Relevant bibliographies by topics / Amyotrophic lateral sclerosis – Research

Academic literature on the topic 'Amyotrophic lateral sclerosis – Research'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Amyotrophic lateral sclerosis – Research"

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Agnello, Luisa, and Marcello Ciaccio. "Molecular Research on Amyotrophic Lateral Sclerosis." International Journal of Molecular Sciences 23, no. 20 (October 11, 2022): 12069. http://dx.doi.org/10.3390/ijms232012069.

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Przedborski, Serge, Hiroshi Mitsumoto, and Lewis P. Rowland. "Recent advances in amyotrophic lateral sclerosis research." Current Neurology and Neuroscience Reports 3, no. 1 (January 2003): 70–77. http://dx.doi.org/10.1007/s11910-003-0041-x.

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Miller, Robert G., Fred Anderson, Benjamin Rix Brooks, Hiroshi Mitsumoto, Walter G. Bradley, and Steven P. Ringel. "Outcomes research in amyotrophic lateral sclerosis: Lessons learned from the amyotrophic lateral sclerosis clinical assessment, research, and education database." Annals of Neurology 65, S1 (January 2009): S24—S28. http://dx.doi.org/10.1002/ana.21556.

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Heo, Gi-yoon, Hee-kyung Kang, Min-hwa Kim, Irang Nam, Mariah Kim, So-yeon Kim, So-jung Park, et al. "A Case Report on a Patient with Amyotrophic Lateral Sclerosis Treated with Korean Medicine." Journal of Internal Korean Medicine 43, no. 5 (October 30, 2022): 891–900. http://dx.doi.org/10.22246/jikm.2022.43.5.891.

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Purpose: The purpose of this paper is to report the improvement of a patient with amyotrophic lateral sclerosis after long-term combined Korean medical treatment.Methods: A patient diagnosed with amyotrophic lateral sclerosis was treated with herbal medicine, acupuncture, pharmacopuncture, moxibustion, and rehabilitation for four separate hospital stays. To evaluate their respiratory discomfort and limb weakness, we used Manual Muscle Testing, the Pulmonary Function Test, and the Korean Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised.Results: The weakness of the muscles of the lower extremities and respiratory function was improved.Conclusion: We consider that combined Korean medicine treatments might be an effective treatment for muscle weakness and respiratory discomfort of amyotrophic lateral sclerosis. To verify the effectiveness of these treatments, further research is required.
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Gregory, Jenna M., Delphine Fagegaltier, Hemali Phatnani, and Matthew B. Harms. "Genetics of Amyotrophic Lateral Sclerosis." Current Genetic Medicine Reports 8, no. 4 (November 7, 2020): 121–31. http://dx.doi.org/10.1007/s40142-020-00194-8.

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Abstract Purpose of Review Amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD) spectrum disorder is a rare fatal disease with strong genetic influences. The implementation of short-read sequencing methodologies in increasingly large patient cohorts has rapidly expanded our knowledge of the complex genetic architecture of the disease. We aim to convey the broad history of ALS gene discovery as context for a focused review of 11 ALS gene associations reported over the last 5 years. We also summarize the current level of genetic evidence for all previously reported genes. Recent Findings The history of ALS gene discovery has occurred in at least four identifiable phases, each powered by different technologies and scale of investigation. The most recent epoch, benefitting from population-scale genome data, large international consortia, and low-cost sequencing, has yielded 11 new gene associations. We summarize the current level of genetic evidence supporting these ALS genes, highlighting any genotype-phenotype or genotype-pathology correlations, and discussing preliminary understanding of molecular pathogenesis. This era has also raised uncertainty around prior ALS-associated genes and clarified the role of others. Summary Our understanding of the genetic underpinning of ALS has expanded rapidly over the last 25 years and has led directly to the clinical application of molecularly driven therapies. Ongoing sequencing efforts in ALS will identify new causative and risk factor genes while clarifying the status of genes reported in prior eras of research.
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Atsuta, Naoki, and Gen Sobue. "Japanese consortium for amyotrophic lateral sclerosis research (JaCALS)." Rinsho Shinkeigaku 50, no. 11 (2010): 928–30. http://dx.doi.org/10.5692/clinicalneurol.50.928.

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Andrews, Jinsy. "Amyotrophic lateral sclerosis: Clinical management and research update." Current Neurology and Neuroscience Reports 9, no. 1 (December 16, 2008): 59–68. http://dx.doi.org/10.1007/s11910-009-0010-0.

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de Carvalho, Mamede. "Advances in amyotrophic lateral sclerosis research in 2022." Lancet Neurology 22, no. 1 (January 2023): 21–22. http://dx.doi.org/10.1016/s1474-4422(22)00490-2.

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9

D’Antona, Salvatore, Martina Caramenti, Danilo Porro, Isabella Castiglioni, and Claudia Cava. "Amyotrophic Lateral Sclerosis: A Diet Review." Foods 10, no. 12 (December 17, 2021): 3128. http://dx.doi.org/10.3390/foods10123128.

