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lbogaine, GDNF & Parkinsons's Disease
GDNF and Ibogaine: Developing an Alternative Treatment for Parkinson's Disease and other Neurodegenerative Conditions

Glial cell line-derived neurotrophic factor (GDNF) is a disulfide-linked , homodimeric protein that promotes the survival and morphological differentiation of midbrain dopamine neuron s (8).The abil ity 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. (6). The lo•ss of dopaminergic neurons in PD leads to deficient levels of dopamine in the striatum and subsequent dysregulation of motor control. Current PD treatments, includ ing methods of dopamine replacement , are largely lim ited 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 neu rorestorative treatment for the symptoms and pathology of PD (3). In chemically induced animal models of PD, GDNF has demonstrated the safety and efficacy prerequ isites for clinical trials in humans (2). Because this 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 mid brain, was utilized in a recent phase I clinical trial (11). 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 resu lts of this study 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 disease state. Improved motor skills and quality oflife were correlated with increased function of m id brain dopaminergic neurons, as evidenced by
18F-dopa PET imaging. Additional molecular evidence suggested that neuronal sprouting may have contributed to this enhanced cellular activity (9). 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 (7). GDNF signaling is reported ly dim inished by drugs of abuse (10), suggesting that GDNF may be involved in the attenuation of addiction by ibogaine (4). Recent studies demonstrated that ibogaine promotes long-lasti ng upregu lation of GDNF expression , secretion and activation of downstream signaling pathways, and that these actions mediate the anti-addiction properties of this alkaloid (4, 5). These data, suggesting that ibogaine may represent a powerful new method to upregu late GDNF in the treatment of neurodegenerative disorders, provide evidence for the hypothesis that ibogaine represents a novel pharmacological treatment for Parki nson's Disease. Multid isciplinary research , using ibogaine as a lead compound, cou ld reshape the lives of those afflicted with Parkinson 's Disease.




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