User:Nkikel/sandbox: Difference between revisions
I am adding health benefits of estrogen beta. |
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<u>Research</u> |
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'''Probiotics''' |
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While [[Germ-free animal|germ-free (GF) mice]] and fecal examination are two ways of examining the [[Microbiota|microbiome]], an effective approach of studying the impact of the microbiome in humans is the utilization of [[Probiotic|probiotics]] due to an element of control. . Probiotics are a combination of various live bacteria and yeasts that are introduced into the digestive system in a powder capsule, or added to food products. A [[systematic review]] from 2016 examined the preclinical and small human trials that have been conducted with certain commercially available strains of probiotic bacteria and found that among those tested, [[Bifidobacterium|''Bifidobacterium'']] and [[Lactobacillus|''Lactobacillus'']] [[genera]] ([[B. longum|''B. longum'']], [[B. breve|''B. breve'']], [[B. infantis|''B. infantis'']], [[L. helveticus|''L. helveticus'']], [[L. rhamnosus|''L. rhamnosus'']], [[Lactobacillus plantarum|''L. plantarum'']], and [[L. casei|''L. casei'']]), had the most potential to be useful for certain [[Central nervous system disorder|central nervous system disorders]]. |
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There is a disparity in prevalence of [[cardiovascular disease]] (CVD) between pre- and post-menopausal women, and the difference can be attributed to estrogen levels. Mutations in ERβ have been shown to influence [[cardiomyocytes]], the cells that comprise the largest part of the heart, and can lead to an increased risk of CVD. Specifically, 17βE2 (a naturally occurring estrogen) improves cardiac metabolism by increasing myocardial ATP levels and respiratory function in the heart. In addition, it can inhibit myocyte cell death due to stress by altering various signaling pathways and can stimulate myocyte regeneration. While ERα has a more profound role in regeneration, ERβ can still increase [[Endothelial progenitor cell|endothelial]] progenitor cell activation and increase cardiac function after a myocardial infarction. The ERβ signaling pathway is also implicated in the role of [[vasodilation]] and arterial dilation, causing an increase in endothelial function and arterial perfusion. As a result, it can lead to a decrease in blood pressure and heart rate<ref>{{Cite journal|last=Luo|first=Tao|last2=Kim|first2=Jin Kyung|date=August 2016|title=The Role of Estrogen and Estrogen Receptors on Cardiomyocytes: An Overview|url=https://www.ncbi.nlm.nih.gov/pubmed/26860777|journal=The Canadian Journal of Cardiology|volume=32|issue=8|pages=1017–1025|doi=10.1016/j.cjca.2015.10.021|issn=1916-7075|pmc=PMC4853290|pmid=26860777}}</ref><ref>{{Cite journal|last=Muka|first=Taulant|last2=Vargas|first2=Kris G.|last3=Jaspers|first3=Loes|last4=Wen|first4=Ke-xin|last5=Dhana|first5=Klodian|last6=Vitezova|first6=Anna|last7=Nano|first7=Jana|last8=Brahimaj|first8=Adela|last9=Colpani|first9=Veronica|date=April 2016|title=Estrogen receptor β actions in the female cardiovascular system: A systematic review of animal and human studies|url=https://www.ncbi.nlm.nih.gov/pubmed/26921926|journal=Maturitas|volume=86|pages=28–43|doi=10.1016/j.maturitas.2016.01.009|issn=1873-4111|pmid=26921926}}</ref>. |
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Researchers can use certain types of probiotics to target specific bacteria and, as a result, the brain networks, behaviors, or cognitive domains affected by those bacteria. Additionally, researchers can control the amount of probiotics used, as well the amount of time participants have to take the treatments. This helps researchers to examine both the behavior of participants who undergo a series of treatments, as well as their neuronal functioning through [[Functional magnetic resonance imaging|fMRI]], [[Electroencephalography|EEG]], and neuropsychological test performance<ref>{{Cite journal|last=Dinan|first=Timothy G.|last2=Stilling|first2=Roman M.|last3=Stanton|first3=Catherine|last4=Cryan|first4=John F.|title=Collective unconscious: How gut microbes shape human behavior|url=http://linkinghub.elsevier.com/retrieve/pii/S0022395615000655|journal=Journal of Psychiatric Research|volume=63|pages=1–9|doi=10.1016/j.jpsychires.2015.02.021}}</ref><ref>{{Cite journal|last=Liu|first=Xiaofei|last2=Cao|first2=Shangqing|last3=Zhang|first3=Xuewu|date=2015-09-16|title=Modulation of Gut Microbiota–Brain Axis by Probiotics, Prebiotics, and Diet|url=http://dx.doi.org/10.1021/acs.jafc.5b02404|journal=Journal of Agricultural and Food Chemistry|volume=63|issue=36|pages=7885–7895|doi=10.1021/acs.jafc.5b02404|issn=0021-8561}}</ref>. |
