<it<ApoE</it< polymorphisms in narcolepsy

<p<Summary</p< <p<Background</p< <p<Narcolepsy is a common neuropsychiatric disorder characterized by increased daytime sleepiness, cataplexy and hypnagogic hallucinations. Deficiency of the hypocretin neurotransmitter system was shown to be involved in the pathogenesis...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Kasten Meike [verfasserIn] Wieczorek Stefan [verfasserIn] Dahmen Norbert [verfasserIn] Gencik Martin [verfasserIn] Gencikova Alexandra [verfasserIn] Epplen Jorg T [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2001

Übergeordnetes Werk:	In: BMC Medical Genetics - BMC, 2003, 2(2001), 1, p 9
Übergeordnetes Werk:	volume:2 ; year:2001 ; number:1, p 9

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2350-2-9

Katalog-ID:	DOAJ085762342

Internformat


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allfields	10.1186/1471-2350-2-9 doi (DE-627)DOAJ085762342 (DE-599)DOAJ199733b94e7749c18060cbba9f488ef2 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Kasten Meike verfasserin aut <it<ApoE</it< polymorphisms in narcolepsy 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Summary</p< <p<Background</p< <p<Narcolepsy is a common neuropsychiatric disorder characterized by increased daytime sleepiness, cataplexy and hypnagogic hallucinations. Deficiency of the hypocretin neurotransmitter system was shown to be involved in the pathogenesis of narcolepsy in animals and men. There are several hints that neurodegeneration of hypocretin producing neurons in the hypothalamus is the pathological correlate of narcolepsy. The <it<ApoE4</it< allele is a major contributing factor to early-onset neuronal degeneration in Alzheimer disease and other neurodegenerative diseases as well.</p< <p<Methods</p< <p<To clarify whether the ApoE4 phenotype predisposes to narcolepsy or associates with an earlier disease onset, we have genotyped the <it<ApoE</it< gene in 103 patients with narcolepsy and 101 healthy controls.</p< <p<Results</p< <p<The frequency of the E4 allele of the <it<ApoE</it< gene was 11% in the patient and 15% in the control groups. Furthermore, the mean age of onset did not differ between the ApoE4<sup<+</sup< and ApoE4<sup<-</sup< patient groups.</p< <p<Conclusion</p< <p<Our results exclude the <it<ApoE4</it< allele as a major risk factor for narcolepsy.</p< Internal medicine Genetics Wieczorek Stefan verfasserin aut Dahmen Norbert verfasserin aut Gencik Martin verfasserin aut Gencikova Alexandra verfasserin aut Epplen Jorg T verfasserin aut In BMC Medical Genetics BMC, 2003 2(2001), 1, p 9 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:2 year:2001 number:1, p 9 https://doi.org/10.1186/1471-2350-2-9 kostenfrei https://doaj.org/article/199733b94e7749c18060cbba9f488ef2 kostenfrei http://www.biomedcentral.com/1471-2350/2/9 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_65 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_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 2 2001 1, p 9
spelling	10.1186/1471-2350-2-9 doi (DE-627)DOAJ085762342 (DE-599)DOAJ199733b94e7749c18060cbba9f488ef2 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Kasten Meike verfasserin aut <it<ApoE</it< polymorphisms in narcolepsy 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Summary</p< <p<Background</p< <p<Narcolepsy is a common neuropsychiatric disorder characterized by increased daytime sleepiness, cataplexy and hypnagogic hallucinations. Deficiency of the hypocretin neurotransmitter system was shown to be involved in the pathogenesis of narcolepsy in animals and men. There are several hints that neurodegeneration of hypocretin producing neurons in the hypothalamus is the pathological correlate of narcolepsy. The <it<ApoE4</it< allele is a major contributing factor to early-onset neuronal degeneration in Alzheimer disease and other neurodegenerative diseases as well.</p< <p<Methods</p< <p<To clarify whether the ApoE4 phenotype predisposes to narcolepsy or associates with an earlier disease onset, we have genotyped the <it<ApoE</it< gene in 103 patients with narcolepsy and 101 healthy controls.</p< <p<Results</p< <p<The frequency of the E4 allele of the <it<ApoE</it< gene was 11% in the patient and 15% in the control groups. Furthermore, the mean age of onset did not differ between the ApoE4<sup<+</sup< and ApoE4<sup<-</sup< patient groups.