After reaching the CNS, TMAO was shown to promote neuronal senescence in the hippocampus and cognitive impairment in mice by increasing oxidative stress, disturbing mitochondrial dysfunction and inhibiting the mammalian target of rapamycin (mTOR) signalling, which increased synaptic damage as well as reduced synaptic plasticity-related proteins [190]. The gene discussed is MTOR; the disease is Cognitive impairment.