Peripartum mood disturbances pathophysiology: Difference between revisions
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*The progression to [disease name] usually involves the [molecular pathway]. | *The progression to [disease name] usually involves the [molecular pathway]. | ||
*The pathophysiology of [disease/malignancy] depends on the histological subtype. | *The pathophysiology of [disease/malignancy] depends on the histological subtype. | ||
Many [[pathological]] mechanisms are involved in [[postpartum]] [[depression]] which interact with one another.<ref name="pmid30552910">{{cite journal |vauthors=Payne JL, Maguire J |title=Pathophysiological mechanisms implicated in postpartum depression |journal=Front Neuroendocrinol |volume=52 |issue= |pages=165–180 |date=January 2019 |pmid=30552910 |pmc=6370514 |doi=10.1016/j.yfrne.2018.12.001 |url=}}</ref> | |||
* '''[[Genetics]] of postpartum depression'''<br>[[Estrogen receptor]] alpha gene, polymorphisms in the [[serotonin transporter]] gene, 5-HTT, and the gene encoding for MAOA and the gene encoding for [[Catechol-O-methyltransferase]] (COMT), Genetic variants for the TPH2 gene, a SNP in OXT was predictive of both variation in breastfeeding duration and postpartum depression scores, an interaction between a SNP in the OXTR gene and methylation state was detected in association with postpartum depression. In a genome-wide linkage and association study, the Hemicentin 1 gene (HMNC1) had the strongest association with postpartum depression. | |||
* '''[[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]]. 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'''<br>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]]. | |||
* '''[[Neurotransmitters]] and postpartum depression'''<br>'''GABA'''-GABA which is an inhibitory [[neurotransmitter]] in the brain, its level is inversely related with the depression symptoms in the [[postpartum]] period.<br> | |||
'''Glutamate'''-Glutamate is the excitatory neurotransmitter in the brain. In women with postpartum depression its level are increased in the medial prefrontal cortex and decreased in the dorsolateral prefrontal cortex.<br> | |||
'''Serotonin'''-The binding of [[Serotonin]] to 5HT1A receptors is decreased in the mesiotemporal and anterior cingulate cortices.<br> | |||
'''Dopamine'''-[[Mutations]] in DR1 is related to the behaviour of mother paying less attention to the baby.<br> | |||
* '''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. | |||
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> | |||
==Genetics== | ==Genetics== | ||
Revision as of 16:49, 2 August 2021
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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
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Physiology
The normal physiology of [name of process] can be understood as follows:
Pathogenesis
- The exact pathogenesis of [disease name] is not completely understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Many pathological mechanisms are involved in postpartum depression which interact with one another.[1]
- Genetics of postpartum depression
Estrogen receptor alpha gene, polymorphisms in the serotonin transporter gene, 5-HTT, and the gene encoding for MAOA and the gene encoding for Catechol-O-methyltransferase (COMT), Genetic variants for the TPH2 gene, a SNP in OXT was predictive of both variation in breastfeeding duration and postpartum depression scores, an interaction between a SNP in the OXTR gene and methylation state was detected in association with postpartum depression. In a genome-wide linkage and association study, the Hemicentin 1 gene (HMNC1) had the strongest 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.
- Neurotransmitters and postpartum depression
GABA-GABA which is an inhibitory neurotransmitter in the brain, its level is inversely related with the depression symptoms in the postpartum period.
Glutamate-Glutamate is the excitatory neurotransmitter in the brain. In women with postpartum depression its level are increased in the medial prefrontal cortex and decreased in the dorsolateral prefrontal cortex.
Serotonin-The binding of Serotonin to 5HT1A receptors is decreased in the mesiotemporal and anterior cingulate cortices.
Dopamine-Mutations in DR1 is related to the behaviour of mother paying less attention to the baby.
- 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.
- ↑ 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.