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Relevant bibliographies by topics / Amyotrophic lateral sclerosis

Academic literature on the topic 'Amyotrophic lateral sclerosis'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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Journal articles on the topic "Amyotrophic lateral sclerosis"

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Nakayama, Yui, Satoru Morimoto, Misao Yoneda, Shigeki Kuzuhara, and Yasumasa Kokubo. "Cerebrospinal Fluid Biomarkers for Kii Amyotrophic Lateral Sclerosis/Parkinsonism-Dementia Complex." Journal of Neurodegenerative Diseases 2013 (March 27, 2013): 1–4. http://dx.doi.org/10.1155/2013/679089.

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Objective. Amyotrophic lateral sclerosis/parkinsonism-dementia complex is classified as one of the tauopathies. Methods. The total tau, phosphorylated tau, and amyloid β42 levels were assayed in cerebrospinal fluid from patients with Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex (), Alzheimer’s disease (), Parkinson’s disease (), amyotrophic lateral sclerosis (), and controls () using specific enzyme-linked immunosorbent assay methods. Results. Total tau and phosphorylated tau did not increase and amyloid β42 was relatively reduced in Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex. Relatively reduced amyloid β42 might discriminate Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex from amyotrophic lateral sclerosis and Parkinson’s disease, and the ratios of phosphorylated-tau to amyloid β42 could discriminate Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex from Alzheimer’s disease. Conclusions. Cerebrospinal fluid analysis may be useful to differentiate amyotrophic lateral sclerosis/parkinsonism-dementia complex from Alzheimer’s disease, amyotrophic lateral sclerosis, and Parkinson’s disease.

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Vlčková, Eva. "Amyotrophic lateral sclerosis." Neurologie pro praxi 17, no. 6 (December 1, 2016): 362–65. http://dx.doi.org/10.36290/neu.2016.076.

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Festoff, Barry W. "Amyotrophic Lateral Sclerosis." Drugs 51, no. 1 (January 1996): 28–44. http://dx.doi.org/10.2165/00003495-199651010-00004.

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Gulecha, VS, MS Mahajan, RA Khandare, HH Gangurde, Aman Upaganlawar, and CD Upasani. "Amyotrophic lateral sclerosis." Annals of Nigerian Medicine 4, no. 2 (2010): 45. http://dx.doi.org/10.4103/0331-3131.78270.

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Dib, Michel. "Amyotrophic Lateral Sclerosis." Drugs 63, no. 3 (2003): 289–310. http://dx.doi.org/10.2165/00003495-200363030-00004.

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Gordon, Paul H. "Amyotrophic Lateral Sclerosis." CNS Drugs 25, no. 1 (January 2011): 1–15. http://dx.doi.org/10.2165/11586000-000000000-00000.

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Askmark, Håkan, and Sten-Magnus Aquilonius. "Amyotrophic Lateral Sclerosis." CNS Drugs 2, no. 2 (August 1994): 102–9. http://dx.doi.org/10.2165/00023210-199402020-00003.

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Brown, Robert H., and Ammar Al-Chalabi. "Amyotrophic Lateral Sclerosis." New England Journal of Medicine 377, no. 2 (July 13, 2017): 162–72. http://dx.doi.org/10.1056/nejmra1603471.

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Rowland, Lewis P., and Neil A. Shneider. "Amyotrophic Lateral Sclerosis." New England Journal of Medicine 344, no. 22 (May 31, 2001): 1688–700. http://dx.doi.org/10.1056/nejm200105313442207.

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Beebe, Winona K., and Kathy Gomez. "Amyotrophic Lateral Sclerosis." Home Healthcare Nurse: The Journal for the Home Care and Hospice Professional 3, no. 3 (May 1985): 8–17. http://dx.doi.org/10.1097/00004045-198505000-00003.

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Dissertations / Theses on the topic "Amyotrophic lateral sclerosis"

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Flowers, Joanna Mary. "Molecular studies in amyotrophic lateral sclerosis." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397027.

