Peripartum mood disturbances pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*[[Genetics]] of [[postpartum]] [[depression]]: <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><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]] [[Hemicentin 1|(HMNC1]]) had the strongest association with [[postpartum]] [[depression]]. | *[[Genetics]] of [[postpartum]] [[depression]]: <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><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]] [[Hemicentin 1|(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]]. | *[[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]]. | *[[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> | *[[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> | '''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|medial prefrontal]] [[cortex]] and decreased in the dorsolateral [[prefrontal cortex]].<br> | '''Glutamate'''-[[Glutamate]] is the [[excitatory neurotransmitter]] in the brain. In women with [[postpartum depression]] its level are increased in the [[Medial prefrontal cortex|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> | '''Serotonin'''-The binding of [[Serotonin]] to [[5HT1A]] [[receptors]] is decreased in the [[mesiotemporal]] and anterior [[cingulate]] [[cortices]].<br> | ||
Revision as of 20:31, 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
Many pathological mechanisms are involved in postpartum depression which interact with one another.
Pathophysiology
Physiology
The normal physiology of [name of process] can be understood as follows:
Pathogenesis
- Genetics of postpartum depression: [1]
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.
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. 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)