Lee et al. (2022) demonstrated that TMAO-treated midbrain organoids showed impaired brain-derived neurotrophic factor signaling, loss of dopaminergic neurons, astrocyte activation, and neuromelanin accumulation. Furthermore, TMAO induced the pathological phosphorylation of α-syn and tau proteins, facilitating their aggregation. Vogt et al. (2018) identified a correlation between elevated TMAO levels and AD pathology and markers of neuronal degeneration in the cerebrospinal fluid. This evidence concerns the gene MAPT and Alzheimer disease.