iboga tree and neurons representing neuroplasticity of iboga and ibogaine

Neuroplasticity of Iboga and Ibogaine

Iboga is a medicinal herb known for its effect on attenuating symptoms of addiction and withdrawal. What is more, a single dose of the shrub is often effective in completely eradicating drug-seeking behavior. Less known benefits include improving mental health conditions, PTSD, trauma, traumatic brain injuries, autoimmune disease, Parkinson’s, and creating new healthy habits. 

These long-term effects are possible thanks to Iboga’s ability to literally rewire the brain. The underlying mechanism is called neuroplasticity and involves the innate ability of the brain to change, repair, and adapt.

Nevertheless, our highly developed central nervous system has a limited ability to recover due to the complex mechanism and factors affecting neuroplasticity.

Iboga may be able to stimulate the majority of these factors in different parts of the brain and boost neuroplasticity which has the potential to provide novel therapeutic options and change neurology forever.

What is Iboga?

Tabernanthe Iboga is a perennial shrub that’s native to the equatorial parts of West Africa. The plant contains several alkaloids which contribute to its psychoactive and medicinal properties.

The main psychoactive alkaloid is called ibogaine and its concentrations are the highest in the roots, more specifically the root bark.

Apart from ibogaine, other alkaloids in the shrub that also contribute to the medicinal properties include tabernanthine, ibogamine, coronaridine, voacangine, and harmaline.

Iboga has been used by the practitioners of the spiritual tradition called Bwiti for thousands of years, but since they pass everything down via oral tradition, not much has been physically documented. 

Data on the benefits of Iboga dates back to 1962, with multiple case studies reporting successful treatments of addictions to heroin, cocaine, morphine, amphetamine, and alcohol (1).

People who have taken Iboga often report that they no longer have a desire to take drugs or experience withdrawal symptoms. That is usually combined with a unique psychedelic experience, which they describe as life-changing.

Currently, it is approved by several countries in the world for medical use in anti-addiction therapy and detox. Furthermore, Ibogaine is also investigated for the benefits of improving mood and boosting neuroplasticity.

What is Neuroplasticity?

Neuroplasticity is the capability of neurons to reorganize, adapt and even form anew. There are two main types of neuroplasticity – structural and functional.

Functional neuroplasticity is more common and it involves the formation of new synapses (connections) between different brain cells. The process plays a key role in normal brain function, adaptation, and the formation of memories.

On the other hand, structural neuroplasticity occurs more slowly and is often called “remapping”. It involves anatomical reorganization of brain cells and even the formation of new ones – a process that was previously considered inactive in adults.

Studies report that there are several growth factors in the brain, which support the growth, survival, and adaptation of old neurons as well as the formation of new ones from progenitor cells (2).

Some of these factors include brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), glial cell-derived neurotrophic factor (GDNF), ciliary neurotrophic factor (CNTF), and others.

According to scientists, both BDNF and GDNF can induce remodeling in the nerve tissue and the formation of new connections (3).

BDNF might also stimulate neurogenesis, which is the formation of new neurons in parts of the adult brain that still retain stem cells (4).

How does Iboga (Ibogaine) increase Neuroplasticity?

Iboga may attenuate drug-seeking behavior and symptoms of depression by affecting several neurotransmitters in the brain. 

Yet, those effects do not explain the long-term effects of Iboga, such as requiring the brain and completely curing addiction. As it turns out, Ibogaine is a potent activator of several neurotrophic factors in the brain, namely NGF, BDNF, and GDNF.

A study on rats reported that 24 hours after administering Ibogaine, the alkaloid leads to a significant increase in the activity of these factors in different parts of the brain (5).

GDNF was significantly upregulated in areas rich in dopaminergic neurons in the midbrain which are linked to reward-driven behavior and are often affected by drugs of abuse.

NGF and BDNF were upregulated in all areas linked to the reward systems in the brain as well.

Furthermore, they were activated in the prefrontal cortex, which is implicated in planning complex cognitive behavior, personality expression, decision making, and moderating social behavior.

Non-hallucinogenic analogs to Ibogaine are not effective in activating neurotrophic factors such as GDNF (6).

What are the benefits of increasing Neuroplasticity?