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Schymick, Jennifer. "The genetics of amyotrophic lateral sclerosis." Thesis, University of Oxford, 2009. http://ora.ox.ac.uk/objects/uuid:f68f15c2-2875-46ba-bf25-8324c1dead91.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterised clinically by rapidly progressive paralysis leading ultimately to death from respiratory failure. There is no cure for ALS and no definitive explanation for the onset and rapid progression of motor neuron degeneration. Genetics is a known risk factor for a portion of familial cases. However, the role of genetics in the commoner sporadic form of the disease is poorly understood, although numerous genes have been implicated. The primary aim of this thesis project is to uncover the genetic causes that underlie ALS. To accomplish this goal, the main focus of this thesis is to perform genome-wide association analysis of sporadic ALS using high density SNP arrays. This thesis describes the first and the largest genome-wide association studies of ALS to date. Results demonstrate that there is no single large effect susceptibility variant underlying a large proportion of ALS, such as ApoE in Alzheimer’s disease. However, the genotyping data has been made publically available and the digital nature of this data means that it is a resource that can grow with future studies. Beyond genome-wide association, this thesis describes work using linkage, haplotype and sequence analysis to investigate the genetic overlap between ALS and frontotemporal dementia. Lastly, this thesis presents a novel method for linkage analysis using high throughput SNP arrays. Ultimately, it is hoped that by uncovering the genes that cause ALS, such knowledge will shed light on the pathogenic mechanisms underlying motor neuron degeneration and potentially lead to new rational therapies effective in slowing or even halting disease progression.

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Tjust, Anton. "Extraocular Muscles in Amyotrophic Lateral Sclerosis." Doctoral thesis, Umeå universitet, Anatomi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-129638.

