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Ibogaine and Parkinsonís Disease

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    Ibogaine and Parkinsonís Disease

    After Alzheimer’s, Parkinson’s Disease is the second most common neurodegenerative disease and is currently not curable. The disease manifests itself by the progressive loss of nerve cells, mainly of dopamine neurons in the Substantia Nigra (part of the mid-brain). This results in a lack of dopamine in the striatum (a subcortical part of the forebrain), as well as a dysfunction in motor functions, tremors, stiffening muscles, language problems and a general loss of balance and coordination.

    These symptoms are also accompanied by psychological effects like dementia and depression. It is thought that the neurodegenerative aspects of Parkinson’s disease are caused by the body’s immune system. Healthy nervous system tissue is attacked when the immune system is no longer able to distinguish between healthy and diseased cells, similar to autoimmune diseases such as multiple sclerosis, fibromyalgia and polyneuropathy.

    GDNF (glial cell line-derived neurotrophic factor) is a protein discovered in 1991 with an extraordinarily positive effect on nerve cell tissue. GDNF stimulates nerve cell growth, especially dopamine neurons. In addition to the ability to regenerate nerve cells in the brain, GDNF also appears to possess neuroprotective properties.

    In an animal experiment in which rats with Parkinson’s disease had GDNF injected directly into the brain, a significant improvement in the symptoms was observed. After one year, there were still no undesirable side effects of GDNF administration.
 Initial studies have shown that GDNF significantly improves the overall condition of Parkinsonian patients. The resulting data suggests that new nerve cells had formed.

    Ibogaine and its metabolite noribogaine lead to a substantial increase in GDNF levels in the brain. This indicates that ibogaine could provide a very effective treatment for neurodegenerative diseases, such as Parkinsons.

    Until now, it was not possible to introduce GDNF directly into the desired regions of the brain. But Ibogaine stimulates the glial cells and neurons to produce GDNF itself, increasing GDNF levels throughout the brain.

 Phytostan, a pharmaceutical company focused on developing ibogaine, has developed an ibogaine-based medicine called CK-BR 12. This consists of Ibogaine HCL and a cocktail composed of 12 vitamins.

    Patient D is a 69-year-old Parkinson’s disease patient and until now the only human treated with Ibogaine for his condition. Patient D reported numerous positive changes regarding his illness: he could swallow again, speech and facial expressions improved noticeably, the control of the hands increased and he could write again legibly. Also, his general motor skills increased.

    He could dress again, eat independently and climb stairs – all activities which were not possible prior to his treatment. The Parkinson’s symptomatology also improved after the treatment was completed. Patient D. was examined by various physicians as well as pharmacologist Dr. Susanne Cappendijk from Semper Clarus Consulting, who presented the promising results at the New York Academy of Sciences conference on April 27, 2015.

    The standard symptomatic treatment, is predominantly carried out with drugs with strong side effects. The quality of life of the patients is often characterised by significant suffering in the terminal phase. In contrast, treatment with ibogaine, in particular through the approach of microdosing, allows an increase in the GDNF levels in the brain, without the side effects of conventionally used medications.

    It was reported that 4mg Ibogaine HCL can increase GDNF levels in the brain by a factor of 12. The neuroplasticity increased by the growth of new neurons promotes the restoration and the construction of nerve tracts. Also, the challenge of introducing GDNF by injection into the brain is obviated. These results could help to redefine the position of Ibogaine in general research and – as ever-unknown healing properties of the plant are discovered – open up new research areas and thereby achieve a wider social and regulatory acceptance.

    At the Ibogaine conference in 2016, Dr. Ignacio Carrera from the Universidad de la Republica Uruguay presented the research of an interdisciplinary group. Novel variations of the ibogaine molecular structure have been developed that enhance the production of GDNF. The group of N-indolylethyl isoquinuclidines appears to be most promising. The synthesis of these molecules is far less complex than that of Ibogaine and there are several promising derivatives. Some of the analogues cause an even higher GDNF-release in vitro than Ibogaine does, but can have cytotoxic effects depending on the structure. The research in this field is still nascent, but it has enormous potential.

    European Ibogaine Forum


    Could Ibogaine be a promising new treatment for Parkinson’s?

    There is reason to believe that ibogaine may be beneficial in Parkinson’s treatment. Columbia’s two-year animal study represents the first time that researchers will probe for a direct link.

