Propofol is a frequently used anesthetic. It can induce neurodegeneration and inhibit neurogenesis in the hippocampus. This effect may be temporary. It can, however, become permanent in vulnerable populations, such as the elderly, who are more susceptible to Alzheimer's disease, and neonates and children, whose brains are still developing and require neurogenesis. Current clinical practice strategies have failed to provide an effective solution to this problem. In addition, the molecular mechanism of this toxicity is not fully understood. Recent advances in molecular research have revealed that apoptosis, in close association with mitochondria, is a crucial mechanism through which propofol contributes to hippocampal toxicity. Preventing the toxicity of propofol on the hippocampus has shown promise in in-vivo, in-vitro, and to a lesser extent human studies. This study seeks to provide a comprehensive literature review of the effects of propofol toxicity on the hippocampus via mitochondria and to suggest translational suggestions based on these molecular results.
Keywords: Anesthesia; Apoptosis; Neurodegeneration; Protection.
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