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'''Alzheimer’s Disease''' |
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'''Autism''' |
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Similar to CVD, post-menopausal women have an increased risk of developing Alzheimer’s disease (AD) due to a loss of estrogen, which affects proper aging of the hippocampus, neural survival and regeneration, and amyloid metabolism. As a result, genetic variation in ERβ is both sex and age dependent and ERβ polymorphism can lead to accelerated brain aging, cognitive impairment, and development of AD pathology. ERβ mRNA is highly expressed in hippocampal formation and contributes to increased neuronal survival against neurodegenerative diseases such as AD. In addition, ERβ upregulates [[insulin-degrading enzyme]] (IDE), which aids in the maintenance of β-amyloid degradation. However, in AD, lack of ERβ causes a decrease in this degradation and an increase in symptoms. ERβ also plays a role in regulating [[Apolipoprotein E|APOE]], a risk factor for AD that redistributes lipids across cells. APOE expression in the hippocampus is specifically regulated by 17βE2, affecting learning and memory in individuals afflicted with AD. Thus, estrogen therapy via an ERβ-targeted approach can be used as a prevention method for AD either before or at the onset of menopause. Interactions between ERα and ERβ can lead to antagonistic actions in the brain, so an ERβ-targeted approach can increase therapeutic neural responses independently of ERα. Therapeutically, ERβ can be used in both men and women in order to regulate plaque formation in the brain<ref>{{Cite journal|last=Zhao|first=Liqin|last2=Woody|first2=Sarah K.|last3=Chhibber|first3=Anindit|date=November 2015|title=Estrogen receptor β in Alzheimer's disease: From mechanisms to therapeutics|url=https://www.ncbi.nlm.nih.gov/pubmed/26307455|journal=Ageing Research Reviews|volume=24|issue=Pt B|pages=178–190|doi=10.1016/j.arr.2015.08.001|issn=1872-9649|pmc=PMC4661108|pmid=26307455}}</ref>. |
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Studies using GF mice indicate a relationship between [[autism]] and microbiome. Three-chamber sociability tests are used to observe autistic behavior in mice, and in these tests mice are placed in a middle chamber and they can make the decision to go to either a chamber with other mice or a chamber with no mice. Typically, a mouse would prefer to go to the chamber containing other mice. However, this is not the case with GF mice. Thus, a lack of a diverse microbiome leads to autistic behavior<ref>{{Cite journal|last=Mulle|first=Jennifer G.|last2=Sharp|first2=William G.|last3=Cubells|first3=Joseph F.|date=2013-02-01|title=The Gut Microbiome: A New Frontier in Autism Research|url=https://link.springer.com/article/10.1007/s11920-012-0337-0|journal=Current Psychiatry Reports|language=en|volume=15|issue=2|pages=337|doi=10.1007/s11920-012-0337-0|issn=1523-3812}}</ref>. Genetic analysis of GF mice via [[RNA extraction]] also shows an upregulation of synaptic plasticity-related genes such as ''[[Brain-derived neurotrophic factor|Bdnf]]'' IV and genes that promote transcription (''[[C-Fos|cFOS]],'' ''Arc'') in the [[amygdala]]. This leads to an over-activation of amygdala activity that mimics amygdala activity in patients with autism<ref>{{Cite journal|last=Stilling|first=Roman M.|last2=Ryan|first2=Feargal J.|last3=Hoban|first3=Alan E.|last4=Shanahan|first4=Fergus|last5=Clarke|first5=Gerard|last6=Claesson|first6=Marcus J.|last7=Dinan|first7=Timothy G.|last8=Cryan|first8=John F.|title=Microbes & neurodevelopment – Absence of microbiota during early life increases activity-related transcriptional pathways in the amygdala|url=http://linkinghub.elsevier.com/retrieve/pii/S0889159115004043|journal=Brain, Behavior, and Immunity|volume=50|pages=209–220|doi=10.1016/j.bbi.2015.07.009}}</ref>. |