    The exact mechanisms of action of ibogaine are still obscure, but the theory for ibogaine’s benefit for Parkinson’s rests on the fact that amongst its other effects, it has been shown to increase the production of a protein called glial cell-derived neurotrophic factor, or GDNF. This and other neurotrophic factors have been shown to stimulate the production of dopaminergic fibers throughout the brain, and some existing research shows that GDNF in particular improves the recovery of dopaminergic neurons and leads to an improvement of Parkinson’s symptoms.

    Previous methods used to increase the expression of GDNF were limited gene therapy and direct brain infusion, but according the research abstract, the research team, led by Dr. Serge Przedborski, President of the World Parkinson Coalition, is exploring whether ibogaine could provide “a safer and more convenient means to enhance GDNF production in the brain.”

    Dr. Jeffrey Kamlet, a Miami medical doctor and board certified addiction specialist has been researching ibogaine for over 20 years, and is a strong advocate for medical supervision. According to Dr. Kamlet, “Ibogaine is the most important discovery in the field of opiate dependency in the history of addiction medicines, and I’m confident that it will one day be a main stay treatment for many addictions.”

    Even with this in mind, some advocates believe that ibogaine’s application as a treatment for Parkinson’s may prove more straightforward for research. In the case of addiction therapy, ibogaine is most often administered in a single large dose, but there is anecdotal evidence that the repeated use of very low sub-perceptual doses, which are generally agreed to be well tolerated in patients, could be sufficient to reverse Parkinson’s symptoms over time.

    Patient D* was 69 years old in 2012 when he was diagnosed with Atypical Parkinson’s, a Parkinson’s-like syndrome that does not include the characteristic palsy. By last year Patient D’s symptoms had advanced to the point where his facial muscles felt frozen. He had difficulty finding his balance, talking or using his hands. As a writer and artist, he noted that emotionally it was the first time in his life he had lost his desire to do anything creative.

    Patient D was treated with CKBR-12, an experimental natural health product and “ibogaine-derivative” at a medical center in Rosarito, Mexico. He took a small dosage twice a day for 30 days, and after the first two weeks began to notice that he could use his fingers to pick up objects again. After a month he had seen a gradual improvement in all of his symptoms to the point where he could carry on normal conversation, and coordinate previously impossible tasks such as buttoning his shirt.

    In a post-treatment interview that was published on YouTube, Patient D says, “It’s difficult to explain what Parkinson’s is, but you lose your edge. And I’ve got my edge back in a few areas… It may be small things to some, but they are big things for me. I’m anxious to see what happens next.”

    When we spoke, to Patient D, he said that he had continued to have improvements with further treatment. His case has been reviewed by several doctors, including Dr. Susanne Cappendijk of Florida State University Medical Center, who relayed some of the results at a conference at the New York Academy of Sciences.

    -Jonathan Dickinson



    Banisteriopsis caapi, also known as ayahuasca, is a South American liana of the family Malpighiaceae. It was shown in the 1920s to alleviate parkinsonism. These pioneering studies were criticized and forgotten for a number of reasons, including questions as to the identity of the active agent and failure to conduct strictly controlled studies. We now report the first double-blind, randomized placebo-controlled trial of a Banisteriopsis caapi (BC) extract for treatment of Parkinson’s disease (PD). A single dose of BC administered to de novo PD patients resulted in significant improvement in motor function evidenced by decline in the Unified Parkinson’s Disease Rating Scale (UPDRS) score. The beneficial effects were maximal by the second hour and persisted until the last evaluation of the patients at 4 hours. However, tremor was not improved and in some patients tremor was exacerbated. All patients also experienced a degree of transient nausea or vomiting. We measured the concentrations of the putative active agents (harmine, harmaline, and tetrahydroharmaline), and hypothesize that the beneficial effects were primarily due to glutamate receptor antagonist actions of the harmalines.


    CKBR-12 for Parkinson’s

    CKBR-12, an Ibogaine derivative medicine is currently being investigated to treat Parkinson’s disease. It has been found to upregulate Glial cell line-Derived Neurotrophic Factor expression in the mid brain, increase GDNF secretion 6, and may represent a powerful new method to upregulate GDNF in the treatment of PD and other neurodegenerative disorders.


