Literatura académica sobre el tema "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
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Artículos de revistas sobre el tema "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Eestnes, Arnulf y Svein Ivar Mellgren. "Familial amyotrophic lateral sclerosis". Acta Neurologica Scandinavica 61, n.º 3 (29 de enero de 2009): 192–99. http://dx.doi.org/10.1111/j.1600-0404.1980.tb01482.x.
Texto completoBoylan, Kevin. "Familial Amyotrophic Lateral Sclerosis". Neurologic Clinics 33, n.º 4 (noviembre de 2015): 807–30. http://dx.doi.org/10.1016/j.ncl.2015.07.001.
Texto completoHand, Collette K. y Guy A. Rouleau. "Familial amyotrophic lateral sclerosis". Muscle & Nerve 25, n.º 2 (febrero de 2002): 135–59. http://dx.doi.org/10.1002/mus.10001.
Texto completoMillichap, J. Gordon. "Juvenile Familial Amyotrophic Lateral Sclerosis". Pediatric Neurology Briefs 12, n.º 7 (1 de julio de 1998): 56. http://dx.doi.org/10.15844/pedneurbriefs-12-7-15.
Texto completoSavinova, A. V., N. A. Shnayder y R. F. Nasyrova. "Genetics of familial amyotrophic lateral sclerosis". Bulletin of Siberian Medicine 20, n.º 3 (22 de octubre de 2021): 193–202. http://dx.doi.org/10.20538/1682-0363-2021-3-193-202.
Texto completoFreischmidt, Axel, Kathrin Müller, Lisa Zondler, Patrick Weydt, Alexander E. Volk, Anže Lošdorfer Božič, Michael Walter et al. "Serum microRNAs in patients with genetic amyotrophic lateral sclerosis and pre-manifest mutation carriers". Brain 137, n.º 11 (5 de septiembre de 2014): 2938–50. http://dx.doi.org/10.1093/brain/awu249.
Texto completoBrenner, David, Kathrin Müller, Thomas Wieland, Patrick Weydt, Sarah Böhm, Dorothée Lulé, Annemarie Hübers et al. "NEK1mutations in familial amyotrophic lateral sclerosis". Brain 139, n.º 5 (5 de marzo de 2016): e28-e28. http://dx.doi.org/10.1093/brain/aww033.
Texto completoValdmanis, P. N. y G. A. Rouleau. "Genetics of familial amyotrophic lateral sclerosis". Neurology 70, n.º 2 (7 de enero de 2008): 144–52. http://dx.doi.org/10.1212/01.wnl.0000296811.19811.db.
Texto completoFang, Fang, Freya Kamel, Paul Lichtenstein, Rino Bellocco, Pär Sparén, Dale P. Sandler y Weimin Ye. "Familial aggregation of amyotrophic lateral sclerosis". Annals of Neurology 66, n.º 1 (julio de 2009): 94–99. http://dx.doi.org/10.1002/ana.21580.
Texto completoByrne, Susan y Orla Hardiman. "Familial aggregation in amyotrophic lateral sclerosis". Annals of Neurology 67, n.º 4 (2 de octubre de 2009): 554. http://dx.doi.org/10.1002/ana.21883.
Texto completoTesis sobre el tema "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Gros-Louis, François. "Genetics of familial and sporadic amyotrophic lateral sclerosis". Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111859.
Texto completoAbalkhail, Halah Abdullah. "Characterisation of a new familial amyotrophic lateral sclerosis". Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419231.
Texto completoGallart, Palau Xavier Ramon. "Synaptic frailty and mitochondrial dysfunction in familial amyotrophic lateral sclerosis". Doctoral thesis, Universitat de Lleida, 2016. http://hdl.handle.net/10803/386410.