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<u>Neuroprotective Benefits</u> |
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'''Pain''' |
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'''Synaptic Strength and Plasticity''' |
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The composition of the gut microbiome can contribute to decreased pain threshold, known as [[visceral hypersensitivity]], in [[Functional gastrointestinal disorder|functional gastrointestinal disorders]] through the sensitization of [[Nociceptor|nociceptors]]. The specific pathway involved starts with nociceptive afferent fibers projecting onto spinal nociceptive neurons in the superficial laminae. Then the [[cingulate cortex]], medial [[thalamus]], [[amygdala]], [[hypothalamus]], [[periaqueductal gray]], and [[solitary tract]] generate the perception of pain and modulate the response<ref>{{Cite journal|last=Chichlowski|first=Maciej|last2=Rudolph|first2=Colin|date=2015-04-30|title=Visceral Pain and Gastrointestinal Microbiome|url=http://dx.doi.org/10.5056/jnm15025|journal=Journal of Neurogastroenterology and Motility|language=en|volume=21|issue=2|pages=172–181|doi=10.5056/jnm15025|issn=2093-0879}}</ref>. |
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Variations in endogenous estrogen levels cause changes in dendritic architecture in the hippocampus, with lower levels leading to decreased dendritic spines. However, treatment of 17βE2 can reverse this affect, giving it the ability to modify hippocampal structure. As a result of the relationship between dendritic architecture and [[long-term potentiation]] (LTP), ERβ can enhance LTP and lead to an increase in synaptic strength. Furthermore, 17βE2 promotes neurogenesis in developing hippocampal neurons and neurons in the [[subventricular zone]] and [[dentate gyrus]] of the adult human brain. Specifically, ERβ increases the proliferation of progenitor cells to create new neurons and can be increased later in life through 17βE2 treatment<ref>{{Cite journal|last=Engler-Chiurazzi|first=E.B.|last2=Brown|first2=C.M.|last3=Povroznik|first3=J.M.|last4=Simpkins|first4=J.W.|title=Estrogens as neuroprotectants: Estrogenic actions in the context of cognitive aging and brain injury|url=http://linkinghub.elsevier.com/retrieve/pii/S0301008215300630|journal=Progress in Neurobiology|volume=157|pages=188–211|doi=10.1016/j.pneurobio.2015.12.008}}</ref><ref>{{Cite journal|last=Vargas|first=Kris G.|last2=Milic|first2=Jelena|last3=Zaciragic|first3=Asija|last4=Wen|first4=Ke-Xin|last5=Jaspers|first5=Loes|last6=Nano|first6=Jana|last7=Dhana|first7=Klodian|last8=Bramer|first8=Wichor M.|last9=Kraja|first9=Bledar|date=November 2016|title=The functions of estrogen receptor beta in the female brain: A systematic review|url=https://www.ncbi.nlm.nih.gov/pubmed/27338976|journal=Maturitas|volume=93|pages=41–57|doi=10.1016/j.maturitas.2016.05.014|issn=1873-4111|pmid=27338976}}</ref>. |
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Specifically, a bacterial composition of ''Lactobacillus rhamnosus'', ''L. farciminis'', ''Bifidobacterium infantis'', and ''B. longum'' have been shown to impact pain. The microbiome can lead to visceral hypersensitivity through activation of receptors involved in peripheral sensitization such as [[Cannabinoid receptor|cannabinoid receptors]] and [[5-HT receptor|serotonin receptors]] via immune response at the mucosal level. It can also stimulate the release of pain-suppressing molecules. These natural biomolecules include opiods from [[Neutrophil|neutrophils]] and [[Monocyte|monocytes]], [[endocannabinoids]], and [[monoamines]]<ref>{{Cite journal|last=Akbar|first=A.|last2=Walters|first2=J. R. F.|last3=Ghosh|first3=S.|date=2009-09-01|title=Review article: visceral hypersensitivity in irritable bowel syndrome: molecular mechanisms and therapeutic agents|url=http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2009.04056.x/abstract|journal=Alimentary Pharmacology & Therapeutics|language=en|volume=30|issue=5|pages=423–435|doi=10.1111/j.1365-2036.2009.04056.x|issn=1365-2036}}</ref><ref>{{Cite journal|last=Oʼ Mahony|first=Siobhain M.|last2=Dinan|first2=Timothy G.|last3=Cryan|first3=John F.|date=2017-04-01|title=The gut microbiota as a key regulator of visceral pain|url=http://Insights.ovid.com/crossref?an=00006396-201704001-00004|journal=PAIN|language=ENGLISH|volume=158|pages=S19–S28|doi=10.1097/j.pain.0000000000000779|issn=0304-3959}}</ref>. |
