The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse

The “slow Wallerian degeneration” (WldS) gene is neuroprotective in numerous models of axonal degeneration. Axonal degeneration is an early feature of disease progression in the SOD1G93A mouse, a widely used model of familial amyotrophic lateral sclerosis (fALS). We crossed the WldS mouse with the S...
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Autor*in:	Lindsey R. Fischer [verfasserIn] Deborah G. Culver [verfasserIn] Albert A. Davis [verfasserIn] Philip Tennant [verfasserIn] Minsheng Wang [verfasserIn] Michael Coleman [verfasserIn] Seneshaw Asress [verfasserIn] Robert Adalbert [verfasserIn] Guillermo M. Alexander [verfasserIn] Jonathan D. Glass [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2005

Schlagwörter:	Axonal degeneration Amyotrophic lateral sclerosis ALS SOD1 WldS Wallerian degeneration

Übergeordnetes Werk:	In: Neurobiology of Disease - Elsevier, 2021, 19(2005), 1, Seite 293-300
Übergeordnetes Werk:	volume:19 ; year:2005 ; number:1 ; pages:293-300

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.nbd.2005.01.008

Katalog-ID:	DOAJ057401365

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spelling	10.1016/j.nbd.2005.01.008 doi (DE-627)DOAJ057401365 (DE-599)DOAJ13be9544346a497092844024b6a267f8 DE-627 ger DE-627 rakwb eng RC321-571 Lindsey R. Fischer verfasserin aut The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The “slow Wallerian degeneration” (WldS) gene is neuroprotective in numerous models of axonal degeneration. Axonal degeneration is an early feature of disease progression in the SOD1G93A mouse, a widely used model of familial amyotrophic lateral sclerosis (fALS). We crossed the WldS mouse with the SOD1G93A mouse to investigate whether the WldS gene could prolong survival and modify neuropathology in these mice. SOD/WldS mice showed levels of motor axon loss similar to that seen in SOD1G93A mice. The presence of the WldS gene, however, modestly prolonged survival and delayed denervation at the neuromuscular junction. Prolonged survival was more prominent in female mice and did not depend on whether animals were heterozygous or homozygous for the WldS gene. We also report that SOD1G93A mice show significant degeneration of sensory axons during the course of disease, supporting previous data from humans demonstrating that ALS is not purely a motor disorder. Axonal degeneration Amyotrophic lateral sclerosis ALS SOD1 WldS Wallerian degeneration Neurosciences. Biological psychiatry. Neuropsychiatry Deborah G. Culver verfasserin aut Albert A. Davis verfasserin aut Philip Tennant verfasserin aut Minsheng Wang verfasserin aut Michael Coleman verfasserin aut Seneshaw Asress verfasserin aut Robert Adalbert verfasserin aut Guillermo M. Alexander verfasserin aut Jonathan D. Glass verfasserin aut In Neurobiology of Disease Elsevier, 2021 19(2005), 1, Seite 293-300 (DE-627)268125414 (DE-600)1471408-5 1095953X nnns volume:19 year:2005 number:1 pages:293-300 https://doi.org/10.1016/j.nbd.2005.01.008 kostenfrei https://doaj.org/article/13be9544346a497092844024b6a267f8 kostenfrei http://www.sciencedirect.com/science/article/pii/S0969996105000227 kostenfrei https://doaj.org/toc/1095-953X 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_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_165 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4700 AR 19 2005 1 293-300
allfields_unstemmed	10.1016/j.nbd.2005.01.008 doi (DE-627)DOAJ057401365 (DE-599)DOAJ13be9544346a497092844024b6a267f8 DE-627 ger DE-627 rakwb eng RC321-571 Lindsey R. Fischer verfasserin aut The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The “slow Wallerian degeneration” (WldS) gene is neuroprotective in numerous models of axonal degeneration. Axonal degeneration is an early feature of disease progression in the SOD1G93A mouse, a widely used model of familial amyotrophic lateral sclerosis (fALS). We crossed the WldS mouse with the SOD1G93A mouse to investigate whether the WldS gene could prolong survival and modify neuropathology in these mice. SOD/WldS