Parkinson’s Disease is classified as a neurodegenerative disorder, one characterized by the progressive atrophy of the central and peripheral nervous system. However, some evidence suggests that the neurodegeneration in Parkinson’s subjects may be caused by the body’s own immune system losing the ability to determine between healthy and unhealthy cells,1 as is the case with autoimmune diseases such as Fibromyalgia, Multiple Sclerosis and others, in which much of the body’s organs and cell tissue deteriorate because of misdirected attack by the immune system.
Although the theory is still untested, there is anecdotal evidence and a theoretical framework that suggests ibogaine may have therapeutic benefits in the treatment of Parkinson, and possibly other disorders that cause the degeneration of brain and cell tissues.
The theoretical case is based on the fact that both ibogaine and its metabolite noribogaine have been shown to lead to an increase in levels of glial cell line-derived neurotrophic factor (GDNF) in the brain.2 It has also been shown to have neuroprotective qualities promoting the survival of both dopaminergic and motor neurons.3
In other research, neutrophic factors, specifically GDNF, have been shown to cause sprouting of dopaminergic fibers, with a resulting improvement of clinical symptoms of Parkinson’s in experimental animal models and humans.4 However, there is little research available using neutrophic factors in the treatment of other neurodegenerative disorders, particularly because administration is usually limited by toxicity or poor bioavailability. Various other methods of administration such as direct brain infusion of GDNF and gene therapy that promotes the expression of neurotrophic factors have been explored.
The direct brain infusion of GDNF into the brains of five rats induced with Parkinson’s disease showed a 39% improvement in 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. After one year, no side effects from the treatment were observed.5
In addition to Parkinson’s, one study using gene therapy that promotes the expression of neurotrophic factors, showed a 50% increase in life span, reduced loss of motor axons and improved neuromuscular function in animal models representing Motor Neuron Diseases. The study suggested further research into neurotrophic factor as a treatment for MND.6
Parkinson’s and similar diseases have no known cure, and these conditions often require management with drugs that have considerable side effects, causing a very poor quality of life for terminal stage sufferers of these diseases.
Ibogaine therapy, especially low-dose regimens, may facilitate the expression of GDNF without the side effects of other medications or the difficulty of other avenues of administering neurotrophic factor. Anecdotal reports suggest that at least several people with Fibromyalgia, Multiple Sclerosis, and Parkinson’s who have been treated with ibogaine have seen an extended remission of symptoms.
Although there is little clinical research into this particular application, one of the first studies to assess ibogaine efficacy, specifically in the treatment of Parkinson disease in animal models, is currently underway at Columbia University.
The information presented here is not intended to promote ibogaine for the treatment of any of the disorders mentioned above. While we believe that the information here warrants further observational and clinical research, the information is presented primarily to inform people who may have encountered claims made elsewhere as to the state of scientific inquiry into this topic.
Carolina Cebrián, Fabio A. Zucca, et al. “MHC-I expression renders catecholaminergic neurons susceptible to T-cell-mediated degeneration.” Nature Communications. March 2014. ↩
Carnicella, S., He, D.Y., Yowell, Q.V., Glick, S.D., Ron, D. Noribogaine, but not 18-MC, exhibits similar actions as ibogaine on GDNF expression and ethanol self-administration. Addiction Biology. October 2010. 15(4):424-33. ↩
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. ↩
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. ↩
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’s disease. Nature Medicine, 9, 589-595. ↩
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. ↩