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<references /> |
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Visceral sensitivity can also be affected by stress-modulate microbiome activity. Stress can lead to decreased gut motility and colonic inertia, which in turn negatively affects the amount and diversity of gut bacteria. Due to the fact that early postnatal life is the critical point to [[Hypothalamic–pituitary–adrenal axis|HPA axis]] development, programming of the neuroendocrine stress response, and establishment of the essential gut microbiota, maternal separation models are used to study the relationship between stress and early life on the microbiota. As a result, these studies suggest that stress in early life leads to increased vulnerability to visceral sensitivity. Furthermore, studies on stress in later life using [[Antibiotics|antibiotic]] studies and GF mice show that animals with a lack of gut bacteria have both an exaggerated stress response and reduced perception of pain<ref>{{Cite journal|last=Moloney|first=Rachel D.|last2=Desbonnet|first2=Lieve|last3=Clarke|first3=Gerard|last4=Dinan|first4=Timothy G.|last5=Cryan|first5=John F.|date=2014-02-01|title=The microbiome: stress, health and disease|url=https://link.springer.com/article/10.1007/s00335-013-9488-5|journal=Mammalian Genome|language=en|volume=25|issue=1-2|pages=49–74|doi=10.1007/s00335-013-9488-5|issn=0938-8990}}</ref>. <references /> |
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Latest revision as of 21:28, 4 December 2017
Research
Probiotics
While germ-free (GF) mice and fecal examination are two ways of examining the microbiome, an effective approach of studying the impact of the microbiome in humans is the utilization of probiotics due to an element of control. . Probiotics are a combination of various live bacteria and yeasts that are introduced into the digestive system in a powder capsule, or added to food products. A systematic review from 2016 examined the preclinical and small human trials that have been conducted with certain commercially available strains of probiotic bacteria and found that among those tested, Bifidobacterium and Lactobacillus genera (B. longum, B. breve, B. infantis, L. helveticus, L. rhamnosus, L. plantarum, and L. casei), had the most potential to be useful for certain central nervous system disorders.
Researchers can use certain types of probiotics to target specific bacteria and, as a result, the brain networks, behaviors, or cognitive domains affected by those bacteria. Additionally, researchers can control the amount of probiotics used, as well the amount of time participants have to take the treatments. This helps researchers to examine both the behavior of participants who undergo a series of treatments, as well as their neuronal functioning through fMRI, EEG, and neuropsychological test performance[1][2].
Autism
Studies using GF mice indicate a relationship between autism and microbiome. Three-chamber sociability tests are used to observe autistic behavior in mice, and in these tests mice are placed in a middle chamber and they can make the decision to go to either a chamber with other mice or a chamber with no mice. Typically, a mouse would prefer to go to the chamber containing other mice. However, this is not the case with GF mice. Thus, a lack of a diverse microbiome leads to autistic behavior[3]. Genetic analysis of GF mice via RNA extraction also shows an upregulation of synaptic plasticity-related genes such as Bdnf IV and genes that promote transcription (cFOS, Arc) in the amygdala. This leads to an over-activation of amygdala activity that mimics amygdala activity in patients with autism[4].