Addiction & Detox

According to researchers, the development of an addiction is related to dysfunction of the neurotrophic growth factors (7).

Long-term addictions lead to unfavorable neural remodeling combined with reduced neuroplasticity, which significantly complicates the treatment process.

Scientists suggest that the activation of these neurotrophic factors, and especially GDNF restores normal neuroplasticity and plays a key role in Ibogaine’s long-lasting anti-addictive properties (8). 

By stimulating neuroplasticity and inducing favorable brain remodeling, Ibogaine may reverse the biochemical adaptations to chronic exposure to drugs of abuse in the reward system. 

Evidence also reveals that the induction of GDNF by ibogaine may activate an autocrine loop, leading to a long-term synthesis and release of GDNF that persists beyond the short-term presence of Ibogaine after the therapy (9). 

Creating new Habits

The release of dopamine controls reward-driven behavior and plays a key role in the formation of habits (10).

Yet, new habits can’t form without the critical role of neuroplasticity, which helps the dopaminergic neurons form new connections and switch the time of dopamine release. 

Furthermore, due to their role in neuroplasticity, BDNF levels can dynamically impact reward-related decision-making and suppress unhealthy habits. 

For example, studies in mice reveal that reduced BDNF expression leads to a loss of control over unhealthy habits such as alcohol consumption (11).

iboga ibogaine neuroplasticity

Traumatic Brain Injuries

Traumatic brain injury (TBI) is damage to the brain that has occurred due to external factors such as sport and work traumas, accidents, violence, etc. The condition can lead to a progressive loss of brain cells and disability.

Neuroplasticity plays a critical role in the ability of the brain to recover different neurological functions after TBI.

The activation of BDNF may induce neuroplastic changes that lead to adaptive neural repair and may have the potential to reverse cognitive and emotional deficits in TBI patients (12).

Currently, animal studies report that the extensive activation of BDNF in zebrafish can lead to a complete brain repair after a TBI (13). 

The neurotrophic factor was able to induce both functional and structural neuroplasticity leading to the formation of new neurons.


Research shows that BDNF increases nerve cell survival in autoimmune diseases that affect the human brain such as autoimmune encephalomyelitis and multiple sclerosis (MS).

In a model of autoimmune encephalomyelitis in mice, experiments reveal that lack of BDNF reduces neuroplasticity and speeds up brain cell death rate (14).

Furthermore, evidence suggests that increasing NGF and GDNF may protect brain cells against cell death and slow down the progression of MS (15).

According to researchers, there are several lines of evidence, both from clinical research and animal models, suggesting that neurotrophic factors play a pivotal role in neuroprotective and neuro-regenerative processes that are often defective in MS (16).

Therefore the scientists suggest that neuroprotective strategies might be used as potentially valuable add-on therapies, alongside traditional immunomodulatory treatment in this condition.

Mental health conditions – depression & anxiety

Mental health conditions such as depression and anxiety disorders appear to be associated with changes in brain neuroplasticity.

For example, a study in almost 2000 individuals with depression reports that the participants had significantly reduced activity of BDNF and neuroplasticity (17).

BDNF was also low in patients with stress-related disorders such as anxiety and chronic fatigue (18).

Furthermore, individuals with genetically determined low expression of GDNF were much more likely to suffer from anxiety disorders (19).


GDNF is investigated as a potential treatment for Parkinson’s since it may help protect and even repair the neurons that are otherwise damaged due to the condition.

Researchers reveal that the activation of GDNF may prevent the death of dopaminergic neurons which can slow down the progression of the disease (20).

Furthermore, case reports suggest that it can induce the formation of new dopamine neurons – the ones damaged and lost in Parkinson’s. 

For example, infusion of GDNF  into the posterior putamen of 62-year-old patients causes similar sprouting of dopaminergic fibers in association with clinical improvement in Parkinson’s disease symptoms by 38% (21).

Another trial in 5 patients supports these findings and reports over 60% improvement in some of the symptoms 1 year after the therapy (22). 


There is a substantial amount of evidence that neuroplasticity may play a role in a wide range of neurological conditions.

Despite that, there are serious obstacles to future research. For example, scientists lack reliable and non-invasive methods to increase the levels of neurotrophic factors in the brain such as GDNF and BDNF (23, 24).