mice showed levels of motor axon loss similar to that seen in SOD1G93A mice. The presence of the WldS gene, however, modestly prolonged survival and delayed denervation at the neuromuscular junction. Prolonged survival was more prominent in female mice and did not depend on whether animals were heterozygous or homozygous for the WldS gene. We also report that SOD1G93A mice show significant degeneration of sensory axons during the course of disease, supporting previous data from humans demonstrating that ALS is not purely a motor disorder. Axonal degeneration Amyotrophic lateral sclerosis ALS SOD1 WldS Wallerian degeneration Neurosciences. Biological psychiatry. Neuropsychiatry Deborah G. Culver verfasserin aut Albert A. Davis verfasserin aut Philip Tennant verfasserin aut Minsheng Wang verfasserin aut Michael Coleman verfasserin aut Seneshaw Asress verfasserin aut Robert Adalbert verfasserin aut Guillermo M. Alexander verfasserin aut Jonathan D. Glass verfasserin aut In Neurobiology of Disease Elsevier, 2021 19(2005), 1, Seite 293-300 (DE-627)268125414 (DE-600)1471408-5 1095953X nnns volume:19 year:2005 number:1 pages:293-300 https://doi.org/10.1016/j.nbd.2005.01.008 kostenfrei https://doaj.org/article/13be9544346a497092844024b6a267f8 kostenfrei http://www.sciencedirect.com/science/article/pii/S0969996105000227 kostenfrei https://doaj.org/toc/1095-953X 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_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_165 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4700 AR 19 2005 1 293-300
allfieldsGer	10.1016/j.nbd.2005.01.008 doi (DE-627)DOAJ057401365 (DE-599)DOAJ13be9544346a497092844024b6a267f8 DE-627 ger DE-627 rakwb eng RC321-571 Lindsey R. Fischer verfasserin aut The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The “slow Wallerian degeneration” (WldS) gene is neuroprotective in numerous models of axonal degeneration. Axonal degeneration is an early feature of disease progression in the SOD1G93A mouse, a widely used model of familial amyotrophic lateral sclerosis (fALS). We crossed the WldS mouse with the SOD1G93A mouse to investigate whether the WldS gene could prolong survival and modify neuropathology in these mice. SOD/WldS mice showed levels of motor axon loss similar to that seen in SOD1G93A mice. The presence of the WldS gene, however, modestly prolonged survival and delayed denervation at the neuromuscular junction. Prolonged survival was more prominent in female mice and did not depend on whether animals were heterozygous or homozygous for the WldS gene. We also report that SOD1G93A mice show significant degeneration of sensory axons during the course of disease, supporting previous data from humans demonstrating that ALS is not purely a motor disorder. Axonal degeneration Amyotrophic lateral sclerosis ALS SOD1 WldS Wallerian degeneration Neurosciences. Biological psychiatry. Neuropsychiatry Deborah G. Culver verfasserin aut Albert A. Davis verfasserin aut Philip Tennant verfasserin aut Minsheng Wang verfasserin aut Michael Coleman verfasserin aut Seneshaw Asress verfasserin aut Robert Adalbert verfasserin aut Guillermo M. Alexander verfasserin aut Jonathan D. Glass verfasserin aut In Neurobiology of Disease Elsevier, 2021 19(2005), 1, Seite 293-300 (DE-627)268125414 (DE-600)1471408-5 1095953X nnns volume:19 year:2005 number:1 pages:293-300 https://doi.org/10.1016/j.nbd.2005.01.008 kostenfrei https://doaj.org/article/13be9544346a497092844024b6a267f8 kostenfrei http://www.sciencedirect.com/science/article/pii/S0969996105000227 kostenfrei https://doaj.org/toc/1095-953X 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_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_165 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4700 AR 19 2005 1 293-300
