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Studies have indicated a significant decrease in steroid hormone synthesis in models with Beclin1 or Atg5 deletion, primarily attributed to a reduction in intracellular cholesterol supply [147, 148], suggesting that the autophagy-lysosome system may indirectly support steroidogenesis by preserving substrate availability [149]

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The effective blood-brain barrier mechanism impeding the transport of monoamines has been attributed to both the presence of tight junctions cementing adjacent endothelial cells of the cerebral capillary walls, along with high concentrations of dopa decarboxylase and monoamine oxidase (MAO) in the cerebral capillary endothelium (Bertler et al, 1966