Texto completoLa Esclerosis Lateral Amiotrófica (ELA) es una enfermedad neurodegenerativa de la motoneurona. Todas las motoneuronas se ven afectadas desde la corteza motora primaria hasta la unión neuromuscular. En 1993 la descubierta de mutaciones en el gen SOD1 abrió nuevos límites experimentales con la creación de los primeros roedores transgénicos para esta enfermedad. Desde ese momento y hasta la actualidad, la mutación más estudiada en la ELA ha sido la mutación SOD1-G93A. Los modelos transgénicos de esta mutación han revelado mecanismos esenciales de la neurodegeneración en la ELA, incluyendo la excitotoxicidad, la disfunción proteica y la degeneración axosináptica entre otras. En este trabajo hemos explorado los cambios moleculares que tienen lugar en los terminales C, unos terminales altamente especializados de las α-motoneuronas, en un modelo murino de ELA con la mutación SOD1-G93A. Además, también hemos focalizado nuestra atención sobre la relación patológica que se establece en la ELA familiar (ELAF) entre la mutación SOD1-G93A y las mitocondrias. En relación a los terminales C durante la ELAF, hemos encontrado cambios asociados con la aparición de síntomas, como por ejemplo el incremento de la expresión del factor neurotrófico Neuregulina-1, localizado por primera vez en la cisterna subsináptica de los terminales C. La Neuregulina-1 en esas estructuras de retículo endoplasmático fue observada dentro de vesículas extracelulares (VEs), sugiriendo que el análisis de la Neuregulina-1 dentro de VEs en la ELA resulta especialmente prometedor como biomarcador potencial para esta enfermedad. Así, nosotros hemos desarrollado también un nuevo método para purificar VEs, dado que este es un paso esencial previo al estudio de las proteínas asociadas con estas estructuras. Nuestro método aplicado a la purificación de VEs de tejidos complejos fue capaz de facilitar la identificación de la Neuregulina en VEs provenientes de tejidos clínicos y fluidos biológicos. En relación a las implicaciones de la mitocondria en la ELA, hemos encontrado que la mutación SOD1-G93A estabiliza la proteína PINK1 en las mitocondrias activando el factor nuclear NFκB en neuronas. La interacción secuencial entre la SOD1 mutante y el NFκB crea una clara disfunción sobre la capacidad proteolítica del proteosoma, la cual a su vez promueve co-agregación de la SOD1 mutante y PINK1 en estas células. Estos resultados suman un sustancial conocimiento mecanístico sobre los roles de la mitocondria en eventos degenerativos clásicos de la ELA, como es la agregación de proteínas disfuncionales en motoneuronas. Siguiendo nuestro estudio de la afectación mitocondrial en la ELA, hemos creado y caracterizado un nuevo modelo de Drosophila que expresa la mutación humana SOD1-G93A en fibras musculares torácicas bajo el promotor 24B. Este modelo de Drosophila transgénica recapitula con éxito en fenotipo mitocondrial característico de la ELA presentando importantes ventajas para la elección de nuevos compuestos terapéuticos. En definitiva, los resultados generados en esta tesis proporcionan evidencia experimental, extensa comprensión molecular y insinúan nuevos horizontes terapéuticos acerca de los mecanismos moleculares y eventos neurodegenerativos asociados con la disfunción sináptica y la disfunción mitocondrial en la ELAF.
Amyotrophic Lateral Sclerosis (ALS) is an orphan age-associated neurodegenerative disease. All motoneurones in ALS are affected by degenerative flow from the primary motor cortex to the neuromuscular junction. In 1993, mutations of the gene SOD1 opened new research avenues allowing for the generation of familial ALS experimental models in rodents. Since then, the FALS mutation SOD1-G93A has been extensively studied worldwide in ALS to date. Transgenic models for this SOD1 mutation have revealed essential mechanisms of neurodegeneration including excitotoxicity, proteinopathy and axosynaptic degeneration among others. In this dissertation, we explored the molecular changes that occur in C-terminals, a very specialised synapse type from α-motoneurones of SOD1-G93A rodents. Also, we focused on the pathological relationship between the FALS mutant SOD1-G93A and mitochondria in motoneurones. With regard to C-terminals in FALS motoneurones, we found changes that were symptomatically associated with the up-regulated expression of the neurotrophic factor Neuregulin-1 located for the first time in the subsurface system of C-boutons juxtaposed to α-motoneurones. Furthermore, Neuregulin-1 in these endoplasmic reticulum structures was observed inside extracellular vesicles, suggesting that analysis of Neuregulin-1 from extracellular vesicles in ALS holds promise as a potential reliable biomarker for that neurodegenerative disease. We therefore have developed a new method for isolation of extracellular vesicles, as this remains as an essential step for the study of molecules associated with these structures. Our method applied to purify extracellular vesicles from complex biological tissues was able to facilitate the identification of Neuregulin-1 in extracellular vessicles from clinical tissues and biological fluids. Regarding implications of mitochondria in ALS, we have found that the FALS mutant hSOD1-G93A stabilises PINK1 in mitochondria and subsequently activates NFκB in neuronal cells. Sequential interaction between hSOD1 and NFκB impairs the proteosome proteolitic function promoting co-aggregation of SOD1 and PINK1 in these cells. These results add substantial mechanistic insight on the roles of mitochondria in classical ALS-associated neurodegenerative events, including aggregation of dysfuntional proteins in motoneurones. Following our study of mitochondria affectation in ALS, we have created and characterised a novel Drosophila model that expresses human SOD1-G93A in thoracic muscles under the genetic muscular promoter 24B. Flies expressing human SOD1-G93A in thoracic muscles successfully recapitulate FALS mitochondrial phenotype with several advantages in front of the current available rodent models for this FALS mutation. Taken together, the results generated in this thesis provide experimental evidence, further molecular comprehension and promise novel therapeutic approaches to the molecular mechanisms and neurodegenerative events associated with synaptic frailty and mitochondrial disfunction in FALS.
