The following is a summary on existing research looking at the influence of ibogaine on glial cell line-derived neurotrophic factor (GDNF) levels in the brain, and the beneficial impact that an increase in this protein can have. While existing studies have examined these areas, very few have identified a possible link between ibogaine, GDNF expression and neurodegenerative diseases, and I believe more research is warranted. I would appreciate feedback off anyone, particularly anyone with a background in neuroscience. Attached is a presentation examining the biochemical background of ibogaine and GDNF in more detail.


One reason ibogaine is so interesting is that it increases levels of glial cell line-derived neurotrophic factor (GDNF) in the brain (He & Ron 2006), and this in turn appears to be a potent survival factor for several different neuronal populations in different brain regions (Boscia et al. 2009) and has neuroprotective properties that promote the survival of both dopaminergic and motor neurons (Bermingham et al. 2004; He and Ron 2006), which may be one of the reasons for the prolonged afterglow often experienced following treatment with the drug. Furthermore, GDNF can cause sprouting of dopaminergic fibers and clinical improvement in experimental animal models of Parkinson’s disease, as well as a similar sprouting of dopaminergic fibers in humans with the disease, with the resultant clinical improvement in symptoms (Love et al. 2005). GDNF has also been identified as having anti-addictive properties (Ron & Janak 2005; Carnicella & Ron 2008.) This may be one of the reasons for ibogaine’s effectiveness in treating drug addicts with impaired receptor function, but this drug may also be a considerable ally to those with degenerative neurological diseases.

Both Parkinson’s disease and Motor neuron disease are chronic disorders with no known cure, and require management with drugs that can have considerable side effects, causing a very poor quality of life for terminal stage sufferers of these diseases. By contrast, a low dose regime of ibogaine or iboga alkaloid extract would be of low toxicity and free of serious side effects.

GDNF has been shown to have potent neurotrophic factor in both rodent and primate models of Parkinson’s disease (Gill et al. 2003). Direct brain infusion of GDNF into the brains of five Parkinson sufferers resulted in a 39% improvement in the off-medication motor sub-score of the Unite Parkinson’s Disease Rating Scale (UPDRS) and a 61% improvement in the activities of daily living sub score (Gill et al. 2003). Positron emission tomography (PET) scans of dopamine uptake showed a significant 28% increase in putamen dopamine storage after 18 months, indicating a direct effect of GDNF on dopamine function. Furthermore, after one year, no serious clinical side effects were observed (Gill et al. 2003). The use of iboga alkaloid extract or ibogaine would provide a longer term and much less invasive method of GDNF administration than direct brain infusion. Thus, further research on ibogaine and GDNF is certainly warranted.

Regarding motor neuron disease, the little research that has occurred in this area, such as gene transfer of neurotrophic factors, suggests potential in the treatment of motor neuron disease (Haase et al. 1997). Again, ibogaine therapy may offer a straightforward, non-invasive, cheap, low-toxicity method of treatment for sufferers of this disease.

Thus based on this previous research, it seems clear to me that further research with ibogaine, GDNF expression and neurodegenerative diseases is certainly warranted, despite the financial and political hurdles of working with ibogaine, a largely scheduled yet natural alkaloid extract from the root bark of the West African shrub iboga (Tabernanthe iboga). The drug is of little financial interest to pharmaceutical companies, and quite inaccurately deemed to be of “no medical value”. Legal red tape is less restrictive for Ibogaine here in the UK than it is in many other parts of the world.



Bermingham, N., Hillermann, R., Gilmour, F., Martin, J. E. and Fisher, E. M. C. (2004) Human glial cell line-derived neurotrophic factor (GDNF) maps to chromosome 5. Human Genetics, 96, (6), 671-673.

Boscia F, Esposito CL, Di Crisci A, de Franciscis V, Annunziato L, et al. (2009) GDNF Selectively Induces Microglial Activation and Neuronal Survival in CA1/CA3 Hippocampal Regions Exposed to NMDA Insult through Ret/ERK Signalling. PLoS ONE 4, 8, e6486. doi:10.1371/journal.pone.0006486

Carnicella, s. & Ron, D. 2008. GDNF – A potential target to treat addiction. Pharmacology & Therapeutics, 122, (1), 9-18.

Gill, S. S., Patel, N. K., Hotton, G. R., O’Sullivan, McCarter, R., Bunnage, M., Brooks, D. J., Svendsen, C. N. and Heywood, P. (2003) Direct brain infusion of glial cell-line derived neurotrophic factor in Parkinson disease. Nature Medicine, 9, 589-595.

Grondin, R., and D. M. Gash. 1998. Glial cell line-derived neurotrophic factor (GDNF): a drug candidate for the treatment of Parkinson's disease. Journal Of Neurology 245, 35-42.