</p< <p<Conclusion</p< <p<Our results exclude the <it<ApoE4</it< allele as a major risk factor for narcolepsy.</p< Internal medicine Genetics Wieczorek Stefan verfasserin aut Dahmen Norbert verfasserin aut Gencik Martin verfasserin aut Gencikova Alexandra verfasserin aut Epplen Jorg T verfasserin aut In BMC Medical Genetics BMC, 2003 2(2001), 1, p 9 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:2 year:2001 number:1, p 9 https://doi.org/10.1186/1471-2350-2-9 kostenfrei https://doaj.org/article/199733b94e7749c18060cbba9f488ef2 kostenfrei http://www.biomedcentral.com/1471-2350/2/9 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_65 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_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 2 2001 1, p 9
allfields_unstemmed	10.1186/1471-2350-2-9 doi (DE-627)DOAJ085762342 (DE-599)DOAJ199733b94e7749c18060cbba9f488ef2 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Kasten Meike verfasserin aut <it<ApoE</it< polymorphisms in narcolepsy 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Summary</p< <p<Background</p< <p<Narcolepsy is a common neuropsychiatric disorder characterized by increased daytime sleepiness, cataplexy and hypnagogic hallucinations. Deficiency of the hypocretin neurotransmitter system was shown to be involved in the pathogenesis of narcolepsy in animals and men. There are several hints that neurodegeneration of hypocretin producing neurons in the hypothalamus is the pathological correlate of narcolepsy. The <it<ApoE4</it< allele is a major contributing factor to early-onset neuronal degeneration in Alzheimer disease and other neurodegenerative diseases as well.</p< <p<Methods</p< <p<To clarify whether the ApoE4 phenotype predisposes to narcolepsy or associates with an earlier disease onset, we have genotyped the <it<ApoE</it< gene in 103 patients with narcolepsy and 101 healthy controls.</p< <p<Results</p< <p<The frequency of the E4 allele of the <it<ApoE</it< gene was 11% in the patient and 15% in the control groups. Furthermore, the mean age of onset did not differ between the ApoE4<sup<+</sup< and ApoE4<sup<-</sup< patient groups.</p< <p<Conclusion</p< <p<Our results exclude the <it<ApoE4</it< allele as a major risk factor for narcolepsy.</p< Internal medicine Genetics Wieczorek Stefan verfasserin aut Dahmen Norbert verfasserin aut Gencik Martin verfasserin aut Gencikova Alexandra verfasserin aut Epplen Jorg T verfasserin aut In BMC Medical Genetics BMC, 2003 2(2001), 1, p 9 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:2 year:2001 number:1, p 9 https://doi.org/10.1186/1471-2350-2-9 kostenfrei https://doaj.org/article/199733b94e7749c18060cbba9f488ef2 kostenfrei http://www.biomedcentral.com/1471-2350/2/9 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_65 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_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 2 2001 1, p 9
allfieldsGer	10.1186/1471-2350-2-9 doi (DE-627)DOAJ085762342 (DE-599)DOAJ199733b94e7749c18060cbba9f488ef2 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Kasten Meike verfasserin aut <it<ApoE</it< polymorphisms in narcolepsy 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Summary</p< <p<Background</p< <p<Narcolepsy is a common neuropsychiatric disorder characterized by increased daytime sleepiness, cataplexy and hypnagogic hallucinations. Deficiency of the hypocretin neurotransmitter system was shown to be involved in the pathogenesis of narcolepsy in animals and men. There are several hints that neurodegeneration of hypocretin producing neurons in the hypothalamus is the pathological correlate of narcolepsy. The <it<ApoE4</it< allele is a major contributing factor to early-onset neuronal degeneration in Alzheimer disease and other neurodegenerative diseases as well.</p< <p<Methods</p< <p<To clarify whether the ApoE4 phenotype predisposes to narcolepsy or associates with an earlier disease onset, we have genotyped the <it<ApoE</it< gene in 103 patients with narcolepsy and 101 healthy controls.