Genetics of migraine: where are we now?

Abstract Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes code for proteins expressed i...
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Autor*in:	Grangeon, Lou [verfasserIn] Lange, Kristin Sophie Waliszewska-Prosół, Marta Onan, Dilara Marschollek, Karol Wiels, Wietse Mikulenka, Petr Farham, Fatemeh Gollion, Cédric Ducros, Anne

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Migraine Familial hemiplegic migraine Genetics Genome-wide association studies Polygenic

Anmerkung:	© The Author(s) 2023

Übergeordnetes Werk:	Enthalten in: The journal of headache and pain - Milano : Springer Italia, 2000, 24(2023), 1 vom: 20. Feb.
Übergeordnetes Werk:	volume:24 ; year:2023 ; number:1 ; day:20 ; month:02

Links:	Volltext

DOI / URN:	10.1186/s10194-023-01547-8

Katalog-ID:	SPR049379283

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allfields	10.1186/s10194-023-01547-8 doi (DE-627)SPR049379283 (SPR)s10194-023-01547-8-e DE-627 ger DE-627 rakwb eng Grangeon, Lou verfasserin aut Genetics of migraine: where are we now? 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes code for proteins expressed in neurons, glial cells, or vessels, all of which increase susceptibility to cortical spreading depression. The study of monogenic migraines has shown that the neurovascular unit plays a prominent role in migraine. Genome-wide association studies have identified numerous susceptibility variants that each result in only a small increase in overall migraine risk. The more than 180 known variants belong to several complex networks of “pro-migraine” molecular abnormalities, which are mainly neuronal or vascular. Genetics has also highlighted the importance of shared genetic factors between migraine and its major co-morbidities, including depression and high blood pressure. Further studies are still needed to map all of the susceptibility loci for migraine and then to understand how these genomic variants lead to migraine cell phenotypes. Migraine (dpeaa)DE-He213 Familial hemiplegic migraine (dpeaa)DE-He213 Genetics (dpeaa)DE-He213 Genome-wide association studies (dpeaa)DE-He213 Polygenic (dpeaa)DE-He213 Lange, Kristin Sophie aut Waliszewska-Prosół, Marta aut Onan, Dilara aut Marschollek, Karol aut Wiels, Wietse aut Mikulenka, Petr aut Farham, Fatemeh aut Gollion, Cédric aut Ducros, Anne aut Enthalten in The journal of headache and pain Milano : Springer Italia, 2000 24(2023), 1 vom: 20. Feb. (DE-627)320600963 (DE-600)2020168-0 1129-2377 nnns volume:24 year:2023 number:1 day:20 month:02 https://dx.doi.org/10.1186/s10194-023-01547-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 1 20 02
spelling	10.1186/s10194-023-01547-8 doi (DE-627)SPR049379283 (SPR)s10194-023-01547-8-e DE-627 ger DE-627 rakwb eng Grangeon, Lou verfasserin aut Genetics of migraine: where are we now? 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes code for proteins expressed in neurons, glial cells, or vessels, all of which increase susceptibility to cortical spreading depression. The study of monogenic migraines has shown that the neurovascular unit plays a prominent role in migraine. Genome-wide association studies have identified numerous susceptibility variants that each result in only a small increase in overall migraine risk. The more than 180 known variants belong to several complex networks of “pro-migraine” molecular abnormalities, which are mainly neuronal or vascular. Genetics has also highlighted the importance of shared genetic factors between migraine and its major co-morbidities, including depression and high blood pressure. Further studies are still needed to map all of the susceptibility loci for migraine and then to understand how these genomic variants lead to migraine cell phenotypes. Migraine (dpeaa)DE-He213 Familial hemiplegic migraine (dpeaa)DE-He213 Genetics (dpeaa)DE-He213 Genome-wide association studies (dpeaa)DE-He213 Polygenic (dpeaa)DE-He213 Lange, Kristin Sophie aut Waliszewska-Prosół, Marta aut Onan, Dilara aut Marschollek, Karol aut Wiels, Wietse aut Mikulenka, Petr aut Farham, Fatemeh aut Gollion, Cédric aut Ducros, Anne aut Enthalten in The journal of headache and pain Milano : Springer Italia, 2000 24(2023), 1 vom: 20. Feb. (DE-627)320600963 (DE-600)2020168-0 1129-2377 nnns volume:24 year:2023 number:1 day:20 month:02 https://dx.doi.org/10.1186/s10194-023-01547-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 1 20 02
