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NeuroVela Home About Services Contact Evidence, uncertainty, and safety Ibogaine Brain De-Aging Early signals of neuroplasticity and network change deserve careful study. They do not yet amount to a validated anti-aging treatment for the aging brain. Starting point Ibogaine is a high-risk neuropsychiatric intervention. Mechanistic hypotheses must be weighed against cardiac liabilities, uncertain cognitive outcomes, and the absence of aging-focused randomized trials. A measured frame What “de-aging” can—and cannot—mean 01—03 Measure, don’t promise In scientific and clinical terms, brain de-aging describes a shift toward younger-like patterns in structure, function, and cognition rather than a claim of literal reversal of time. It must be anchored in reliable measures across imaging, physiology, and behavior. Composite brain-age models, MRI, EEG, memory, and attention can help define a testable question. Use converging signals Researchers often estimate brain aging with composite “brain age” models from MRI or EEG, task-based performance on memory and attention, and systemic signals such as inflammation markers. Because definitions vary, reproducibility demands pre-registered endpoints and harmonized analytics. No single metric defines cognitive decline or clinical relevance. Keep uncertainty visible For a complex agent like ibogaine, the prudent lens is hypothesis testing, not hype. Clear baselines, blinded raters where feasible, and multi-modal biomarker panels are essential to separate genuine signal from placebo effects and expectation bias. Early reports are not proof of cognitive rejuvenation. Measurement what brain de-aging means and how it is measured Clinically, brain de-aging is inferred from convergence: improved cognitive composites, normalized brain connectivity, and favorable shifts in blood or CSF biomarkers. Imaging may include default-mode reconfiguration and hippocampal volume trajectories. Common test domains include memory, executive function, atte

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