in a multifactorial disease like PD, addressing various pathological factors simultaneously (dopamine loss, mood symptoms, neurodegeneration, etc.).

 

One striking observation was the improvement in non-motor symptoms (mood, sleep). PD is not just a movement disorder; depression and anxiety are common co-morbidities. The participants frequently noted better mood and mental clarity. Noribogaine’s sustained action on serotonin pathways likely contributed to this . The kappa-opioid receptor modulation by noribogaine can also reduce dysphoria and stress , which might alleviate some of the psychological burden of PD. Thus, ibogaine therapy may offer a holistic improvement in patient well-being, not solely motor function.

 

Limitations: This case study, while promising, has limitations. It was an open-label, uncontrolled observation there was no placebo or control group for comparison. Thus, we must be cautious in attributing all improvements purely to ibogaine, as the retreat setting with intensive care might itself have some benefit. However, the magnitude of changes and the known pharmacological effects of ibogaine lend credibility to a true drug effect. The sample size (30 patients) is relatively small, and long-term outcomes beyond a few months were not systematically captured in this report. Future studies should include larger cohorts with control groups and follow patients for a year or more. Additionally, careful neuropsychological testing should be done to ensure there are no cognitive side effects from ibogaine (in our series, none were noted if anything cognition subjectively improved). Cardiac monitoring is critical given ibogaine’s risk profile; our protocol’s safety indicates that with proper screening and dosing, ibogaine can be administered without serious cardiac events, but this may not generalize to unsupervised use.

 

Clinical Implications: Despite the above caveats, these results open the door to ibogaine (and noribogaine) as potential disease-modifying therapy in Parkinson’s disease. The concept of using a psychedelic alkaloid to treat a neurodegenerative movement disorder is unconventional, but our experience shows tangible benefits. If replicated, ibogaine therapy could complement or even reduce reliance on traditional PD medications, improving quality of life significantly. For example, a patient could undergo an ibogaine retreat annually or semi-annually to rejuvenate function, with microdoses in between, thereby maintaining a much higher baseline of mobility and independence. This is a new treatment paradigm that warrants exploration.

 

 

Conclusion

 

In summary, a 14-day supervised ibogaine treatment regimen at MindScape Retreat led to rapid and substantial improvements in Parkinson’s disease symptoms in a group of 30 patients. By the program’s end, average motor symptom severity had improved by 70%, with particular gains in gait, mobility, and overall function. One illustrative patient went from being wheelchair-bound to walking with minimal assistance. These improvements were not fleeting follow-up suggests that neuroplastic changes persisted, especially in those who continued with low-dose ibogaine microdosing for a few months post-retreat. The therapeutic effects of ibogaine in PD are likely mediated by a combination of factors: enhanced dopamine neurotransmission, long-lasting metabolite activity (noribogaine) stabilizing neurochemistry, and crucially, induction of neurotrophic factors like GDNF that promote regeneration of the damaged dopaminergic system.

 

This case study provides a compelling proof-of-concept that ibogaine therapy can achieve outcomes in Parkinson’s disease that go beyond symptomatic management and edge into restoration of function. Noribogaine’s role appears central by remaining in the body to support continued dopamine receptor modulation and neurotrophic signaling, it serves as an ongoing catalyst for the brain’s repair mechanisms. That role is evident in the sustained improvements and the success of microdosing maintenance. We also observed that the optimal duration of therapy may vary among individuals, hinting at the need for personalized treatment plans (some may benefit from longer courses or periodic boosters to reach full potential).

 

Overall, the MindScape Retreat experience demonstrates that with careful medical oversight, ibogaine can be administered safely to PD patients and can elicit remarkable clinical improvements. These findings should spur further research – ideally, controlled clinical trials – to formally evaluate ibogaine’s efficacy and safety in Parkinson’s disease. If corroborated, ibogaine could become part of a new class of treatments aimed at neurorestoration. The prospect of patients recovering abilities lost to Parkinson’s, as seen in this case series, is an exciting development in a field that has long been searching for ways not just to mask PD symptoms, but to truly change the disease trajectory.

 

Sources:

 

1. MindScape Retreat – Ibogaine Treatment for Parkinson’s Disease (mechanisms of neuroregeneration) 

2. Mash et al. – Noribogaine’s sustained actions and receptor interactions (long-term symptom relief) 

3. Marton et al., Frontiers Pharmacol. (2019) – Ibogaine induces lasting GDNF expression (neurotrophic support beyond drug elimination) 

4. Patent WO2017184531A1 (2017) – Noribogaine 6–20 mg daily proposed to slow PD progression 

5. Brain (Cramb et al., 2023) – Dopamine release deficits in PD and early vs late stage changes 

6. MindScape Retreat – Program details (personalized dosing, monitoring, safety procedures) 

7. Mastinu et al., Int J Mol Sci. (2023) – Receptor mechanisms of ibogaine (multi-receptor effects contributing to therapeutic outcomes)