The reason is that there is a barrier between the brain and the rest of the circulation in your body, called the blood-brain barrier, and infusion with neurotrophic factors is ineffective in reaching the central nervous system.

On the other hand, Ibogaine and other alkaloids present in Iboga can easily pass through this barrier and rich all parts of the brain.

Besides, Iboga happens to increase GDNF, BDNF, and NGF levels in the brain including areas affected by specific neurological disorders such as addictions, withdrawal, mental health conditions, Parkinson’s, MS, and encephalomyelitis.

Hopefully, future research will investigate the effectiveness of Tabernanthe Iboga and its potent alkaloids on improving neuroplasticity, brain recovery, and remapping.


  1. Lotsof, H. S., & Alexander, N. E. (2001). Case studies of ibogaine treatment: implications for patient management strategies. The Alkaloids. Chemistry and biology56, 293–313. https://doi.org/10.1016/s0099-9598(01)56020-4 
  2. Deister, C., & Schmidt, C. E. (2006). Optimizing neurotrophic factor combinations for neurite outgrowth. Journal of neural engineering3(2), 172–179. https://doi.org/10.1088/1741-2560/3/2/011 
  3. Lu,, B. & Figurov,, A. (1997). Role of Neurotrophins in Synapse Development and Plasticity. Reviews in the Neurosciences8(1), 1-12. https://doi.org/10.1515/REVNEURO.1997.8.1.1
  4. Zigova, T., Pencea, V., Wiegand, S. J., & Luskin, M. B. (1998). Intraventricular administration of BDNF increases the number of newly generated neurons in the adult olfactory bulb. Molecular and cellular neurosciences11(4), 234–245. https://doi.org/10.1006/mcne.1998.0684 
  5. Marton, S., González, B., Rodríguez-Bottero, S., Miquel, E., Martínez-Palma, L., Pazos, M., Prieto, J. P., Rodríguez, P., Sames, D., Seoane, G., Scorza, C., Cassina, P., & Carrera, I. (2019). Ibogaine Administration Modifies GDNF and BDNF Expression in Brain Regions Involved in Mesocorticolimbic and Nigral Dopaminergic Circuits. Frontiers in pharmacology10, 193. https://doi.org/10.3389/fphar.2019.00193
  6. Carnicella, S., He, D. Y., Yowell, Q. V., Glick, S. D., & Ron, D. (2010). Noribogaine, but not 18-MC, exhibits similar actions as ibogaine on GDNF expression and ethanol self-administration. Addiction Biology15(4), 424–433. https://doi.org/10.1111/j.1369-1600.2010.00251.x 
  7. Angelucci, F., Ricci, V., Pomponi, M., Conte, G., Mathé, A. A., Attilio Tonali, P., & Bria, P. (2007). Chronic heroin and cocaine abuse is associated with decreased serum concentrations of the nerve growth factor and brain-derived neurotrophic factor. Journal of psychopharmacology (Oxford, England)21(8), 820–825. https://doi.org/10.1177/0269881107078491 
  8. Corne, R., & Mongeau, R. (2019). Utilisation des psychédéliques en psychiatrie : lien avec les neurotrophines [Neurotrophic mechanisms of psychedelic therapy]. Biologie aujourd’hui213(3-4), 121–129. https://doi.org/10.1051/jbio/2019015 
  9. He, D. Y., & Ron, D. (2006). Autoregulation of glial cell line-derived neurotrophic factor expression: implications for the long-lasting actions of the anti-addiction drug, Ibogaine. FASEB journal: official publication of the Federation of American Societies for Experimental Biology20(13), 2420–2422. https://doi.org/10.1096/fj.06-6394fje 
  10. Neal, D. T., Wood, W., & Quinn, J. M. (2006). Habits—A repeat performance. Current directions in psychological science15(4), 198-202. https://doi.org/10.1111/j.1467-8721.2006.00435.x
  11. Pitts, E. G., Li, D. C., & Gourley, S. L. (2018). Bidirectional coordination of actions and habits by TrkB in mice. Scientific reports8(1), 4495. https://doi.org/10.1038/s41598-018-22560-x 
