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It has long been known that the pathophysiology of depression is associated with a reduction in the brain concentrations of monoamines, that is, serotonin, noradrenaline, and dopamine. Although conventional antidepressant drugs increase monoamine contents immediately after their administration, it takes several weeks or more before their clinical efficacy becomes evident. The mechanism of the delayed onset of antidepressant effects remains elusive. Furthermore, over 30–50% of patients with depression show resistance to antidepressant drug treatment. Thus, two major questions remain to be resolved—(1) delayed clinical efficacy of antidepressant drugs, and (2) a large percentage of treatment-resistant depression. First, this review describes the evidence, obtained from animal and human studies, that similar to early-stage Parkinson’s disease, depression is a neurodegenerative disease characterized by the degeneration of monoamine axons and the delayed clinical efficacy of antidepressants is due to their regenerative action on damaged monoamine axons. Moreover, the causes of treatment-resistant depression are discussed in relation to inflammation as a cause of neurodegeneration. This review provides new insights into not only the pathophysiology of depression but also the diagnosis and therapy of early stages of neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease.

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Perspective Chapter: Depression as a Disorder of Monoamine Axon Degeneration May Hold an Answer to Two Antidepressant Questions - Delayed Clinical Efficacy and Treatment-Resistant Depression