Pramatarova, Albéna. "Role of CuZn superoxide dismutase in familial amyotrophic lateral sclerosis". Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36684.
Texto completoIt has been hypothesized that the pathology observed in FALS cases with SOD1 mutations is due to a gain of a new deleterious function of the mutant enzyme and not to a simple loss of dismutase activity. However the exact mechanism of SOD1 toxicity is still unknown and the specificity of the degenerating cell populations remains to be addressed. In this work, we investigated whether the damage seen in ALS with SOD1 mutations results from direct motor neuron toxicity. We have generated transgenic animals carrying a human SOD1 cDNA with the G37R mutation associated with FALS, driven by the neurofilament light chain promoter in order to specifically express the mutant protein in neuronal tissues. We show that transgenic animals express high levels of the human SOD1 protein in neuronal tissues, especially in the spinal cord where the motor neurons are concentrated, but develop no apparent motor deficit at up to 2 years of age. Our animal model suggests that neuron specific expression of mutant human SOD1 might not be sufficient for the development of the disease in mice, and hints towards the involvement of additional yet unidentified cell types/mechanisms.
Forsberg, Karin. "Misfolded superoxide dismutase-1 in sporadic and familial Amyotrophic Lateral Sclerosis". Doctoral thesis, Umeå universitet, Patologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-47550.
Texto completoPramatarova, Albéna. "Role of Cu/Zn superoxide dismutase in familial amyotrophic lateral sclerosis". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0030/NQ64647.pdf.
Texto completoSchaldecker, Christina [Verfasser]. "Metabolism in presymptomatic mutation carriers of familial Amyotrophic Lateral Sclerosis / Christina Schaldecker". Ulm : Universität Ulm, 2019. http://d-nb.info/1189734001/34.
Texto completoFujita, Hibiki Kawamata. "Copper, zinc superoxide dismutase and mitochondria : implications for familial amyotrophic lateral sclerosis /". Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1619236681&sid=6&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Texto completoWu, Chi-Hong. "Functional Characterization of Novel PFN1 Mutations Causative for Familial Amyotrophic Lateral Sclerosis: A Dissertation". eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/815.
Texto completoWu, Chi-Hong. "Functional Characterization of Novel PFN1 Mutations Causative for Familial Amyotrophic Lateral Sclerosis: A Dissertation". eScholarship@UMMS, 2012. http://escholarship.umassmed.edu/gsbs_diss/815.
Texto completoLibros sobre el tema "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Hiroshi, Mitsumoto, ed. Amyotrophic lateral sclerosis: A guide for patients and families. 3a ed. New York, NY: Demos Health, 2009.
Buscar texto completoHiroshi, Mitsumoto y Munsat Theodore L. 1930-, eds. Amyotrophic lateral sclerosis: A guide for patients and families. 2a ed. New York: Demos, 2001.
Buscar texto completoMassachusetts. Bureau of Environmental Health. Environmental Epidemiology Program. The Amyotrophic Lateral Sclerosis (ALS) Disease Registry: Frequently asked questions for patients and families. Boston, Mass.]: Massachusetts Department of Public Health, Bureau of Environmental Health, Environmental Epidemiology Program, 2009.
Buscar texto completoBrown, Robert H., Michael Swash y Piera Pasinelli. Amyotrophic Lateral Sclerosis. 2a ed. London: CRC Press, 2021. http://dx.doi.org/10.1201/9781003076445.
Texto completoCosi, V., Ann C. Kato, W. Parlette, P. Pinelli y M. Poloni, eds. Amyotrophic Lateral Sclerosis. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5302-7.
Texto completoMD, Brown Robert H., Swash Michael y Pasinelli Piera, eds. Amyotrophic lateral sclerosis. 2a ed. Abingdon [England]: Informa Healthcare, 2006.
