Neurorestorative Properties of Ibogaine: Linking Multi-Receptor Affinities to Remyelination and Metabolic Restoration
Tanya Calvey, D. Govender, Gavin Owen, Nancy Tumba, Dirk Lang, Bernard Lerer, Dan J Stein, Steven Shoptaw
Acta Neuropsychiatrica February 13, 2026 DOI: 10.1017/neu.2026.10059 via OpenAlex
Summary
AI-generated from the abstractIbogaine, 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.
Study at a glance
| Characteristics | Review Peer reviewed |
|---|---|
| Topics | Neuroplasticity |
| Keywords | Remyelination Neuroscience Neuroprotection Medicine Central nervous system |
| Key finding | Ibogaine's multi-receptor actions reduce excitotoxicity, regulate metabolism, and promote neuroplasticity and immunomodulation, facilitating neuronal repair and remyelination in disorders such as opioid use disorder, multiple sclerosis, and traumatic brain injury. |
Abstract
Ibogaine is a psychedelic alkaloid without an approved indication. Observational clinical research shows linkages between single administration of ibogaine and relief of symptoms of neuropsychiatric conditions including substance use disorder, multiple sclerosis, and traumatic brain injury. Ibogaine has multi-receptor actions, but the neurobiological mechanisms underlying such putative effects is unknown. Here we review and discuss the relevant literature, focusing on remyelination and metabolic restoration. We provide evidence that ibogaine upregulates markers of myelination following opioid administration; that conditions such as opioid use disorder, multiple sclerosis and traumatic brain injury are characterized by white matter pathology; that decreased myelination is related to dysregulated metabolic homeostasis, ischemia and hypoxia which may also play a role in these disorders. We conclude that multi-receptor actions of ibogaine, especially its affinities for the NMDA, kappa opioid and sigma receptors, in turn account for reduction in excitotoxicity, metabolic regulation, lasting neuroplasticity and immunomodulation that facilitates neuronal repair and remyelination providing a rationale for future investigation of its use as a therapeutic agent for these common central nervous system disorders.