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Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease of motor neurons characterized by muscle paralysis and death within 3-5 years of onset. However, due to unknown mechanisms, the extraocular muscles (EOMs) remain remarkably unaffected. The EOMs are highly specialized muscles that differ from other muscles in many respects, including innervation and satellite cells (SCs). Understanding whether these factors play a role in the relative sparing of EOMs in ALS could provide useful clues on how to slow down the progression of ALS in other muscles. The EOMs and limb muscles from terminal ALS patients and age-matched controls as well as the commonly used SOD1G93A ALS mouse model were studied with immunofluorescence. Antibodies against neurofilament and synaptophysin were used to identify nerves and neuromuscular junctions (NMJs); against Pax7, NCAM, MyoD, myogenin, Ki-67, dystrophin and laminin, to identify SCs and their progeny in EOMs and limb muscles. The proportion and fiber size of myofibers containing myosin heavy chain (MyHC) slow tonic and MyHC slow twitch were also determined in human EOMs. The abundance of SCs differed extensively along the length of control human EOMs, being twice as abundant in the anterior portion. Pax7-positive cells were also detected in non-traditional SC positions. EOMs from terminal ALS patients showed similar numbers of resting and activated SCs as the controls. In limb muscles of ALS patients, the number of resting and activated SCs ranged from low (similar to normal aged, sedentary individuals) to high numbers, especially in muscles with long duration of disease and varied between the upper and lower limbs. The EOMs maintained a high degree of innervation compared to hindlimb muscles of symptomatic SOD1G93A mice. MyHC slow tonic fibers were less abundant in ALS patients than in controls. The change seemed more pronounced in bulbar onset patients, and in this group of subjects only, there was a strong association between decline in MyHC slow tonic fibers and age of death. Notably, the decline in MyHC slow tonic fibers was unrelated to disease duration. Our data suggested that SCs play a minor role in the progression of ALS in general and in the sparing of the EOMs in particular. The generally preserved innervation in the EOMs of G93A mice may reflect distinct intrinsic properties relevant for sparing of the oculomotor system. Even though the EOMs are relatively spared in ALS, MyHC slow tonic myofibers were selectively affected and this may reflect differences in innervation, as these fibers are multiply innervated.
Amyotrofisk lateralskleros (ALS) är en obotlig neurodegenerativ sjukdom som främst påverkar kroppens viljestyrda motoriska nervceller. ALS leder till förlamning, muskelförtvining och slutligen döden genom andningssvikt, vanligen inom tre till fem år efter sjukdomsdebuten. Av okända anledningar så bibehålls ögonmusklernas funktion mycket bättre vid ALS i jämförelse med andra muskler och är hos merparten av patienter i stort sett opåverkade. Ögonmusklerna är mycket specialiserade muskler som skiljer sig från andra muskler i kroppen på flera sätt, bland annat genom deras unika nervförsörjning och genom de satellitceller – muskelspecifika stamceller, som finns i dem. En ökad förståelse för hur dessa faktorer inverkar på ögonmusklernas motståndskraft vid ALS skulle kunna ge värdefulla ledtrådar till hur man skulle kunna sakta ned sjukdomens fortskridande i andra muskler vid ALS. Ögonmuskler och extremitetsmuskler från avlidna ALS-patienter och åldersmatchade friska kontroller, tillsammans med transgena möss med den sjukdomsalstrande mutationen SOD1G93A, studerades genom immunfluorescens och efterföljande mikroskopering. Antikroppar mot molekylerna Pax7, NCAM, MyoD, myogenin, Ki-67, laminin och dystrofin användes för att identifiera satellitceller och deras dotterceller i ögonmuskler och extremitetsmuskler. Antikroppar mot neurofilament och synaptofysin användes för att identifiera nerver och neuromuskulära synapser hos transgena SOD1-möss. Antikroppar mot toniska (tonic) och ryckande (twitch) muskelmyosinkedjor användes för att bestämma proportionen av och storleken på dessa typer av muskelfibrer i ögonmuskler från avlidna ALS-patienter och friska kontroller. Mängden satellitceller varierade mellan de främre och de mer bakre delarna i friska, humana ögonmuskler och var dubbelt så många i den främre delen av muskeln jämfört med den mellersta och bakre delen av muskeln. Celler som uttryckte satellitcellsmarkören Pax7 hittades även i icke-traditionella satellitcellspositioner i ögonmusklerna. Mängden satellitceller i ögonmusklerna från ALS-patienter var samma som hos friska kontroller. I extremitetsmusklerna hos ALS-patienter varierade mängden satellitceller mellan låga nivåer (liknande de hos friska åldrade, inaktiva individer) till höga nivåer, särskilt i muskler där sjukdomen fortskridit under lång tid. Dessutom varierade mängden satellitceller mellan övre och nedre extremiteter. Hos symptomatiska SOD1G93A-möss hade ögonmusklerna en mycket välbevarad innervation jämfört med bakbensmusklerna, där många neuromuskulära synapser saknade kontakt mellan nerven och motorändplattan. Proportionen muskelfibrer med toniska muskelmyosinkedjor var lägre hos ALS-patienter jämfört med friska kontroller. Denna minskning var tydligare hos patienter där sjukdomssymtomen hade debuterat i tugg- och ansiktsmuskulaturen – så kallad bulbär ALS. Dessutom fanns det i den här gruppen, men ingen annan studerad grupp, en stark korrelation mellan nedgången i toniska fibrer och patientens ålder. Värt att notera är att minskningen av toniska muskelfibrer saknade korrelation med hur länge patienten hade varit sjuk i ALS. Den generellt välbevarade innervationen i ögonmusklerna hos SOD1G93A-möss kan spegla distinkta inneboende egenskaper hos ögonmusklerna som är av vikt för bevarandet av ögonrörligheten vid ALS. Gällande satellitceller så antyder våra data att satellitceller och deras regenerativa kapacitet spelar en försumbar roll vid ALS i allmänhet och vid ögonmusklernas bevarande i synnerhet. Slutligen, även om ögonmuskler generellt är välbevarade vid ALS så är toniska muskelfibrer märkbart påverkade och detta kan spegla skillnader mellan olika nervcellsgruppers känslighet vid ALS.

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Valbuena, Gabriel. "Metabolomic studies of amyotrophic lateral sclerosis." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/49719.

