This paper examines how ibogaine may enhance synaptic plasticity and neural repair. Extracellular efflux analysis showed that ibogaine (3, 10 or 30 μM) produced a rapid (<5 min) and concentration-dependent suppression of mitochondrial function and glycolysis in mouse cortical neurons.

The “Stanford Study” looked at 30 retired Special Operations veterans with traumatic brain injury who showed major improvement across disability, post-traumatic stress, depression and anxiety. This paper helped spark a major upsurge in ibogaine research and state-level funding initiatives in the US.

Ambio’s preliminary case report on two MS patients (one relapsing remitting, one secondary progressive). We observed broad symptomatic improvement alongside structural changes in the brain; the RRMS case showed a 71% reduction in white-matter lesion volume post-treatment.

In rats given morphine, a team led by Prof. Tanya Calvey found ibogaine switched on the molecular machinery for remyelination — rebuilding the protective “insulation” around nerve fibers — with the effect strongest about 72 hours after treatment.

Marton et al. (2019) gave rats a single dose of ibogaine and measured neurotrophic factors — proteins that help neurons grow, survive and rewire. GDNF rose specifically in the VTA at 24 hours, after ibogaine had cleared the brain, pointing to a self-sustaining mechanism that could explain why ibogaine’s effects outlast the drug itself.

The foundational study tying ibogaine’s effect to a growth factor. A single dose raised GDNF in the midbrain of rats and mice; delivering ibogaine into the VTA produced a lasting drop in alcohol self-administration, and blocking GDNF cancelled the effect. The paper #4 builds on.

The paper that coined “psychoplastogen.” A range of psychedelics increased the growth of neurites and dendritic spines (where neurons form new connections); ibogaine’s long-lived metabolite, noribogaine, was among the compounds shown to spur this growth. A broad frame for why these substances may support repair.