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Статті в журналах з теми "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Eestnes, Arnulf, and Svein Ivar Mellgren. "Familial amyotrophic lateral sclerosis." Acta Neurologica Scandinavica 61, no. 3 (January 29, 2009): 192–99. http://dx.doi.org/10.1111/j.1600-0404.1980.tb01482.x.
Повний текст джерелаBoylan, Kevin. "Familial Amyotrophic Lateral Sclerosis." Neurologic Clinics 33, no. 4 (November 2015): 807–30. http://dx.doi.org/10.1016/j.ncl.2015.07.001.
Повний текст джерелаHand, Collette K., and Guy A. Rouleau. "Familial amyotrophic lateral sclerosis." Muscle & Nerve 25, no. 2 (February 2002): 135–59. http://dx.doi.org/10.1002/mus.10001.
Повний текст джерелаMillichap, J. Gordon. "Juvenile Familial Amyotrophic Lateral Sclerosis." Pediatric Neurology Briefs 12, no. 7 (July 1, 1998): 56. http://dx.doi.org/10.15844/pedneurbriefs-12-7-15.
Повний текст джерелаSavinova, A. V., N. A. Shnayder, and R. F. Nasyrova. "Genetics of familial amyotrophic lateral sclerosis." Bulletin of Siberian Medicine 20, no. 3 (October 22, 2021): 193–202. http://dx.doi.org/10.20538/1682-0363-2021-3-193-202.
Повний текст джерелаFreischmidt, 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, no. 11 (September 5, 2014): 2938–50. http://dx.doi.org/10.1093/brain/awu249.
Повний текст джерелаBrenner, David, Kathrin Müller, Thomas Wieland, Patrick Weydt, Sarah Böhm, Dorothée Lulé, Annemarie Hübers, et al. "NEK1mutations in familial amyotrophic lateral sclerosis." Brain 139, no. 5 (March 5, 2016): e28-e28. http://dx.doi.org/10.1093/brain/aww033.
Повний текст джерелаValdmanis, P. N., and G. A. Rouleau. "Genetics of familial amyotrophic lateral sclerosis." Neurology 70, no. 2 (January 7, 2008): 144–52. http://dx.doi.org/10.1212/01.wnl.0000296811.19811.db.
Повний текст джерелаFang, Fang, Freya Kamel, Paul Lichtenstein, Rino Bellocco, Pär Sparén, Dale P. Sandler, and Weimin Ye. "Familial aggregation of amyotrophic lateral sclerosis." Annals of Neurology 66, no. 1 (July 2009): 94–99. http://dx.doi.org/10.1002/ana.21580.
Повний текст джерелаByrne, Susan, and Orla Hardiman. "Familial aggregation in amyotrophic lateral sclerosis." Annals of Neurology 67, no. 4 (October 2, 2009): 554. http://dx.doi.org/10.1002/ana.21883.
Повний текст джерелаДисертації з теми "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.
Повний текст джерелаAbalkhail, 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.
Повний текст джерелаGallart, 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.
Повний текст джерелаLa 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.
Повний текст джерелаIt 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.
Повний текст джерелаPramatarova, 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.
Повний текст джерелаSchaldecker, Christina [Verfasser]. "Metabolism in presymptomatic mutation carriers of familial Amyotrophic Lateral Sclerosis / Christina Schaldecker." Ulm : Universität Ulm, 2019. http://d-nb.info/1189734001/34.
Повний текст джерелаFujita, 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.
Повний текст джерелаWu, 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.
Повний текст джерелаWu, 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.
Повний текст джерелаКниги з теми "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Hiroshi, Mitsumoto, ed. Amyotrophic lateral sclerosis: A guide for patients and families. 3rd ed. New York, NY: Demos Health, 2009.
Знайти повний текст джерелаHiroshi, Mitsumoto, and Munsat Theodore L. 1930-, eds. Amyotrophic lateral sclerosis: A guide for patients and families. 2nd ed. New York: Demos, 2001.
Знайти повний текст джерелаMassachusetts. 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.
Знайти повний текст джерелаBrown, Robert H., Michael Swash, and Piera Pasinelli. Amyotrophic Lateral Sclerosis. 2nd ed. London: CRC Press, 2021. http://dx.doi.org/10.1201/9781003076445.