allfieldsSound	10.1016/j.nbd.2005.01.008 doi (DE-627)DOAJ057401365 (DE-599)DOAJ13be9544346a497092844024b6a267f8 DE-627 ger DE-627 rakwb eng RC321-571 Lindsey R. Fischer verfasserin aut The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The “slow Wallerian degeneration” (WldS) gene is neuroprotective in numerous models of axonal degeneration. Axonal degeneration is an early feature of disease progression in the SOD1G93A mouse, a widely used model of familial amyotrophic lateral sclerosis (fALS). We crossed the WldS mouse with the SOD1G93A mouse to investigate whether the WldS gene could prolong survival and modify neuropathology in these mice. SOD/WldS mice showed levels of motor axon loss similar to that seen in SOD1G93A mice. The presence of the WldS gene, however, modestly prolonged survival and delayed denervation at the neuromuscular junction. Prolonged survival was more prominent in female mice and did not depend on whether animals were heterozygous or homozygous for the WldS gene. We also report that SOD1G93A mice show significant degeneration of sensory axons during the course of disease, supporting previous data from humans demonstrating that ALS is not purely a motor disorder. Axonal degeneration Amyotrophic lateral sclerosis ALS SOD1 WldS Wallerian degeneration Neurosciences. Biological psychiatry. Neuropsychiatry Deborah G. Culver verfasserin aut Albert A. Davis verfasserin aut Philip Tennant verfasserin aut Minsheng Wang verfasserin aut Michael Coleman verfasserin aut Seneshaw Asress verfasserin aut Robert Adalbert verfasserin aut Guillermo M. Alexander verfasserin aut Jonathan D. Glass verfasserin aut In Neurobiology of Disease Elsevier, 2021 19(2005), 1, Seite 293-300 (DE-627)268125414 (DE-600)1471408-5 1095953X nnns volume:19 year:2005 number:1 pages:293-300 https://doi.org/10.1016/j.nbd.2005.01.008 kostenfrei https://doaj.org/article/13be9544346a497092844024b6a267f8 kostenfrei http://www.sciencedirect.com/science/article/pii/S0969996105000227 kostenfrei https://doaj.org/toc/1095-953X 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_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_165 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4700 AR 19 2005 1 293-300
language	English
source	In Neurobiology of Disease 19(2005), 1, Seite 293-300 volume:19 year:2005 number:1 pages:293-300
sourceStr	In Neurobiology of Disease 19(2005), 1, Seite 293-300 volume:19 year:2005 number:1 pages:293-300
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Axonal degeneration Amyotrophic lateral sclerosis ALS SOD1 WldS Wallerian degeneration Neurosciences. Biological psychiatry. Neuropsychiatry
isfreeaccess_bool	true
container_title	Neurobiology of Disease
authorswithroles_txt_mv	Lindsey R. Fischer @@aut@@ Deborah G. Culver @@aut@@ Albert A. Davis @@aut@@ Philip Tennant @@aut@@ Minsheng Wang @@aut@@ Michael Coleman @@aut@@ Seneshaw Asress @@aut@@ Robert Adalbert @@aut@@ Guillermo M. Alexander @@aut@@ Jonathan D. Glass @@aut@@
publishDateDaySort_date	2005-01-01T00:00:00Z
hierarchy_top_id	268125414
id	DOAJ057401365
language_de	englisch
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callnumber-first	R - Medicine
author	Lindsey R. Fischer
spellingShingle	Lindsey R. Fischer misc RC321-571 misc Axonal degeneration misc Amyotrophic lateral sclerosis misc ALS misc SOD1 misc WldS misc Wallerian degeneration misc Neurosciences. Biological psychiatry. Neuropsychiatry The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse
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topic_title	RC321-571 The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse Axonal degeneration Amyotrophic lateral sclerosis ALS SOD1 WldS Wallerian degeneration
topic	misc RC321-571 misc Axonal degeneration misc Amyotrophic lateral sclerosis misc ALS misc SOD1 misc WldS misc Wallerian degeneration misc Neurosciences. Biological psychiatry. Neuropsychiatry
topic_unstemmed	misc RC321-571 misc Axonal degeneration misc Amyotrophic lateral sclerosis misc ALS misc SOD1 misc WldS misc Wallerian degeneration misc Neurosciences. Biological psychiatry. Neuropsychiatry
topic_browse	misc RC321-571 misc Axonal degeneration misc Amyotrophic lateral sclerosis misc ALS misc SOD1 misc WldS misc Wallerian degeneration misc Neurosciences. Biological psychiatry. Neuropsychiatry
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title	The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse