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Amyotrophic Lateral Sclerosis (ALS) is a relentlessly progressive neurodegenerative disease, and is fatal within 3-5 years of onset. Metabolic dysfunctions have consistently been identified in ALS, although its role in pathogenesis remains unclear. In this thesis, I apply a metabolomic approach using 1H NMR spectroscopy and Gas Chromatography-Mass Spectrometry in a range of disease models of increasing biological complexity, as well as patient tissues, in order to reveal perturbations to the metabolic network that may impact the course of the disease. I examined alterations to metabolism in the motor neuron-like NSC-34 cell line, and found that mutant SOD1 led to increased glycolysis to divert glucose from oxidative metabolism, and a broad intracellular amino acid depletion. The contribution of non-cell autonomous processes were also investigated in an astrocyte-motor neuron co-culture model, where mutant SOD1 produced varying perturbations to glycolysis and oxidative stress responses in each cell type, together with decreased branched-chain amino acid catabolism and glutamine-glutamate production that may indicate impaired neurotransmitter recycling. I also found different metabolic responses to mutant SOD1 in two strains with varying rates of disease progression, suggesting a role for early metabolic responses to mutant SOD1 in affecting the course of disease. In addition, I identify a metabolic signature for C9ORF72 ALS in cerebellum tissue, providing evidence that the hexanucleotide repeat expansion leads to distinctive metabolic changes in the CNS. Overall, I demonstrate the applicability of metabolomics in ALS research, particularly in revealing hidden metabolic subtypes of the disease. This opens opportunities to improve our understanding of the processes leading to motor neuron death in ALS, and highlights the potential use of metabolomics as a tool to develop therapies targeted to the individual metabolic responses of individuals susceptible to ALS.

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Seals, Ryan M. "Risk Factors for Amyotrophic Lateral Sclerosis." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:23205175.

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Amyotrophic lateral sclerosis (ALS) is a progressive debilitating disease of the upper and lower motor neurons. Median survival of ALS patients is consistently estimated at between 2-3 years from symptom onset, with some evidence that survival is increasing due to improved care. There are few well-established risk factors for ALS, and there is conflicting evidence regarding the trends in ALS incidence and mortality over the past several decades. In Chapter I we investigate the trends in ALS incidence and mortality in Denmark between 1970 and 2009. We employed age-period-cohort models to model both the incidence and mortality rates of ALS over time for the first time. We found a significant rise in ALS incidence and mortality over several decades, and we observed evidence for a birth cohort component to the rise in ALS, which is consistent with an environmental cause of ALS. In Chapter II we investigate the role of physical trauma – both head and other – in the development of ALS. We employed the Danish registries and linked health data from the hospital system to prior diagnoses for physical trauma. We found a borderline significant association between physical trauma and ALS, which grew stronger upon restricting to physical traumas before the age of 55. Chapter III concerns the risk of ALS in those employed by the military in Denmark. We linked occupational records from the Danish Pension Fund to health records of the hospital system. We found a significantly elevated rate of ALS among those who had been previously employed by the military, with the highest rates in the decade immediately following cessation of employment. These analyses strengthen the knowledge base for the epidemiology of ALS, and suggest future avenues of research to further understand the etiology of the disease.

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Fang, Fang. "Epidemiologic studies of amyotrophic lateral sclerosis." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-671-2/.

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Johnston, Pamela. "Echovirus aetiology in amyotrophic lateral sclerosis." Thesis, Glasgow Caledonian University, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.688246.

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McHenry, Kristen L. "Respiratory Compromise in Amyotrophic Lateral Sclerosis." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/2539.

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Jonsson, P. Andreas. "Superoxide dismutase 1 and amyotrophic lateral sclerosis." Doctoral thesis, Umeå : Medical Biosciences, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-611.

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Enayat, Zinat Ellaheh. "Superoxide dismutase mutations and amyotrophic lateral sclerosis." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400500.

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Books on the topic "Amyotrophic lateral sclerosis"

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Brown, Robert H., Michael Swash, and Piera Pasinelli. Amyotrophic Lateral Sclerosis. 2nd ed. London: CRC Press, 2021. http://dx.doi.org/10.1201/9781003076445.

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Cosi, 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.

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MD, Brown Robert H., Swash Michael, and Pasinelli Piera, eds. Amyotrophic lateral sclerosis. 2nd ed. Abingdon [England]: Informa Healthcare, 2006.

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1947-, Brown Robert H., Meininger Vincent, and Swash Michael, eds. Amyotrophic lateral sclerosis. London: Martin Dunitz, 2000.

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National 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.

