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. 2024 Feb 9;9:30. doi: 10.1038/s41392-024-01738-y

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — An outline map of the hypotheses to explain MDD pathogenesis. (I) HPA axis dysfunction hypothesis: high levels of glucocorticoids (GCs) play a core role in the pathogenesis of MDD, and thyroid hormone (TH) and estrogen are also involved in functions of the HPA axis; (II) the monoamine hypothesis: the functional deficiency of serotonin (5-HT), dopamine (DA) and norepinephrine (NE) are the main pathogenesis of MDD; (III) the inflammatory hypothesis: the neuro-inflammation induced by reactive oxygen species (ROS), inflammatory cytokines and inflammasomes activation is suggested to promote the occurrence of MDD; (IV) the genetic and epigenetic anomaly hypothesis: some genes are susceptible in the patients with MDD, including presynaptic vesicle trafficking (PCLO), D2 subtype of the dopamine receptor (DRD2), glutamate ionotropic receptor kainate type subunit 5 (GRIK5), metabotropic glutamate receptor 5 (GRM5), calcium voltage-gated channel subunit alpha1 E (CACNA1E), calcium voltage-gated channel auxiliary subunit alpha2 delta1(CACNA2D1), DNA methyltransferases (DNMTs), transcription levels of somatostatin (SST), fatty acid desaturase (FADS); (V) the structural and functional brain remodeling hypothesis: the postmortem results of patients with MDD are mostly associated with the reduced densities of glial cells in the prefrontal cortex (PFC), hippocampus, and amygdala; (VI) the social psychological hypothesis: the traumatic or stressful life events are the high risks of the occurrence of MDD. Adobe Illustrator was used to generate this figure