Progress in brain research
January 1, 2018
Joseph P Barsuglia, Martin Polanco, Robert Palmer et al.
37 citations
A 31-year-old male military veteran with moderate alcohol use disorder received sequential treatment with ibogaine hydrochloride (1550mg, 17.9mg/kg) on day 1 and vaporized 5-MeO-DMT (bufotoxin source 50mg, estimated 5-7mg) on day 3 at an inpatient clinic in Mexico. SPECT neuroimaging before and 3 days after treatment showed increased brain perfusion in bilateral caudate nuclei, left putamen, right insula, and temporal, occipital, and cerebellar regions. The patient reported improved mood, cessation of alcohol use, and reduced cravings at 5 days, sustained at 1 month, with partial return to mild alcohol use at 2 months. The findings suggest short-term therapeutic outcomes and warrant further investigation.
Frontiers in neuroscience
January 1, 2024
Demi Govender, Leila Moloko, Maria Papathanasopoulos et al.
10 citations
Ibogaine, a psychedelic alkaloid being investigated for opioid use disorder, upregulates genes and proteins involved in remyelination in rats. In an experiment with 50 Sprague Dawley rats, morphine upregulated CNPase, while ibogaine alone had no effect on CNP mRNA or protein expression. However, ibogaine given after repeated morphine immediately increased CNP mRNA expression, which diminished after 72 hours but resulted in highly significant upregulation of CNPase protein at 72 hours. Ibogaine alone significantly upregulated protein expression but downregulated MBP mRNA expression. Ibogaine after morphine significantly upregulated MBP mRNA expression, increasing at 72 hours and leading to highly significant upregulation of MBP protein at 72 hours. These findings indicate ibogaine can upregulate remyelination-related genes and proteins after opioid use.
Acta Neuropsychiatrica
February 13, 2026
Tanya Calvey, D. Govender, Gavin Owen et al.
Ibogaine, a psychedelic alkaloid with no approved medical use, has been linked in observational studies to symptom relief for substance use disorder, multiple sclerosis, and traumatic brain injury after a single dose. This review examines the neurobiological mechanisms behind these effects, focusing on remyelination and metabolic restoration. Evidence indicates ibogaine increases markers of myelination after opioid administration, and that these disorders involve white matter pathology and disrupted metabolic homeostasis, ischemia, and hypoxia. The authors conclude that ibogaine's multi-receptor actions—particularly on NMDA, kappa opioid, and sigma receptors—reduce excitotoxicity, regulate metabolism, promote lasting neuroplasticity, and modulate immunity, facilitating neuronal repair and remyelination, supporting further research as a therapeutic agent for these central nervous system disorders.