  12. Kaplan, G. B., Vasterling, J. J., & Vedak, P. C. (2010). Brain-derived neurotrophic factor in traumatic brain injury, post-traumatic stress disorder, and their comorbid conditions: role in pathogenesis and treatment. Behavioral pharmacology21(5-6), 427–437. https://doi.org/10.1097/FBP.0b013e32833d8bc9 
  13. Cacialli, P., Palladino, A., & Lucini, C. (2018). Role of brain-derived neurotrophic factor during the regenerative response after traumatic brain injury in adult zebrafish. Neural regeneration research13(6), 941–944. https://doi.org/10.4103/1673-5374.233430 
  14. Linker, R. A., Lee, D. H., Demir, S., Wiese, S., Kruse, N., Siglienti, I., Gerhardt, E., Neumann, H., Sendtner, M., Lühder, F., & Gold, R. (2010). Functional role of brain-derived neurotrophic factor in neuroprotective autoimmunity: therapeutic implications in a model of multiple sclerosis. Brain: a journal of neurology133(Pt 8), 2248–2263. https://doi.org/10.1093/brain/awq179 
  15. Razavi, S., Nazem, G., Mardani, M., Esfandiari, E., Salehi, H., & Esfahani, S. H. (2015). Neurotrophic factors and their effects in the treatment of multiple sclerosis. Advanced biomedical research4, 53. https://doi.org/10.4103/2277-9175.151570
  16. Kalinowska-Lyszczarz, A., & Losy, J. (2012). The role of neurotrophins in multiple sclerosis-pathological and clinical implications. International journal of molecular sciences13(10), 13713–13725. https://doi.org/10.3390/ijms131013713
  17. Bus, B. A., Molendijk, M. L., Tendolkar, I., Penninx, B. W., Prickaerts, J., Elzinga, B. M., & Voshaar, R. C. (2015). Chronic depression is associated with a pronounced decrease in serum brain-derived neurotrophic factors over time. Molecular psychiatry20(5), 602–608. https://doi.org/10.1038/mp.2014.83 
  18. Sjörs Dahlman, A., Blennow, K., Zetterberg, H., Glise, K., & Jonsdottir, I. H. (2019). Growth factors and neurotrophins in patients with stress-related exhaustion disorder. Psychoneuroendocrinology109, 104415. https://doi.org/10.1016/j.psyneuen.2019.104415 
  19. Kotyuk, E., Keszler, G., Nemeth, N., Ronai, Z., Sasvari-Szekely, M., & Szekely, A. (2013). Glial cell line-derived neurotrophic factor (GDNF) as a novel candidate gene of anxiety. PloS one8(12), e80613. https://doi.org/10.1371/journal.pone.0080613 
  20. Oo, T. F., Kholodilov, N., & Burke, R. E. (2003). Regulation of natural cell death in dopaminergic neurons of the substantia nigra by striatal glial cell line-derived neurotrophic factor in vivo. The Journal of neuroscience : the official journal of the Society for Neuroscience23(12), 5141–5148. https://doi.org/10.1523/JNEUROSCI.23-12-05141.2003 
  21. Love, S., Plaha, P., Patel, N. K., Hotton, G. R., Brooks, D. J., & Gill, S. S. (2005). Glial cell line-derived neurotrophic factor induces neuronal sprouting in human brain. Nature medicine11(7), 703–704. https://doi.org/10.1038/nm0705-703 
  22. Gill, S. S., Patel, N. K., Hotton, G. R., O’Sullivan, K., McCarter, R., Bunnage, M., Brooks, D. J., Svendsen, C. N., & Heywood, P. (2003). Direct brain infusion of glial cell line-derived neurotrophic factor in Parkinsons disease. Nature medicine9(5), 589–595. https://doi.org/10.1038/nm850 
  23. Peterson, A. L., & Nutt, J. G. (2008). Treatment of Parkinson’s disease with trophic factors. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics5(2), 270–280. https://doi.org/10.1016/j.nurt.2008.02.003 
  24. Chan, S. J., Love, C., Spector, M., Cool, S. M., Nurcombe, V., & Lo, E. H. (2017). Endogenous regeneration: Engineering growth factors for stroke. Neurochemistry international107, 57–65. https://doi.org/10.1016/j.neuint.2017.03.024