allfields_unstemmed	10.1186/s10194-023-01547-8 doi (DE-627)SPR049379283 (SPR)s10194-023-01547-8-e DE-627 ger DE-627 rakwb eng Grangeon, Lou verfasserin aut Genetics of migraine: where are we now? 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes code for proteins expressed in neurons, glial cells, or vessels, all of which increase susceptibility to cortical spreading depression. The study of monogenic migraines has shown that the neurovascular unit plays a prominent role in migraine. Genome-wide association studies have identified numerous susceptibility variants that each result in only a small increase in overall migraine risk. The more than 180 known variants belong to several complex networks of “pro-migraine” molecular abnormalities, which are mainly neuronal or vascular. Genetics has also highlighted the importance of shared genetic factors between migraine and its major co-morbidities, including depression and high blood pressure. Further studies are still needed to map all of the susceptibility loci for migraine and then to understand how these genomic variants lead to migraine cell phenotypes. Migraine (dpeaa)DE-He213 Familial hemiplegic migraine (dpeaa)DE-He213 Genetics (dpeaa)DE-He213 Genome-wide association studies (dpeaa)DE-He213 Polygenic (dpeaa)DE-He213 Lange, Kristin Sophie aut Waliszewska-Prosół, Marta aut Onan, Dilara aut Marschollek, Karol aut Wiels, Wietse aut Mikulenka, Petr aut Farham, Fatemeh aut Gollion, Cédric aut Ducros, Anne aut Enthalten in The journal of headache and pain Milano : Springer Italia, 2000 24(2023), 1 vom: 20. Feb. (DE-627)320600963 (DE-600)2020168-0 1129-2377 nnns volume:24 year:2023 number:1 day:20 month:02 https://dx.doi.org/10.1186/s10194-023-01547-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 1 20 02
allfieldsGer	10.1186/s10194-023-01547-8 doi (DE-627)SPR049379283 (SPR)s10194-023-01547-8-e DE-627 ger DE-627 rakwb eng Grangeon, Lou verfasserin aut Genetics of migraine: where are we now? 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes code for proteins expressed in neurons, glial cells, or vessels, all of which increase susceptibility to cortical spreading depression. The study of monogenic migraines has shown that the neurovascular unit plays a prominent role in migraine. Genome-wide association studies have identified numerous susceptibility variants that each result in only a small increase in overall migraine risk. The more than 180 known variants belong to several complex networks of “pro-migraine” molecular abnormalities, which are mainly neuronal or vascular. Genetics has also highlighted the importance of shared genetic factors between migraine and its major co-morbidities, including depression and high blood pressure. Further studies are still needed to map all of the susceptibility loci for migraine and then to understand how these genomic variants lead to migraine cell phenotypes. Migraine (dpeaa)DE-He213 Familial hemiplegic migraine (dpeaa)DE-He213 Genetics (dpeaa)DE-He213 Genome-wide association studies (dpeaa)DE-He213 Polygenic (dpeaa)DE-He213 Lange, Kristin Sophie aut Waliszewska-Prosół, Marta aut Onan, Dilara aut Marschollek, Karol aut Wiels, Wietse aut Mikulenka, Petr aut Farham, Fatemeh aut Gollion, Cédric aut Ducros, Anne aut Enthalten in The journal of headache and pain Milano : Springer Italia, 2000 24(2023), 1 vom: 20. Feb. (DE-627)320600963 (DE-600)2020168-0 1129-2377 nnns volume:24 year:2023 number:1 day:20 month:02 https://dx.doi.org/10.1186/s10194-023-01547-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 1 20 02
allfieldsSound	10.1186/s10194-023-01547-8 doi (DE-627)SPR049379283 (SPR)s10194-023-01547-8-e DE-627 ger DE-627 rakwb eng Grangeon, Lou verfasserin aut Genetics of migraine: where are we now? 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes code for proteins expressed in neurons, glial cells, or vessels, all of which increase susceptibility to cortical spreading depression. The study of monogenic migraines has shown that the neurovascular unit plays a prominent role in migraine. Genome-wide association studies have identified numerous susceptibility variants that each result in only a small increase in overall migraine risk. The more than 180 known variants belong to several complex networks of “pro-migraine” molecular abnormalities, which are mainly neuronal or vascular. Genetics has also highlighted the importance of shared genetic factors between migraine and its major co-morbidities, including depression and high blood pressure. Further studies are still needed to map all of the susceptibility loci for migraine and then to understand how these genomic variants lead to migraine cell phenotypes. Migraine (dpeaa)DE-He213 Familial hemiplegic migraine (dpeaa)DE-He213 Genetics (dpeaa)DE-He213 Genome-wide association studies (dpeaa)DE-He213 Polygenic (dpeaa)DE-He213 Lange, Kristin Sophie aut Waliszewska-Prosół, Marta aut Onan, Dilara aut Marschollek, Karol aut Wiels, Wietse aut Mikulenka, Petr aut Farham, Fatemeh aut Gollion, Cédric aut Ducros, Anne aut Enthalten in The journal of headache and pain Milano : Springer Italia, 2000 24(2023), 1 vom: 20. Feb. (DE-627)320600963 (DE-600)2020168-0 1129-2377 nnns volume:24 year:2023 number:1 day:20 month:02 https://dx.doi.org/10.1186/s10194-023-01547-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 1 20 02