Buscar texto completoNational Institute of Neurological Disorders and Stroke (U.S.). Office of Communications and Public Liaison, ed. Amyotrophic lateral sclerosis. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 2000.
Buscar texto completo1949-, Chad David A. y Pioro Erik P. 1955-, eds. Amyotrophic lateral sclerosis. Philadelphia: F.A. Davis, 1998.
Buscar texto completoHiroshi, Mitsumoto, Przedborski Serge y Gordon Paul H, eds. Amyotrophic lateral sclerosis. Boca Raton: Taylor & Francis, 2006.
Buscar texto completoClifford, Rose F., ed. Amyotrophic lateral sclerosis. New York, N.Y: Demos, 1990.
Buscar texto completoCapítulos de libros sobre el tema "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Siddique, T., D. Nijhawan y A. Hentati. "Familial amyotrophic lateral sclerosis". En Advances in Research on Neurodegeneration, 219–33. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6844-8_23.
Texto completoBrockington, Alice y Pamela J. Shaw. "Familial motor neuron diseases other than amyotrophic lateral sclerosis". En Amyotrophic Lateral Sclerosis, 141–86. 2a ed. London: CRC Press, 2021. http://dx.doi.org/10.1201/9781003076445-11.
Texto completoMorita, M. y R. H. Brown, Jr. "Familial Amyotrophic Lateral Sclerosis: A Review". En Monographs in Clinical Neuroscience, 177–89. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000061621.
Texto completoNorris, F. H., D. Holden, K. Kandal y E. Stanley. "Home Nursing Care by Families for Severely Paralyzed ALS Patients". En Amyotrophic Lateral Sclerosis, 231–38. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5302-7_35.
Texto completoGregoire, N. y G. Serratrice. "Atypical Forms of Familial Amyotrophic Lateral Sclerosis". En Advances in Experimental Medicine and Biology, 159–64. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5302-7_27.
Texto completoWong, Philip C., David R. Borchelt, Michael K. Lee, Carlos A. Pardo, Gopal Thinakaran, Lee J. Martin, Sangram S. Sisodia y Donald L. Price. "Familial Amyotrophic Lateral Sclerosis and Alzheimer’s Disease". En Advances in Experimental Medicine and Biology, 145–59. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4869-0_9.
Texto completoWhitson, Lisa J. y P. John Hart. "Copper-Zinc Superoxide Dismutase and Familial Amyotrophic Lateral Sclerosis". En Neurodegenerative Diseases and Metal Ions, 179–205. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470028114.ch8.
Texto completoHart, P. John y Joan Selverstone Valentine. "Metal-Deficient Copper-Zinc Superoxide Dismutase and Familial Amyotrophic Lateral Sclerosis". En ACS Symposium Series, 348–65. Washington, DC: American Chemical Society, 2005. http://dx.doi.org/10.1021/bk-2005-0903.ch019.
Texto completoWinkler, Duane D., Mercedes Prudencio, Celeste Karch, David R. Borchelt y John Hart. "Copper-Zinc Superoxide Dismutase, Its Copper Chaperone, and Familial Amyotrophic Lateral Sclerosis". En Protein Misfolding Diseases, 381–401. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470572702.ch17.
Texto completoAzzouz, Mimoun, Nathalie Leclerc, Mark Gurney, Jean-Marie Warter, Philippe Poindron y Jacques Borg. "Progressive Motor Neuron Impairment in an Animal Model of Familial Amyotrophic Lateral Sclerosis". En Neurochemistry, 485–90. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_81.
Texto completoActas de conferencias sobre el tema "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Youn, Clover y Michael Weiss. "C9orf72-related Familial Amyotrophic Lateral Sclerosis Manifesting as Monomelic Amyotrophy of the Lower Extremity (P10-8.010)". En 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000202042.
Texto completoMarzocchi, N., S. Severi, M. Pieri, C. Zona y S. Cavalcanti. "Numerical simulation of motor neuron excitability in a transgenic mouse model of familial amyotrophic lateral sclerosis". En BIOMEDICINE 2005. Southampton, UK: WIT Press, 2005. http://dx.doi.org/10.2495/bio050221.
Texto completoWolmer, Paulo Schneider, Thiago Junqueira Ribeiro de Rezende, Fabrício Castro de Borba y Marcondes Cavalcante França Junior. "Distinct patterns of cerebellar damage in sporadic and ATXN2- related amyotrophic lateral sclerosis". En XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.511.