</p< <p<Results</p< <p<The frequency of the E4 allele of the <it<ApoE</it< gene was 11% in the patient and 15% in the control groups. Furthermore, the mean age of onset did not differ between the ApoE4<sup<+</sup< and ApoE4<sup<-</sup< patient groups.</p< <p<Conclusion</p< <p<Our results exclude the <it<ApoE4</it< allele as a major risk factor for narcolepsy.</p< Internal medicine Genetics Wieczorek Stefan verfasserin aut Dahmen Norbert verfasserin aut Gencik Martin verfasserin aut Gencikova Alexandra verfasserin aut Epplen Jorg T verfasserin aut In BMC Medical Genetics BMC, 2003 2(2001), 1, p 9 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:2 year:2001 number:1, p 9 https://doi.org/10.1186/1471-2350-2-9 kostenfrei https://doaj.org/article/199733b94e7749c18060cbba9f488ef2 kostenfrei http://www.biomedcentral.com/1471-2350/2/9 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_65 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_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 2 2001 1, p 9
allfieldsSound	10.1186/1471-2350-2-9 doi (DE-627)DOAJ085762342 (DE-599)DOAJ199733b94e7749c18060cbba9f488ef2 DE-627 ger DE-627 rakwb eng RC31-1245 QH426-470 Kasten Meike verfasserin aut <it<ApoE</it< polymorphisms in narcolepsy 2001 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Summary</p< <p<Background</p< <p<Narcolepsy is a common neuropsychiatric disorder characterized by increased daytime sleepiness, cataplexy and hypnagogic hallucinations. Deficiency of the hypocretin neurotransmitter system was shown to be involved in the pathogenesis of narcolepsy in animals and men. There are several hints that neurodegeneration of hypocretin producing neurons in the hypothalamus is the pathological correlate of narcolepsy. The <it<ApoE4</it< allele is a major contributing factor to early-onset neuronal degeneration in Alzheimer disease and other neurodegenerative diseases as well.</p< <p<Methods</p< <p<To clarify whether the ApoE4 phenotype predisposes to narcolepsy or associates with an earlier disease onset, we have genotyped the <it<ApoE</it< gene in 103 patients with narcolepsy and 101 healthy controls.</p< <p<Results</p< <p<The frequency of the E4 allele of the <it<ApoE</it< gene was 11% in the patient and 15% in the control groups. Furthermore, the mean age of onset did not differ between the ApoE4<sup<+</sup< and ApoE4<sup<-</sup< patient groups.</p< <p<Conclusion</p< <p<Our results exclude the <it<ApoE4</it< allele as a major risk factor for narcolepsy.</p< Internal medicine Genetics Wieczorek Stefan verfasserin aut Dahmen Norbert verfasserin aut Gencik Martin verfasserin aut Gencikova Alexandra verfasserin aut Epplen Jorg T verfasserin aut In BMC Medical Genetics BMC, 2003 2(2001), 1, p 9 (DE-627)326643788 (DE-600)2041359-2 14712350 nnns volume:2 year:2001 number:1, p 9 https://doi.org/10.1186/1471-2350-2-9 kostenfrei https://doaj.org/article/199733b94e7749c18060cbba9f488ef2 kostenfrei http://www.biomedcentral.com/1471-2350/2/9 kostenfrei https://doaj.org/toc/1471-2350 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_65 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_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 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 2 2001 1, p 9
language	English
source	In BMC Medical Genetics 2(2001), 1, p 9 volume:2 year:2001 number:1, p 9
sourceStr	In BMC Medical Genetics 2(2001), 1, p 9 volume:2 year:2001 number:1, p 9
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Internal medicine Genetics
isfreeaccess_bool	true
container_title	BMC Medical Genetics
authorswithroles_txt_mv	Kasten Meike @@aut@@ Wieczorek Stefan @@aut@@ Dahmen Norbert @@aut@@ Gencik Martin @@aut@@ Gencikova Alexandra @@aut@@ Epplen Jorg T @@aut@@
publishDateDaySort_date	2001-01-01T00:00:00Z
hierarchy_top_id	326643788
id	DOAJ085762342
language_de	englisch
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callnumber-first	R - Medicine
author	Kasten Meike
spellingShingle	Kasten Meike misc RC31-1245 misc QH426-470 misc Internal medicine misc Genetics <it<ApoE</it< polymorphisms in narcolepsy
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topic_title	RC31-1245 QH426-470 <it<ApoE</it< polymorphisms in narcolepsy
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title	<it<ApoE</it< polymorphisms in narcolepsy
ctrlnum	(DE-627)DOAJ085762342 (DE-599)DOAJ199733b94e7749c18060cbba9f488ef2