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source	Enthalten in The journal of headache and pain 24(2023), 1 vom: 20. Feb. volume:24 year:2023 number:1 day:20 month:02
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author	Grangeon, Lou
spellingShingle	Grangeon, Lou misc Migraine misc Familial hemiplegic migraine misc Genetics misc Genome-wide association studies misc Polygenic Genetics of migraine: where are we now?
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topic_title	Genetics of migraine: where are we now? Migraine (dpeaa)DE-He213 Familial hemiplegic migraine (dpeaa)DE-He213 Genetics (dpeaa)DE-He213 Genome-wide association studies (dpeaa)DE-He213 Polygenic (dpeaa)DE-He213
topic	misc Migraine misc Familial hemiplegic migraine misc Genetics misc Genome-wide association studies misc Polygenic
topic_unstemmed	misc Migraine misc Familial hemiplegic migraine misc Genetics misc Genome-wide association studies misc Polygenic
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title_sort	genetics of migraine: where are we now?
title_auth	Genetics of migraine: where are we now?
abstract	Abstract Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes code for proteins expressed in neurons, glial cells, or vessels, all of which increase susceptibility to cortical spreading depression. The study of monogenic migraines has shown that the neurovascular unit plays a prominent role in migraine. Genome-wide association studies have identified numerous susceptibility variants that each result in only a small increase in overall migraine risk. The more than 180 known variants belong to several complex networks of “pro-migraine” molecular abnormalities, which are mainly neuronal or vascular. Genetics has also highlighted the importance of shared genetic factors between migraine and its major co-morbidities, including depression and high blood pressure. Further studies are still needed to map all of the susceptibility loci for migraine and then to understand how these genomic variants lead to migraine cell phenotypes. © The Author(s) 2023
abstractGer	Abstract Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes code for proteins expressed in neurons, glial cells, or vessels, all of which increase susceptibility to cortical spreading depression. The study of monogenic migraines has shown that the neurovascular unit plays a prominent role in migraine. Genome-wide association studies have identified numerous susceptibility variants that each result in only a small increase in overall migraine risk. The more than 180 known variants belong to several complex networks of “pro-migraine” molecular abnormalities, which are mainly neuronal or vascular. Genetics has also highlighted the importance of shared genetic factors between migraine and its major co-morbidities, including depression and high blood pressure. Further studies are still needed to map all of the susceptibility loci for migraine and then to understand how these genomic variants lead to migraine cell phenotypes. © The Author(s) 2023
abstract_unstemmed	Abstract Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes code for proteins expressed in neurons, glial cells, or vessels, all of which increase susceptibility to cortical spreading depression. The study of monogenic migraines has shown that the neurovascular unit plays a prominent role in migraine. Genome-wide association studies have identified numerous susceptibility variants that each result in only a small increase in overall migraine risk. The more than 180 known variants belong to several complex networks of “pro-migraine” molecular abnormalities, which are mainly neuronal or vascular. Genetics has also highlighted the importance of shared genetic factors between migraine and its major co-morbidities, including depression and high blood pressure. Further studies are still needed to map all of the susceptibility loci for migraine and then to understand how these genomic variants lead to migraine cell phenotypes. © The Author(s) 2023
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title_short	Genetics of migraine: where are we now?
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