Postpartum depression: A mini-review
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Keywords:Anhedonia, depression, post-partum, stress
Stress and traumatic past experiences are two of the main risk factors for the development of postpartum depression. Reprogramming of the HPA axis and epigenetic alterations, which can also affect HPA function, are two neuroendocrine changes reported in postpartum depression that is linked to stress and negative life events. Because it is well established that stress hormones affect neuroinflammation, altered HPA axis function may have an impact on peripartum neuroimmune alterations that affect postpartum depression. On the other hand, neuroinflammation can affect how well the HPA axis functions, which may possibly be a factor in postpartum depression. By highlighting both clinical and fundamental science research findings, this review attempts to highlight the numerous potential pathophysiological pathways that contribute to postpartum depression. The discussion of postpartum depression risk factors may reveal information regarding potential neurological causes. The biology of postpartum depression is examined along with the evidence that suggests the involvement of neuroendocrine alterations, neuroinflammation, altered neurotransmitters, circuit malfunction, genetics, and epigenetics. This review emphasized neuroendocrine changes.
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