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10.1186/s10194-021-01271-1 http://scihub22266oqcxt.onion/10.1186/s10194-021-01271-1 34112082!8192049!34112082     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Headache+Pain 2021 ; 22 (1): 55 Nephropedia Template TP {{tp|p=34112082|t=2021. Migraine and neuroinflammation: the inflammasome perspective |pdf=|usr=}}{{34112082}} gab.com Text Migraine and neuroinflammation: the inflammasome perspective JO: J Headache Pain http://www.kidney.de/pget.php?&tw=1&pmid=34112082 #FOAvip BACKGROUND: Neuroinflammation has an important role in the pathophysiology of migraine, which is a complex neuro-glio-vascular disorder. The main aim of this review is to highlight findings of cortical spreading depolarization (CSD)-induced neuroinflammatory signaling in brain parenchyma from the inflammasome perspective. In addition, we discuss the limited data of the contribution of inflammasomes to other aspects of migraine pathophysiology, foremost the activation of the trigeminovascular system and thereby the generation of migraine pain. MAIN BODY: Inflammasomes are signaling multiprotein complexes and key components of the innate immune system. Their activation causes the production of inflammatory cytokines that can stimulate trigeminal neurons and are thus relevant to the generation of migraine pain. The contribution of inflammasome activation to pain signaling has attracted considerable attention in recent years. Nucleotide-binding domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) is the best characterized inflammasome and there is emerging evidence of its role in a variety of inflammatory pain conditions, including migraine. In this review, we discuss, from an inflammasome point of view, cortical spreading depolarization (CSD)-induced neuroinflammatory signaling in brain parenchyma, the connection with genetic factors that make the brain vulnerable to CSD, and the relation of the inflammasome with diseases that are co-morbid with migraine, including stroke, epilepsy, and the possible links with COVID-19 infection. CONCLUSION: Neuroinflammatory pathways, specifically those involving inflammasome proteins, seem promising candidates as treatment targets, and perhaps even biomarkers, in migraine. Twit Text FOAVip Migraine and neuroinflammation: the inflammasome perspective ????J Headache Pain http://www.kidney.de/pget.php?&tw=1&pmid=34112082 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34112082 #FOAvip English Wikipedia <ref>{{Cite pmid|34112082}}</ref> Migraine and neuroinflammation: the inflammasome perspective #MMPMID34112082 Kursun O; Yemisci M; van den Maagdenberg AMJM; Karatas H J Headache Pain 2021[Jun]; 22 (1): 55 PMID34112082show ga BACKGROUND: Neuroinflammation has an important role in the pathophysiology of migraine, which is a complex neuro-glio-vascular disorder. The main aim of this review is to highlight findings of cortical spreading depolarization (CSD)-induced neuroinflammatory signaling in brain parenchyma from the inflammasome perspective. In addition, we discuss the limited data of the contribution of inflammasomes to other aspects of migraine pathophysiology, foremost the activation of the trigeminovascular system and thereby the generation of migraine pain. MAIN BODY: Inflammasomes are signaling multiprotein complexes and key components of the innate immune system. Their activation causes the production of inflammatory cytokines that can stimulate trigeminal neurons and are thus relevant to the generation of migraine pain. The contribution of inflammasome activation to pain signaling has attracted considerable attention in recent years. Nucleotide-binding domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) is the best characterized inflammasome and there is emerging evidence of its role in a variety of inflammatory pain conditions, including migraine. In this review, we discuss, from an inflammasome point of view, cortical spreading depolarization (CSD)-induced neuroinflammatory signaling in brain parenchyma, the connection with genetic factors that make the brain vulnerable to CSD, and the relation of the inflammasome with diseases that are co-morbid with migraine, including stroke, epilepsy, and the possible links with COVID-19 infection. CONCLUSION: Neuroinflammatory pathways, specifically those involving inflammasome proteins, seem promising candidates as treatment targets, and perhaps even biomarkers, in migraine. |*COVID-19[MESH] |*Migraine Disorders[MESH] |Humans[MESH] |Inflammasomes[MESH] |NLR Family, Pyrin Domain-Containing 3 Protein[MESH]Migraine and neuroinflammation: the inflammasome perspective (epmc).pdf DeepDyve Pubget Overpricing