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1949-, Chad David A., and Pioro Erik P. 1955-, eds. Amyotrophic lateral sclerosis. Philadelphia: F.A. Davis, 1998.

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Clifford, Rose F., ed. Amyotrophic lateral sclerosis. New York, N.Y: Demos, 1990.

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1952-, Brown Robert H., Meininger Vincent, and Swash Michael, eds. Amyotrophic lateral sclerosis. London: Martin Dunitz, 2000.

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Hiroshi, Mitsumoto, Przedborski Serge, and Gordon Paul H, eds. Amyotrophic lateral sclerosis. Boca Raton: Taylor & Francis, 2006.

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A, Murray Christine, ed. Amyotrophic lateral sclerosis: New research. New York: Nova Biomedical Books, 2006.

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Book chapters on the topic "Amyotrophic lateral sclerosis"

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Öztürk, Şerefnur. "Amyotrophic Lateral Sclerosis." In Neurological Disorders in Clinical Practice, 101–5. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23168-6_16.

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Donati, Stéphane Yannis, Didier Demory, and Jean-Michel Arnal. "Amyotrophic Lateral Sclerosis." In Uncommon Diseases in the ICU, 115–23. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-04576-4_11.

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Rana, Abdul Qayyum, Ali T. Ghouse, and Raghav Govindarajan. "Amyotrophic Lateral Sclerosis." In Neurophysiology in Clinical Practice, 139–45. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39342-1_17.

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Haase, Georg. "Amyotrophic Lateral Sclerosis." In Neuroprotection, 51–69. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527603867.ch3.

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Tröster, Alexander I. "Amyotrophic Lateral Sclerosis." In Encyclopedia of Clinical Neuropsychology, 217–21. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_514.

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Lang, Bethan. "Amyotrophic Lateral Sclerosis." In Diagnostic Criteria in Autoimmune Diseases, 417–20. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-285-8_76.

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Turner, Martin R. "Amyotrophic Lateral Sclerosis." In PET and SPECT in Neurology, 639–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54307-4_29.

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Oskarsson, Björn, Yvonne D. Rollins, and Steven P. Ringel. "Amyotrophic Lateral Sclerosis." In International Neurology, 199–202. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444317008.ch52.

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Breakwell, Susan. "Amyotrophic Lateral Sclerosis." In Clinical Case Studies in Home Health Care, 459–66. West Sussex UK: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118785744.ch43.

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Hardiman, Orla, Matthew C. Kiernan, and Leonard H. van den Berg. "Amyotrophic Lateral Sclerosis." In Neurodegenerative Disorders, 145–65. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23309-3_8.

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Conference papers on the topic "Amyotrophic lateral sclerosis"

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Aquino, 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.

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Introduction: Amyotrophic Lateral Sclerosis (ALS) is a progressive and degenerative motor disease of the nervous system. Symptoms are variable, the main one being muscle weakness. Treatment is based on medication and monitoring by a multidisciplinary team to maintain quality of life (QoL) and autonomy. There are barriers, like mobility, and telehealth (TH) can be a possibility of care. Objectives: To identify evidence of the use of TH in patients with ALS to improve symptoms and QoL. Design and settings: Study carried out at Centro Universitario São Camilo. Methodology: Literature review in the PubMed, Lilacs and PEDro, between 2011 and 2021, in Portuguese, English or Spanish, with “ALS”, “telemedicine”, “TH”. Results: Of the 14 studies found, 13 were selected after review. The majority (93%) made use of video and telephone calls for monitoring and new orientations, after face-to-face evaluation; but all showed the possibility of remote assessment, associated or no with technological resources (such apps, accelerometers, smartwatches). 31% of the studies reported indication of TH for respiratory care in critically ill patients. In general, 93% of the papers demonstrated that TH brought benefits in maintaining QoL and improving respiratory parameters. Conclusion: Use of TH in patients with ALS seems to be to viable, safe and beneficial for assessment and monitoring, especially in advanced stages and for respiratory symptoms.

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Bentley, 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.

