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 (MS), and traumatic brain injury. Ibogaine has multi-receptor actions, but the neurobiological mechanisms underlying such putative effects are 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, MS and traumatic brain injury are characterised by white matter pathology; that decreased myelination is related to dysregulated metabolic homeostasis, ischaemia 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.