Peripartum mood disturbances pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sunita Kumawat, M.B.B.S[2]
Overview
Many pathological mechanisms are involved in postpartum depression which interact with one another.
Pathophysiology
Pathophysiology Of Peripartum mood disturbances- Pathophysiology of Peripartum mood disturbances includes the role of various genes and hormones as described below
- Genetic Mechanism of postpartum depression: [1]Numerous gene playing significant role in deciding the pathophysiology are:
- Estrogen receptor alpha gene,
- Polymorphisms in the serotonin transporter gene,
- 5-HTT
- gene encoding for MAOA and the
- gene encoding for Catechol-O-methyltransferase (COMT),
- Genetic variants for the TPH2 gene,
- SNP in OXT; SNP in the OXTR gene and methylation state was detected in association with postpartum depression.
- Hemicentin 1 gene (HMNC1) and its association with postpartum depression.
- Epigenetic mechanisms of postpartum depression
- In women with postpartum depression, there was a substantial interaction between OXTR DNA methylation, estradiol, and the ratio of allopregnanolone to progesterone.
- Alterations in DNA methylation of the OXTR gene are adversely linked with blood estradiol levels in women with postpartum depression.
- As a result, epigenetic alterations can affect metabolic processes linked to postpartum depression.
- Neuroendocrine mechanisms of postpartum depression:
- In postpartum depression, there is an interaction between the Hypothalamus-pituitary-gonadal (HPG) and Hypothalamus-Pituitary-Adrenal(HPA) axis.
- HPA axis function has been found to be influenced by reproductive hormones and vice versa.
- As a result, any change in reproductive hormones may cause stress hormone levels to fluctuate, resulting in postpartum depression.
- Alterations of the HPA axis' function may also affect reproductive hormone levels, contributing to postpartum depression.
| GABA | Glutamate | Serotonin | Dopamine |
|---|---|---|---|
| GABA which is an inhibitory neurotransmitter in the brain | Glutamate is the excitatory neurotransmitter in the brain | Serotonin to 5HT1A receptors is decreased in the following brain regions | Mutations in DR1 |
| Level is inversely related with the depression symptoms in the postpartum period | postpartum depression its level are increased in the medial prefrontal cortex | mesiotemporal and anterior cingulate cortices. | Relates to the attention and affection of mother for the baby |
| In postpartum depression decreased in the dorsolateral prefrontal cortex. |
- Neuroinflammatory mechanisms in postpartum depression:
There is a negative relationship between T-cell number and postpartum depression symptoms, whereas IL-6 and IL-1β have a significant positive relationship with it.
- It is thought that in postpartum psychosis, immunoneuroendocrine set point is dysregulated with overactivation of the immune system's macrophage and monocyte arm. [2]
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Payne JL, Maguire J (January 2019). "Pathophysiological mechanisms implicated in postpartum [[depression]]". Front Neuroendocrinol. 52: 165–180. doi:10.1016/j.yfrne.2018.12.001. PMC 6370514. PMID 30552910. URL–wikilink conflict (help)
- ↑ Davies W (June 2017). "Understanding the pathophysiology of [[postpartum]] [[psychosis]]: Challenges and new approaches". World J Psychiatry. 7 (2): 77–88. doi:10.5498/wjp.v7.i2.77. PMC 5491479. PMID 28713685. URL–wikilink conflict (help)