Texto completoAthayde, Natália Merten, Wladimir Bocca Vieira de Rezende Pinto, Paulo Victor Sgobbi de Souza, Acary Souza Bulle Oliveira y Alzira Alves de Siqueira Carvalho. "Expansion of the phenotype in ALS19". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.455.
Texto completoAlbuquerque Filho, José Marcos Vieira de, Natália Merten Athayde, Alzira Alves de Siqueira Carvalho, Igor Braga Farias, Roberta Ismael Lacerda Machado y Marco Antônio Troccoli Chieia. "Familial ALS Type 25 – A Brazillian Case Serie". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.186.
Texto completoCambraia, Amanda, Mario Campos Junior, Fernanda Gubert, Juliana Ferreira Vasques, Marli Pernes da Silva Loureiro, Claudio Heitor Gress, José Mauro Bráz de Lima, Rosalia Mendez Otero y Verônica Marques Zembrzuski. "A novel mutation in the RRM2 domain of TDP-43 in a Brazilian sporadic ALS patient." En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.486.
Texto completoAndrade, Isabela Mascarenhas de y Adriele Ribeiro França Viriato. "Prognostic factors related to mortality in motor neuron disease at an outpatient care center in Salvador (BA)". En XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.330.
Texto completoAquino, Letícia, Juliana Victor dos Santos, Jaqueline Donola Scandoleira, Jéssica Elen Gonçalves Nascimento y Letícia Moraes de Aquino. "Telerehabilitation in Amyotrophic Lateral Sclerosis". En XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.528.
Texto completoBentley, Brenda, Moira O’Connor y Lauren Breen. "Counselling People with Amyotrophic Lateral Sclerosis". En Annual Worldwide Nursing Conference (WNC 2017). Global Science & Technology Forum (GSTF), 2017. http://dx.doi.org/10.5176/2315-4330_wnc17.131.
Texto completoDash, Debadatta, Paul Ferrari, Angel Hernandez, Daragh Heitzman, Sara G. Austin y Jun Wang. "Neural Speech Decoding for Amyotrophic Lateral Sclerosis". En Interspeech 2020. ISCA: ISCA, 2020. http://dx.doi.org/10.21437/interspeech.2020-3071.
Texto completoInformes sobre el tema "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Anklesaria, Pervin. Preclinical Development of Therapeutics for Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, octubre de 2009. http://dx.doi.org/10.21236/ada541412.
Texto completoConnor, James R. Apo-Ferritin as a Therapeutic Treatment for Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 2012. http://dx.doi.org/10.21236/ada567828.
Texto completoPrzedborski, Serge. Neuroprotective Small Molecules for the Treatment of Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 2012. http://dx.doi.org/10.21236/ada567841.
Texto completoConnor, James R. Apo-Ferritin as a Therapeutic Treatment for Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, diciembre de 2013. http://dx.doi.org/10.21236/ada598852.
Texto completoGrill, Raymond J. Targeted Riluzole Delivery by Antioxidant Nanovectors for Treating Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, octubre de 2014. http://dx.doi.org/10.21236/ada613439.
Texto completoGrill, Raymond J. Targeted Riluzole Delivery by Antioxidant Nanovectors for Treating Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, octubre de 2013. http://dx.doi.org/10.21236/ada598451.
Texto completoLoGrasso, Philip y Serge Przedborski. c-jun-N-Terminal Kinase (JNK) for the Treatment of Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, octubre de 2013. http://dx.doi.org/10.21236/ada596507.
Texto completoSantos, Ana Lúcia Yaeko da Silva, Deyse Mayara Rodrigues Caron, Livia Shirahige y Abrahão Fontes Baptista. Alterations in Corticomotor Excitability in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, mayo de 2023. http://dx.doi.org/10.37766/inplasy2023.5.0078.
Texto completoWackerman, Brooke L., B. L. Cox, K. L. Grayson, Shari L. Shanklin y Wilson W. McGriff. Case Series Investigation of Amyotrophic Lateral Sclerosis (ALS) Among Former Kelly Air Force Base Workers. Fort Belvoir, VA: Defense Technical Information Center, abril de 2005. http://dx.doi.org/10.21236/ada437518.
Texto completoZhu, Qiaochu, Jin Zhou, Hai Huang, Jie Han, Biwei Cao, Dandan Xu, Yan Zhao y Gang Chen. Risk factors associated with amyotrophic lateral sclerosis: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, septiembre de 2022. http://dx.doi.org/10.37766/inplasy2022.9.0118.
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