Pain
The composition of the gut microbiome can contribute to decreased pain threshold, known as visceral hypersensitivity, in functional gastrointestinal disorders through the sensitization of nociceptors. The specific pathway involved starts with nociceptive afferent fibers projecting onto spinal nociceptive neurons in the superficial laminae. Then the cingulate cortex, medial thalamus, amygdala, hypothalamus, periaqueductal gray, and solitary tract generate the perception of pain and modulate the response[5].
Specifically, a bacterial composition of Lactobacillus rhamnosus, L. farciminis, Bifidobacterium infantis, and B. longum have been shown to impact pain. The microbiome can lead to visceral hypersensitivity through activation of receptors involved in peripheral sensitization such as cannabinoid receptors and serotonin receptors via immune response at the mucosal level. It can also stimulate the release of pain-suppressing molecules. These natural biomolecules include opiods from neutrophils and monocytes, endocannabinoids, and monoamines[6][7].
Visceral sensitivity can also be affected by stress-modulate microbiome activity. Stress can lead to decreased gut motility and colonic inertia, which in turn negatively affects the amount and diversity of gut bacteria. Due to the fact that early postnatal life is the critical point to HPA axis development, programming of the neuroendocrine stress response, and establishment of the essential gut microbiota, maternal separation models are used to study the relationship between stress and early life on the microbiota. As a result, these studies suggest that stress in early life leads to increased vulnerability to visceral sensitivity. Furthermore, studies on stress in later life using antibiotic studies and GF mice show that animals with a lack of gut bacteria have both an exaggerated stress response and reduced perception of pain[8].
- ^ Dinan, Timothy G.; Stilling, Roman M.; Stanton, Catherine; Cryan, John F. "Collective unconscious: How gut microbes shape human behavior". Journal of Psychiatric Research. 63: 1–9. doi:10.1016/j.jpsychires.2015.02.021.
- ^ Liu, Xiaofei; Cao, Shangqing; Zhang, Xuewu (2015-09-16). "Modulation of Gut Microbiota–Brain Axis by Probiotics, Prebiotics, and Diet". Journal of Agricultural and Food Chemistry. 63 (36): 7885–7895. doi:10.1021/acs.jafc.5b02404. ISSN 0021-8561.
- ^ Mulle, Jennifer G.; Sharp, William G.; Cubells, Joseph F. (2013-02-01). "The Gut Microbiome: A New Frontier in Autism Research". Current Psychiatry Reports. 15 (2): 337. doi:10.1007/s11920-012-0337-0. ISSN 1523-3812.
- ^ Stilling, Roman M.; Ryan, Feargal J.; Hoban, Alan E.; Shanahan, Fergus; Clarke, Gerard; Claesson, Marcus J.; Dinan, Timothy G.; Cryan, John F. "Microbes & neurodevelopment – Absence of microbiota during early life increases activity-related transcriptional pathways in the amygdala". Brain, Behavior, and Immunity. 50: 209–220. doi:10.1016/j.bbi.2015.07.009.
- ^ Chichlowski, Maciej; Rudolph, Colin (2015-04-30). "Visceral Pain and Gastrointestinal Microbiome". Journal of Neurogastroenterology and Motility. 21 (2): 172–181. doi:10.5056/jnm15025. ISSN 2093-0879.
- ^ Akbar, A.; Walters, J. R. F.; Ghosh, S. (2009-09-01). "Review article: visceral hypersensitivity in irritable bowel syndrome: molecular mechanisms and therapeutic agents". Alimentary Pharmacology & Therapeutics. 30 (5): 423–435. doi:10.1111/j.1365-2036.2009.04056.x. ISSN 1365-2036.
- ^ Oʼ Mahony, Siobhain M.; Dinan, Timothy G.; Cryan, John F. (2017-04-01). "The gut microbiota as a key regulator of visceral pain". PAIN. 158: S19 – S28. doi:10.1097/j.pain.0000000000000779. ISSN 0304-3959.
- ^ Moloney, Rachel D.; Desbonnet, Lieve; Clarke, Gerard; Dinan, Timothy G.; Cryan, John F. (2014-02-01). "The microbiome: stress, health and disease". Mammalian Genome. 25 (1–2): 49–74. doi:10.1007/s00335-013-9488-5. ISSN 0938-8990.