*[[Epigenetic]] mechanisms of [[postpartum depression]]<br>
*[[Epigenetic]] mechanisms of [[postpartum depression]]<br>
**In women with [[postpartum depression]], there was a substantial interaction between [[OXTR]] [[DNA methylation]], [[estradiol]], and the ratio of [[allopregnanolone]] to [[progesterone]].
**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]].
**[[File:A-hypothetical-mechanism-by-which-depression-during-pregnancy-and-postpartum-may.png|alt=Pathophysiology|290x290px|left|thumb]]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]].
**As a result, [[epigenetic]] alterations can affect [[metabolic]] processes linked to [[postpartum depression]].
*[[Neuroendocrine]] mechanisms of [[postpartum depression]]: <br>
*[[Neuroendocrine]] mechanisms of [[postpartum depression]]: <br>
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*[[Neuroinflammatory]] mechanisms in [[postpartum depression]]: <br>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.
*[[Neuroinflammatory]] mechanisms in [[postpartum depression]]: <br>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.<br />
<br />
*It is thought that in [[postpartum]] [[psychosis]], immunoneuroendocrine set point is dysregulated with overactivation of the [[immune system]]'s [[macrophage]] and [[monocyte]] arm. <ref name="pmid28713685">{{cite journal |vauthors=Davies W |title=Understanding the pathophysiology of [[postpartum]] [[psychosis]]: Challenges and new approaches |journal=World J Psychiatry |volume=7 |issue=2 |pages=77–88 |date=June 2017 |pmid=28713685 |pmc=5491479 |doi=10.5498/wjp.v7.i2.77 |url=}}</ref>
*It is thought that in [[postpartum]] [[psychosis]], immunoneuroendocrine set point is dysregulated with overactivation of the [[immune system]]'s [[macrophage]] and [[monocyte]] arm. <ref name="pmid28713685">{{cite journal |vauthors=Davies W |title=Understanding the pathophysiology of [[postpartum]] [[psychosis]]: Challenges and new approaches |journal=World J Psychiatry |volume=7 |issue=2 |pages=77–88 |date=June 2017 |pmid=28713685 |pmc=5491479 |doi=10.5498/wjp.v7.i2.77 |url=}}</ref>
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==Genetics==
<br />
[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].
Pathophysiology Of Peripartum mood disturbances- Pathophysiology of Peripartum mood disturbances includes the role of various genes and hormones as described below