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title_full	The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse
author_sort	Lindsey R. Fischer
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author_browse	Lindsey R. Fischer Deborah G. Culver Albert A. Davis Philip Tennant Minsheng Wang Michael Coleman Seneshaw Asress Robert Adalbert Guillermo M. Alexander Jonathan D. Glass
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title_sort	wlds gene modestly prolongs survival in the sod1g93a fals mouse
callnumber	RC321-571
title_auth	The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse
abstract	The “slow Wallerian degeneration” (WldS) gene is neuroprotective in numerous models of axonal degeneration. Axonal degeneration is an early feature of disease progression in the SOD1G93A mouse, a widely used model of familial amyotrophic lateral sclerosis (fALS). We crossed the WldS mouse with the SOD1G93A mouse to investigate whether the WldS gene could prolong survival and modify neuropathology in these mice. SOD/WldS mice showed levels of motor axon loss similar to that seen in SOD1G93A mice. The presence of the WldS gene, however, modestly prolonged survival and delayed denervation at the neuromuscular junction. Prolonged survival was more prominent in female mice and did not depend on whether animals were heterozygous or homozygous for the WldS gene. We also report that SOD1G93A mice show significant degeneration of sensory axons during the course of disease, supporting previous data from humans demonstrating that ALS is not purely a motor disorder.
abstractGer	The “slow Wallerian degeneration” (WldS) gene is neuroprotective in numerous models of axonal degeneration. Axonal degeneration is an early feature of disease progression in the SOD1G93A mouse, a widely used model of familial amyotrophic lateral sclerosis (fALS). We crossed the WldS mouse with the SOD1G93A mouse to investigate whether the WldS gene could prolong survival and modify neuropathology in these mice. SOD/WldS mice showed levels of motor axon loss similar to that seen in SOD1G93A mice. The presence of the WldS gene, however, modestly prolonged survival and delayed denervation at the neuromuscular junction. Prolonged survival was more prominent in female mice and did not depend on whether animals were heterozygous or homozygous for the WldS gene. We also report that SOD1G93A mice show significant degeneration of sensory axons during the course of disease, supporting previous data from humans demonstrating that ALS is not purely a motor disorder.
abstract_unstemmed	The “slow Wallerian degeneration” (WldS) gene is neuroprotective in numerous models of axonal degeneration. Axonal degeneration is an early feature of disease progression in the SOD1G93A mouse, a widely used model of familial amyotrophic lateral sclerosis (fALS). We crossed the WldS mouse with the SOD1G93A mouse to investigate whether the WldS gene could prolong survival and modify neuropathology in these mice. SOD/WldS mice showed levels of motor axon loss similar to that seen in SOD1G93A mice. The presence of the WldS gene, however, modestly prolonged survival and delayed denervation at the neuromuscular junction. Prolonged survival was more prominent in female mice and did not depend on whether animals were heterozygous or homozygous for the WldS gene. We also report that SOD1G93A mice show significant degeneration of sensory axons during the course of disease, supporting previous data from humans demonstrating that ALS is not purely a motor disorder.
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title_short	The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse
url	https://doi.org/10.1016/j.nbd.2005.01.008 https://doaj.org/article/13be9544346a497092844024b6a267f8 http://www.sciencedirect.com/science/article/pii/S0969996105000227 https://doaj.org/toc/1095-953X
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The WldS gene modestly prolongs survival in the SOD1G93A fALS mouse

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