title_full	<it<ApoE</it< polymorphisms in narcolepsy
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author_browse	Kasten Meike Wieczorek Stefan Dahmen Norbert Gencik Martin Gencikova Alexandra Epplen Jorg T
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author2-role	verfasserin
title_sort	<it<apoe</it< polymorphisms in narcolepsy
callnumber	RC31-1245
title_auth	<it<ApoE</it< polymorphisms in narcolepsy
abstract	<p<Summary</p< <p<Background</p< <p<Narcolepsy is a common neuropsychiatric disorder characterized by increased daytime sleepiness, cataplexy and hypnagogic hallucinations. Deficiency of the hypocretin neurotransmitter system was shown to be involved in the pathogenesis of narcolepsy in animals and men. There are several hints that neurodegeneration of hypocretin producing neurons in the hypothalamus is the pathological correlate of narcolepsy. The <it<ApoE4</it< allele is a major contributing factor to early-onset neuronal degeneration in Alzheimer disease and other neurodegenerative diseases as well.</p< <p<Methods</p< <p<To clarify whether the ApoE4 phenotype predisposes to narcolepsy or associates with an earlier disease onset, we have genotyped the <it<ApoE</it< gene in 103 patients with narcolepsy and 101 healthy controls.</p< <p<Results</p< <p<The frequency of the E4 allele of the <it<ApoE</it< gene was 11% in the patient and 15% in the control groups. Furthermore, the mean age of onset did not differ between the ApoE4<sup<+</sup< and ApoE4<sup<-</sup< patient groups.</p< <p<Conclusion</p< <p<Our results exclude the <it<ApoE4</it< allele as a major risk factor for narcolepsy.</p<
abstractGer	<p<Summary</p< <p<Background</p< <p<Narcolepsy is a common neuropsychiatric disorder characterized by increased daytime sleepiness, cataplexy and hypnagogic hallucinations. Deficiency of the hypocretin neurotransmitter system was shown to be involved in the pathogenesis of narcolepsy in animals and men. There are several hints that neurodegeneration of hypocretin producing neurons in the hypothalamus is the pathological correlate of narcolepsy. The <it<ApoE4</it< allele is a major contributing factor to early-onset neuronal degeneration in Alzheimer disease and other neurodegenerative diseases as well.</p< <p<Methods</p< <p<To clarify whether the ApoE4 phenotype predisposes to narcolepsy or associates with an earlier disease onset, we have genotyped the <it<ApoE</it< gene in 103 patients with narcolepsy and 101 healthy controls.</p< <p<Results</p< <p<The frequency of the E4 allele of the <it<ApoE</it< gene was 11% in the patient and 15% in the control groups. Furthermore, the mean age of onset did not differ between the ApoE4<sup<+</sup< and ApoE4<sup<-</sup< patient groups.</p< <p<Conclusion</p< <p<Our results exclude the <it<ApoE4</it< allele as a major risk factor for narcolepsy.</p<
abstract_unstemmed	<p<Summary</p< <p<Background</p< <p<Narcolepsy is a common neuropsychiatric disorder characterized by increased daytime sleepiness, cataplexy and hypnagogic hallucinations. Deficiency of the hypocretin neurotransmitter system was shown to be involved in the pathogenesis of narcolepsy in animals and men. There are several hints that neurodegeneration of hypocretin producing neurons in the hypothalamus is the pathological correlate of narcolepsy. The <it<ApoE4</it< allele is a major contributing factor to early-onset neuronal degeneration in Alzheimer disease and other neurodegenerative diseases as well.</p< <p<Methods</p< <p<To clarify whether the ApoE4 phenotype predisposes to narcolepsy or associates with an earlier disease onset, we have genotyped the <it<ApoE</it< gene in 103 patients with narcolepsy and 101 healthy controls.</p< <p<Results</p< <p<The frequency of the E4 allele of the <it<ApoE</it< gene was 11% in the patient and 15% in the control groups. Furthermore, the mean age of onset did not differ between the ApoE4<sup<+</sup< and ApoE4<sup<-</sup< patient groups.</p< <p<Conclusion</p< <p<Our results exclude the <it<ApoE4</it< allele as a major risk factor for narcolepsy.</p<
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title_short	<it<ApoE</it< polymorphisms in narcolepsy
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