    1. Decreased or elimination of Saliva and drooling. No problems in swallowing
    2. Loss of any depression or anxiety.
    3. Improvement in his speech, diction, and tongue control.
    4. Increased facial activity, muscles coming alive. Loss of facial rigidity.
    5. Regaining hand movement and use.
    6. Free flowing handwriting.
    7. Motor Skills: 50% or 75% better within 30 days.
    8. Return of self dressing and dexterity with fingers
    9. Naturally eating, cutting own food, don’t need assistance. Able to hold a fork and knife differently .
    10. Balance: Standing up for long periods of time and regaining a sense of balance. Loss of feeling of falling.
    11. Walking: Able to walk up and down stairs much faster and longer distances.
    12. Loss of tremors.

    Parkinson’s Disease, Motor Neuron Disease and Alzheimer’s Disease are chronic disorders that are normally treated with prescription medications that can have considerable side effects which may cause a very poor quality of life for terminal sufferers. In turn, Ibogaine may be very beneficial to those with degenerative neurological diseases.



    Ibogaine and Parkinson’s Disease – Case Study

    By Trevor Millar

    It’s been recently discovered that Ibogaine may work to reverse the debilitating effects of Parkinson’s Disease (PD). A recent article published on the Global Ibogaine Therapy Alliance website prompted a PD sufferer to contact Liberty Root to see if we might be able to help him follow a protocol to work on his disease. Having heard that the study at Columbia University was using a low-dose protocol, a mere 4 mg of ibogaine a couple of times a day, which is sub-perceptual, and very low-risk dose, we were excited to provide this gentleman with some medicine and see what the effects might be.

    Bill is a 52 year old male who was diagnosed with PD more than two years ago, but had early signs four years ago. He’s been very proactive since his diagnosis in trying to mitigate the onset of the symptoms of the disease, which include tremors, slow movement, rigid muscles, impaired posture and balance, loss of automatic movements; speech and writing impairment. Bill has changed his lifestyle so as to include daily exercise (yoga, cycling, PD specific exercises) as well as switched to a clean diet, avoiding processed food, and including organic vegetables and other nutrient dense foods. He’s been taking Apo-Levocarb daily, which is a dopamine medicine that helps reduce the symptoms of PD, but as Bill told me, it has diminishing returns – the more you take, the less effective it is.

    Bill has been spending the winters in Tucson, Arizona, as it’s got a large community of PD patients, and specifically the Parkinson’s Wellness Recovery, which Bill speaks very highly of. When I first met him, he had just finished driving from AZ to BC, and stopped by our facility on the last leg of his journey to pick up some tablets that contain Ibogaine prior to heading to his home on Vancouver Island. Meeting Bill it was obvious he suffered from PD, especially after that long drive. He was bent over, had a hard time walking, was shaky, his speech was slurred, with a slight facial paralysis. During our initial consultation he needed to sit, and had a hard time getting up afterward. Some other symptoms he described to me were a loss of movements that had been automatic, like with using the turn signal on his car he needed to be very conscious when making that happen, or once he finished urinating in the toilet, that first step backing up afterward needed to be very consciously thought out; it didn’t just happen automatically anymore.

    Initially we gave Bill a supply of tablets each containing 4 milligrams of Ibogaine HCL and once we saw there was no adverse reaction, with plenty of improvement, some 10 mg doses were compounded. As mentioned, this is a very low dose of Ibogaine compared to what we would give to a person so as to interrupt an addiction (we might use a gram and a half or more of ibogaine for addiction therapy). Bill started by taking one of these in the morning, along with his dopamine med, and then one in the afternoon. Here are some comments relating to his couple of months with low-dose protocol and its effects:

    10 mgs or less of Ibogaine twice daily:
    – Feeling of looseness in my arms neck, shoulders and chest
    – Able to shoulder check when driving
    – More power in left arm while driving
    – Able to back up easier when driving with left-handed steering
    – Easier exiting car
    – Easier doing up seatbelt (reaching and clasping)
    – More torque in left hand when turning on water taps and door knobs
    – Opening jars much easier
    – Sweeping and raking much easier
    – Able to let go of objects without thinking about it first (left hand)
    – Dopamine medicine much more effective, works faster lasts a little longer
    – Fewer left hand cramps
    – Less restless arm and legs at night
    – Stronger voice
    – Way less need to stretch during the day and morning
    – Just more coordination in left hand and right hand as well
    – Walking gate improved, less clop in left foot longer steps
    – Late night and early morning walking more steady (getting up to pee in the night and waking up in the morning )
    – Don’t feel a sense of depression on off days and haven’t cried since starting Ibogaine

    Once we started seeing such great improvements in Bill’s condition, we upped the dosage and compounded some 20 mg caplets of Ibogaine, which is still a very low dose; he continued to experience zero psychedelic effects.