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De Benito Zorrero, Esther, Julia Rodriguez Medina, Carlos Carrera Cuevas, Pilar Zamorano, Emilia Barrot Cortes, and Candelaria Caballero Eraso. "Amyotrophic lateral sclerosis and organ donation." In Respiratory Failure and Mechanical Ventilation Conference 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/23120541.rfmv-2024.144.

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Dash, 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.

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Pascual Martinez, Natalia, María Melgar Herrero, Cristina Gómez Rebollo, and Elisa Martínez Repiso. "How Our Amyotrophic Lateral Sclerosis Patients Die." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3419.

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Kaltsakas, Georgios, Michael Rentzos, Theodoros Alexakis, Vassiliki Zouvelou, Anastasios F. Palamidas, Sofia Antiopi Gennimata, Sophia Xirou, Ioannis Evdokimidis, and Nickolaos G. Koulouris. "Upper airway dysfunction in amyotrophic lateral sclerosis." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4610.

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Vieira, Marina Duarte Gama, Anna Letícia Siqueira de Medeiros, Narayna Suellen Santos da Silva, and Edlene Lima Ribeiro. "Dysphagia in patients with amyotrophic lateral sclerosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.398.

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Background: Amyotrophic lateral sclerosis is a rare neurodegenerative disease that acts on the upper and lower motor neurons, causing muscle weakness.¹²³Dysphagia occurs due to malfunction of the swallowing mechanisms and generates functional problems.⁴⁵⁶ Objectives: Describe the pathophysiology of dysphagia and discuss strategies for symptom relief. Design and setting: Systematic review, Faculdade Integrada Tiradentes, Jaboatão dos Guararapes - PE. Methods: Systematic review of 10 articles from the last years. Results: Dysarthria and dysphagia are common signs of upper motor neuron involvement and 80% of ALS cases exhibit asymmetric limb weakness.⁶ Conclusions: To improve the nutrition of patients with dysphagia, is suggested the use of supplements, changes in diet and food consistency, along with education on safe swallowing modes. Also percutaneous endoscopic gastrostomy can be used as an alternative. ⁷⁸⁹¹⁰

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Pyarali, F., R. Lewis, F. Diaz, and A. Elsayegh. "Differentiating Spirometric Features Between Patients with Amyotrophic Lateral Sclerosis and Primary Lateral Sclerosis." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2207.

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Visi, Federico, Duncan Williams, Eduardo Pontes Miranda, and Giovanni Dothel. "An Immersive Media Model of Amyotrophic Lateral Sclerosis." In Electronic Visualisation and the Arts (EVA 2014). BCS Learning & Development, 2014. http://dx.doi.org/10.14236/ewic/eva2014.52.

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Fernandes Palheiros Conde, Bebiana Da Conceição, Maria Esteves Brandão, Sara Raimundo, Ana Ferreira, and Joao Carlos Winck. "Amyotrophic lateral sclerosis: a not-so-rare disease." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2148.

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Reports on the topic "Amyotrophic lateral sclerosis"

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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.

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Connor, 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.

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Przedborski, 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.

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Connor, 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.

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Grill, 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.

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Grill, 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.

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Santos, 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.

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Review question / Objective: To systematically evaluate the utility of TMS to follow up on ALS patients using neurophysiological metrics and to quantify corticomotor excitability compared to sham controls or other neuromuscular diseases. Condition being studied: Amyotrophic Lateral Sclerosis (ALS) is the third most common neurodegenerative disease (BRUNET et al., 2020). The condition is characterized by progressive muscle atrophy due to upper and lower motor neuron death (GOETZ, 2000).

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LoGrasso, 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.

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Wackerman, 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.

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Zhu, 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.

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Review question / Objective: To identify and list the risk factors associated with the onset and progression of ALS. Condition being studied: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder affecting the upper and lower motor neurons in the spinal bulb, cerebral cortex, and spinal cord. The clinical processing symptoms accompany muscle atrophy, fasciculation, and fatigue of limbs, which can lead to general paralysis and death from respiratory failure within 3-5 years after the onset of this disease. Though the pathogenesis of ALS is still unclear, exploring the associations between risk factors and ALS can provide reliable evidence to find the pathogenesis in the future. This meta-analysis aims to synthesize all related risk factors on ALS, comprehensively understand this disease, and provide clues to mechanism research and clinicians.

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