Повний текст джерелаCosi, V., Ann C. Kato, W. Parlette, P. Pinelli, and M. Poloni, eds. Amyotrophic Lateral Sclerosis. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5302-7.
Повний текст джерелаMD, Brown Robert H., Swash Michael, and Pasinelli Piera, eds. Amyotrophic lateral sclerosis. 2nd ed. Abingdon [England]: Informa Healthcare, 2006.
Знайти повний текст джерелаNational 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.
Знайти повний текст джерела1949-, Chad David A., and Pioro Erik P. 1955-, eds. Amyotrophic lateral sclerosis. Philadelphia: F.A. Davis, 1998.
Знайти повний текст джерелаHiroshi, Mitsumoto, Przedborski Serge, and Gordon Paul H, eds. Amyotrophic lateral sclerosis. Boca Raton: Taylor & Francis, 2006.
Знайти повний текст джерелаClifford, Rose F., ed. Amyotrophic lateral sclerosis. New York, N.Y: Demos, 1990.
Знайти повний текст джерелаЧастини книг з теми "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Siddique, T., D. Nijhawan, and A. Hentati. "Familial amyotrophic lateral sclerosis." In Advances in Research on Neurodegeneration, 219–33. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6844-8_23.
Повний текст джерелаBrockington, Alice, and Pamela J. Shaw. "Familial motor neuron diseases other than amyotrophic lateral sclerosis." In Amyotrophic Lateral Sclerosis, 141–86. 2nd ed. London: CRC Press, 2021. http://dx.doi.org/10.1201/9781003076445-11.
Повний текст джерелаMorita, M., and R. H. Brown, Jr. "Familial Amyotrophic Lateral Sclerosis: A Review." In Monographs in Clinical Neuroscience, 177–89. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000061621.
Повний текст джерелаNorris, F. H., D. Holden, K. Kandal, and E. Stanley. "Home Nursing Care by Families for Severely Paralyzed ALS Patients." In Amyotrophic Lateral Sclerosis, 231–38. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5302-7_35.
Повний текст джерелаGregoire, N., and G. Serratrice. "Atypical Forms of Familial Amyotrophic Lateral Sclerosis." In 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.
Повний текст джерелаWong, Philip C., David R. Borchelt, Michael K. Lee, Carlos A. Pardo, Gopal Thinakaran, Lee J. Martin, Sangram S. Sisodia, and Donald L. Price. "Familial Amyotrophic Lateral Sclerosis and Alzheimer’s Disease." In 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.
Повний текст джерелаWhitson, Lisa J., and P. John Hart. "Copper-Zinc Superoxide Dismutase and Familial Amyotrophic Lateral Sclerosis." In Neurodegenerative Diseases and Metal Ions, 179–205. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470028114.ch8.
Повний текст джерелаHart, P. John, and Joan Selverstone Valentine. "Metal-Deficient Copper-Zinc Superoxide Dismutase and Familial Amyotrophic Lateral Sclerosis." In ACS Symposium Series, 348–65. Washington, DC: American Chemical Society, 2005. http://dx.doi.org/10.1021/bk-2005-0903.ch019.
Повний текст джерелаWinkler, Duane D., Mercedes Prudencio, Celeste Karch, David R. Borchelt, and John Hart. "Copper-Zinc Superoxide Dismutase, Its Copper Chaperone, and Familial Amyotrophic Lateral Sclerosis." In Protein Misfolding Diseases, 381–401. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470572702.ch17.
Повний текст джерелаAzzouz, Mimoun, Nathalie Leclerc, Mark Gurney, Jean-Marie Warter, Philippe Poindron, and Jacques Borg. "Progressive Motor Neuron Impairment in an Animal Model of Familial Amyotrophic Lateral Sclerosis." In Neurochemistry, 485–90. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_81.
Повний текст джерелаТези доповідей конференцій з теми "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Youn, Clover, and Michael Weiss. "C9orf72-related Familial Amyotrophic Lateral Sclerosis Manifesting as Monomelic Amyotrophy of the Lower Extremity (P10-8.010)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000202042.