    20 mgs of Ibogaine twice daily:
    – All of the above with more vigour, speed, and strength
    – Knocked 10 minutes off time for regular 34 km bike ride; way stronger on hills and head winds
    – Less fatigue when walking and more improvements in gate
    – Grades less noticeable when walking uphill
    – Stepping backwards easier with larger steps
    – Less shaking on exertion with left arm (lifting weights)
    – Much easier pulling up spandex cycling shorts
    – Reduction of getting stuck (less often and shorter duration)

    As a general rule, with Ibogaine and addiction interruption, the more you take, the better it works, to a point at least. So we figured we’d bring Bill into our facility for a larger dose. After clearing it with his doctor, and having the standard tests we have done prior to a larger dose (ECG, blood work) we welcomed Bill to Liberty Root for him to go on a little ‘journey’ with the medicine. After two days of larger dosing (>250 mgs) Bill had this to report:

    – Feel no need for dopamine, moving better than even with dopamine supplement
    – Left hand no longer hyper-extended at rest and has stopped “locking” open
    – Using left hand in more spontaneous fashion, no self-correction
    – Washing easier, dressing easier, tying shoes easier
    – Improved sense of smell and taste
    – Haven’t been stuck since last dosage

    It’s only been a few days since Bill left our facility. In speaking with him today, he mentioned that his left hand has become a bit more stiff than it was upon his departure. There is obviously a lot more research and experimentation that needs be done, but the preliminary findings are very encouraging, and have offered Bill a degree of liberty he hasn’t seen in years.


    I had drug-induced Parkinsonism and after microdosing for a week and then a flood dose of ibogaine, all my symptoms of that particular illness were gone. I know it is different from Parkinson's itself but the symptoms aren't all that different. I believe this could be the best medicine for those suffering from Parkinson's disease.

    -Christian Forbes


    Ibogaine, GDNF expression and neurodegenerative diseases

    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, few have identified a possible link between Ibogaine, GDNF expression and neurodegenerative 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.

    Last edited by Sherman Peabody; 09-25-2017, 11:12 AM.

    Ibogaine & Parkinson’s Disease

    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, 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. It has also been shown to have neuroprotective qualities promoting the survival of both dopaminergic and motor neurons.

    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. 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.

    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.

    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.

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      From the Neurotalk Forum 2012 I posted this:
      New :
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      Each time I read about GDNF and the BBB problems, I am reminded of the following compound and wonder WHY no one has looked at it for PD. One answer I received is that the drug induces hallucinations for the initial 24 hr period after it is given. Oh yeah--ignore that sinemet does the same though having to take it daily means the hallucinations are spread out over a much longer period of time. Have attempted to find the researcher/author, but have failed to do so. Madelyn
      Former posting:
      (seems researchers have been thinking about/looking into utilizing Ibogaine for PD
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      Benjamin Chemel September 6, 2005
      GDNF and Ibogaine: Developing a Cure for Parkinson’s Disease
      Glial cell line-derived neurotrophic factor (GDNF) is a disulfide-linked,
      homodimeric protein that promotes the survival and morphological differentiation
      of midbrain dopamine neurons (7).The ability of GDNF to act as a growth factor
      for dopamine neurons suggests that it could be a valuable treatment for
      Parkinson’s Disease (PD), a debilitating neurodegenerative disorder caused by a
      loss of dopamine neurons in the substantia nigra. (5). The loss of dopaminergic
      neurons in PD leads to deficient levels of dopamine in the striatum and
      subsequent dysregulation of motor control. Current PD treatments, including
      methods of dopamine replacement, are limited to ameliorating symptoms. In
      contrast, an ideal therapeutic approach would aim to halt the progressive cell
      loss or improve function in spared neurons.