Haase, G., Kennel, B., Pettmann, B., Vigne, E., Akil, S., Revah, F., Schmalbruch, H. and Kahn, A. (1997) Gene therapy of murine motor neuron disease using adenoviral vectors for neurotrophic factors. Nature Medicine, 3, 429-436.

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. The FASEB Journal, 20, 2420-2422.

Kirik, D., B. Georgievska, and A. Bjorklund. (2004) Localized striatal delivery of GDNF as a treatment for Parkinson disease. Nature Neuroscience 7:105-110.

Love, S., P. Plaha, N. K. Patel, G. R. Hotton, D. J. Brooks, and Gill, S. S. (2005) Glial cell line-derived neurotrophic factor induces neuronal sprouting in human brain. Nature Medicine 11:703-704.

Ron, D. & Janak, P. H. (2005) GDNF and addiction. Reviews in the Neurosciences, 16, (4), 277-285.

Bancopuma-fascinating article.

I studied neuroscience back in the early 90s and as Im sure you know, you just retain what you need to , to fulfil the requirements of your job.My work still requires me to have a pretty full understanding of neurology but in a clinical capacity.

I wont pretend to have a full understanding of the details of all the pathways/receptors etc but I agree, its quite clear that GDNF levels in vital central structures are raised by ibogaine and the effect on neurodegeneration of certain cell-types is to promote regeneration.I believe some of the 'subsets' of GDNF have a role to play in conditions such as Hirschsprungs disease and also some renal effects.

I suspect that at some point, these aspects of ibogaines effects will be revisited.It may not result in iboga being used but analysing this property may allow a fuller understanding of GDNP and how it achieves its effects; it may also open up therapeutic options with compounds related to iboga.

Once again-absolutely fascinating.

Hi corpus,

Many thanks for your feedback and the information, I'll look into it further. My background isn't in neuroscience although it is an area I find fascinating. I kind of feel this works against me though when trying to contact other scientists with experience in this area, its likely I'm not going to be taken very seriously not having any previous education in this area.

This is also interesting for specific drug addictions. I consider methamphetaime one drug with the most potential for harm, abuse causing dopaminergic dendrite degeneration, while GDNF (expressed via Ibogaine) may actually cause sprouting of dopaminergic fibres, and this could allow one to repair damaged areas of the brain, to at least some degree. Apparently exercise also raises ones levels of GDNF.

I hear what you say about scientists, particularly in the medical and allied fields, not really giving the time of day to those who are not formally qualified.I think this is in part due to a degree of arrogance on their parts.

I was at the Royal College of Physicians in London last week attending a symposium on headaches which was pretty good and this prompted me to make a post here at the Nexus about cluster headaches.Whilst down there listening to all the eminent bods doing their spiel, I was SO tempted to raise the issue of LSD as a possible treatment but thought better of it-I dont need their quizzical looks and disapproving grimaces coming my way.Little consolation for you but it goes to show that even those of us who are legitimately 'accepted' as being worthy of attending their club have to play the game to remain accepted.

The anecdotal evidence for using ibogaine to treat addictions is strong-I think opiate-addiction was first found to be helped by ibogaine.There are similarities between addiction to theses compounds and others which require dopaminergic pathways to subserve the addiction and meth is one of these.

All this talk of ibogaine.....ALMOST makes me want to fish out my gram and give it a bash!!

Sounds like it would be a very powerfull medicine against a whole range of psychiatric disorders. That's probably also why not much research is likely to be done: if you'd have a pill you could take that would solve many problems at once or within only a few weeks, where existing medication is used chronically than you'd lose a lot of your income as a pharmaceutical company...

Could part of it's effects on all kinds of addictions that are more psychological than physical be that it sort of allows the brain to 'rewire' a bit, like normally only happens before someone reaches adolescence?

I reckon iboga will in part exert its effects through GDNF and some 're-wiring';there may be ethical problems analyzing how the pre/peri-adolescent brain'wires' itself as observation of this may alter the process itself.

A little interesting feedback regarding this, I have been contacting Iboga(ine) people and scientists working in this area.

This is a reply I got from Dr Kenneth Alper. Kenneth is a psychiatrist specializing in addiction and clinical neurophysiology, with an interest in the potentials of Ibogaine.


"The expression of GDNF by ibogaine is a clinical application in Parkinson's that has been considered, but the necessary clinical work remains to be done. I recently searched the literature on any evidence of the therapeutic application of ibogaine to Parkinson's using both academic Medline/ISI/Pubmed approaches as well as Google and found nothing, not for want of effort on my part. But I agree with you regarding the theoretical case."


So this seems quite interesting...I feel that the necessary research hasn't been done to provide a conclusive answer, but there could be something here. Possibly an avenue for future research, or one would hope so.