Повний текст джерелаMarzocchi, N., S. Severi, M. Pieri, C. Zona, and S. Cavalcanti. "Numerical simulation of motor neuron excitability in a transgenic mouse model of familial amyotrophic lateral sclerosis." In BIOMEDICINE 2005. Southampton, UK: WIT Press, 2005. http://dx.doi.org/10.2495/bio050221.
Повний текст джерелаWolmer, Paulo Schneider, Thiago Junqueira Ribeiro de Rezende, Fabrício Castro de Borba, and Marcondes Cavalcante França Junior. "Distinct patterns of cerebellar damage in sporadic and ATXN2- related amyotrophic lateral sclerosis." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.511.
Повний текст джерелаAthayde, Natália Merten, Wladimir Bocca Vieira de Rezende Pinto, Paulo Victor Sgobbi de Souza, Acary Souza Bulle Oliveira, and Alzira Alves de Siqueira Carvalho. "Expansion of the phenotype in ALS19." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.455.
Повний текст джерелаAlbuquerque Filho, José Marcos Vieira de, Natália Merten Athayde, Alzira Alves de Siqueira Carvalho, Igor Braga Farias, Roberta Ismael Lacerda Machado, and Marco Antônio Troccoli Chieia. "Familial ALS Type 25 – A Brazillian Case Serie." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.186.
Повний текст джерелаCambraia, 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, and Verônica Marques Zembrzuski. "A novel mutation in the RRM2 domain of TDP-43 in a Brazilian sporadic ALS patient." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.486.
Повний текст джерелаAndrade, Isabela Mascarenhas de, and Adriele Ribeiro França Viriato. "Prognostic factors related to mortality in motor neuron disease at an outpatient care center in Salvador (BA)." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.330.
Повний текст джерелаAquino, Letícia, Juliana Victor dos Santos, Jaqueline Donola Scandoleira, Jéssica Elen Gonçalves Nascimento, and Letícia Moraes de Aquino. "Telerehabilitation in Amyotrophic Lateral Sclerosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.528.
Повний текст джерелаBentley, Brenda, Moira O’Connor, and Lauren Breen. "Counselling People with Amyotrophic Lateral Sclerosis." In Annual Worldwide Nursing Conference (WNC 2017). Global Science & Technology Forum (GSTF), 2017. http://dx.doi.org/10.5176/2315-4330_wnc17.131.
Повний текст джерелаDash, Debadatta, Paul Ferrari, Angel Hernandez, Daragh Heitzman, Sara G. Austin, and Jun Wang. "Neural Speech Decoding for Amyotrophic Lateral Sclerosis." In Interspeech 2020. ISCA: ISCA, 2020. http://dx.doi.org/10.21437/interspeech.2020-3071.
Повний текст джерелаЗвіти організацій з теми "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"
Anklesaria, Pervin. Preclinical Development of Therapeutics for Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, October 2009. http://dx.doi.org/10.21236/ada541412.
Повний текст джерелаConnor, James R. Apo-Ferritin as a Therapeutic Treatment for Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada567828.
Повний текст джерелаPrzedborski, Serge. Neuroprotective Small Molecules for the Treatment of Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada567841.
Повний текст джерелаConnor, James R. Apo-Ferritin as a Therapeutic Treatment for Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada598852.
Повний текст джерелаGrill, Raymond J. Targeted Riluzole Delivery by Antioxidant Nanovectors for Treating Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613439.
Повний текст джерелаGrill, Raymond J. Targeted Riluzole Delivery by Antioxidant Nanovectors for Treating Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada598451.
Повний текст джерелаLoGrasso, Philip, and Serge Przedborski. c-jun-N-Terminal Kinase (JNK) for the Treatment of Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada596507.
Повний текст джерелаSantos, Ana Lúcia Yaeko da Silva, Deyse Mayara Rodrigues Caron, Livia Shirahige, and 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, May 2023. http://dx.doi.org/10.37766/inplasy2023.5.0078.
Повний текст джерелаWackerman, Brooke L., B. L. Cox, K. L. Grayson, Shari L. Shanklin, and 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, April 2005. http://dx.doi.org/10.21236/ada437518.
Повний текст джерелаZhu, Qiaochu, Jin Zhou, Hai Huang, Jie Han, Biwei Cao, Dandan Xu, Yan Zhao, and 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, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0118.
Повний текст джерела