      It has been hypothesized that GDNF represents a neuroprotective
      and neurorestorative treatment for the symptoms and pathology of PD (3).
      In chemically induced animal models of PD, GDNF has demonstrated the safety
      and efficacy prerequisites for clinical trials in humans (2). Because this 134
      amino acid protein cannot cross the blood brain barrier, new techniques are
      being developed to deliver GDNF into target tissues deep within the brain (1).
      One such approach, which employs an intraparenchymal catheter to infuse
      recombinant protein directly into the midbrain, was utilized in a recent phase I
      clinical trial (10). In this open-label trial, symptomatic evaluations were conducted
      using the Universal Parkinson’s Disease Rating Scale (UPDRS), while midbrain
      neuronal function was assessed using 18F-dopa positron emission tomography
      (PET) imaging. The results suggested that the long-term, continuous infusion of
      GDNF was well tolerated, with no apparent side effects. Additionally, all test
      subjects displayed a significant amelioration of their PD disease state. Improved
      motor skills and quality of life were correlated with increased function of midbrain
      dopaminergic neurons, as evidenced by 18F-dopa PET imaging. Additional
      molecular evidence suggested that neuronal sprouting may have contributed to
      this enhanced cellular activity (8). Phase II studies were aborted by the parent
      company, citing lack of functional improvements and safety concerns, yet for the
      patients and researchers involved, GDNF remains a promising treatment for PD.

      A pharmacological means of regulating endogenous GDNF could improve
      safety and delivery issues. One such compound is the hallucinogenic alkaloid,
      ibogaine. The ability of ibogaine to treat drug addiction and withdrawal has been
      anecdotally reported and verified in animal models of opiate, stimulant, and
      alcohol abuse (6). GDNF signaling is reportedly diminished by drugs of abuse
      (9), suggesting that GDNF may be involved in the attenuation of addiction by
      ibogaine (4).

      These observations provide evidence for my original
      hypothesis, that ibogaine represents a novel means of regulating GDNF
      and can be used to treat Parkinson’s Disease. In a recent study, ibogaine was
      found to upregulate GDNF expression in the midbrain and increase GDNF
      secretion and GDNF-dependent activation of downstream signaling pathways in
      vitro (4). These data suggest that ibogaine may represent a powerful new
      method to upregulate GDNF in the treatment of neurodegenerative disorders.
      Multidisciplinary research, using ibogaine as a lead compound, could reshape
      the lives of those afflicted with Parkinson’s Disease.

      1. Aebischer, P., and J. L. Ridet. 2001. Recombinant proteins for
      neurodegenerative diseases: the delivery issue. Trends In Neurosciences
      2. Bjorklund, A., and O. Lindvall. 2000. Parkinson disease gene therapy
      moves toward the clinic. Nature Medicine 6:1207-1208.
      3. 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:P35-P42.
      4. He, D. Y., N. N. H. McGough, A. Ravindranathan, J. Jeanblanc, M. L.
      Logrip, K. Phamluong, P. H. Janak, and D. Ron. 2005. Glial cell linederived
      neurotrophic factor mediates the desirable actions of the antiaddiction
      drug ibogaine against alcohol consumption. Journal Of
      Neuroscience 25:619-628.
      5. Kirik, D., B. Georgievska, and A. Bjorklund. 2004. Localized striatal
      delivery of GDNF as a treatment for Parkinson disease. Nature
      Neuroscience 7:105-110.
      6. Levi, M. S., and R. F. Borne. 2002. A review of chemical agents in the
      pharmacotherapy of addiction. Current Medicinal Chemistry 9:1807-1818.
      7. Lin, L. F. H., D. H. Doherty, J. D. Lile, S. Bektesh, and F. Collins. 1993.
      Gdnf - A Glial-Cell Line Derived Neurotrophic Factor For Midbrain
      Dopaminergic-Neurons. Science 260:1130-1132.
      8. Love, S., P. Plaha, N. K. Patel, G. R. Hotton, D. J. Brooks, and S. S.
      Gill. 2005. Glial cell line-derived neurotrophic factor induces neuronal
      sprouting in human brain. Nature Medicine 11:703-704.
      9. Messer, C. J., A. J. Eisch, W. A. Carlezon, K. Whisler, L. Shen, D. H.
      Wolf, H. Westphal, F. Collins, D. S. Russell, and E. J. Nestler. 2000.
      Role for GDNF in biochemical and behavioral adaptations to drugs of
      abuse. Neuron 26:247-257.
      10. Patel, N. K., M. Bunnage, P. Plaha, C. N. Svendsen, P. Heywood, and
      S. S. Gill. 2005. Intraputamenal infusion of glial cell line-derived
      neurotrophic factor in PD: A two-year outcome study. Annals Of Neurology
      11. Sariola, H., and M. Saarma. 2003. Novel functions and signalling
      pathways for GDNF. Journal Of Cell Science 116:Only registered and activated users can see links., Click Here To Register....