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Amyotrophic lateral sclerosis (ALS) is a fatal disease related to upper and lower motor neurons degeneration. Although the environmental and genetic causes of this disease are still unclear, some factors involved in ALS onset such as oxidative stress may be influenced by diet. A higher risk of ALS has been correlated with a high fat and glutamate intake and β-methylamino-L-alanine. On the contrary, a diet based on antioxidant and anti-inflammatory compounds, such as curcumin, creatine, coenzyme Q10, vitamin E, vitamin A, vitamin C, and phytochemicals could reduce the risk of ALS. However, data are controversial as there is a discrepancy among different studies due to a limited number of samples and the many variables that are involved. In addition, an improper diet could lead to an altered microbiota and consequently to an altered metabolism that could predispose to the ALS onset. In this review we summarized some research that involve aspects related to ALS such as the epidemiology, the diet, the eating behaviour, the microbiota, and the metabolic diseases. Further research is needed to better comprehend the role of diet and the metabolic diseases in the mechanisms leading to ALS onset and progression.
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Lulé, Dorothée. "Neuroimaging Advances in Amyotrophic Lateral Sclerosis." European Neurological Review 5, no. 2 (2010): 54. http://dx.doi.org/10.17925/enr.2010.05.02.54.

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The development of non-invasive functional imaging techniques has allowed neuroscientists to investigate the physiological parameters of the clinical features of amyotrophic lateral sclerosis (ALS), a severe neurological disease. Modern neuroimaging techniques enable anatomy and function to be connectedin vivowith an acceptable balance between low patient load and high information capacity, making them ideal for clinical research in patients with physical restrictions, such as those with ALS. Structural imaging techniques in ALS include T1/T2-weighted structural magnetic resonance imaging, diffusion tensor imaging and voxel-based morphometry. Functional neuroimaging enables the acquisition of dynamic cortical function either in a passive (or resting) state or via active paradigms. The main technique used is functional magnetic resonance imaging. Structural and functional neuroimaging has provided evidence of alterations in motor and non-motor cortical pathways in ALS. In the future, neuroimaging may provide early diagnostic criteria to support the clinical diagnosis of ALS, help us to understand the aetiological background of the disease and pave the way for a new viewpoint on the functional capacities of these patients, which may have a major impact on our way of thinking about end-of-life decisions.
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Dissertations / Theses on the topic "Amyotrophic lateral sclerosis – Research"

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Frakes, Ashley E. "The Role of Neuroinflammation in the Pathogenesis of Amyotrophic Lateral Sclerosis." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1417649954.

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Likhite, Shibi B. "Therapeutic suppression of mutant SOD1 by AAV9-mediated gene therapy approach in Amyotrophic Lateral Sclerosis." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1417394084.

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Rajagopalan, Venkateswaran. "Evaluation of Upper Motor Neuron Pathology in Amyotrophic Lateral Sclerosis by MRI: Towards Identifying Noninvasive Biomarkers of the Disease." Cleveland State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=csu1288020485.

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Toro, Gabriela. "Gene Therapy for Amyotrophic Lateral Sclerosis: An AAV Mediated RNAi Approach for Autosomal Dominant C9ORF72 Associated ALS." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1020.

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Amyotrophic lateral sclerosis (ALS) is a terminal neurodegenerative disease that affects motor neurons causing progressive muscle weakness and respiratory failure. In 2011, the presence of a hexanucleotide repeat expansion within chromosome 9 open reading frame 72(C9ORF72) was identified in ALS patient samples, becoming the major known genetic cause for ALS and frontotemporal dementia (FTD). Carriers of this mutation present reduced levels of C9ORF72 mRNA, RNA foci produced by the aggregating expansion and toxic dipeptides generated through repeat-associated non-ATG translation. These findings have led to multiple hypotheses on the pathogenesis of C9ORF72: 1) Haploinsufficiency, 2) RNA gain-of-function, 3) RAN Translation, and 4) Disrupted nucleocytoplasmic trafficking. Due to lack of treatments for this disease, we have pursued an AAV-RNAi dependent gene therapy approach, using an artificial microRNA (amiR) packaged in a recombinant adeno-associated virus (rAAV). After validating our in vitro results, we advanced to in vivo experiments using transgenic mice that recapitulate the major histopathological features seen in human ALS/FTD patients. Adult and neonate mice were injected through clinically relevant routes and our results indicate that AAV9-mediated amiR silencing not only reduced mRNA and protein levels of C9ORF72 but also the expansion derived toxic GP dipeptides. Although our amiR is not targeting the expansion itself but exon 3, we illustrate here that the evident dipeptide decrease is achievable due to the presence of aberrant transcripts in the cytoplasm containing miss-spliced Intron-HRE-C9ORF72 species. These encouraging results have led to the continued testing of this treatment as a therapeutic option for C9ORF72 - ALS patients.
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Draper, Christiana S. I. "ALS-induced Excitability Changes in Individual Motorneurons and the Spinal Motorneuron Network in SOD1-G93A Mice at Symptom Onset." Wright State University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wright1621064515386592.

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Caroppo, Paola. "Study of the clinical and preclinical stages of genetic forms of frontotemporal lobar degeneration (FTLD) and research of biomarkers of progression of the disease." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066116.

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Les dégénérescences lobaires fronto-temporale (DLFT) sont des démences neurodégénératives rares. 30-50% des DLFT a une cause génétique, la plupart sont des mutations des gènes C9orf72 et progranuline (GRN). L'objectif de la thèse a été d'élargir le spectre mutationnel et phénotypique des mutations GRN. Nous avons identifié les premières délétions partielles du gène GRN chez des patients avec progranulinémie baisse (la progranulinémie est abaissée en cas de mutation), mais sans mutation détectée par séquençage. Nous avons contribué à élargir le spectre clinique de la maladie en décrivant un phénotype d'atrophie corticale postérieure et des lésions de la substance blanche cérébrale chez des patients GRN, caractéristique évocatrice de cette forme génétique. Enfin, nous avons étudié la phase présymptomatique de la maladie, alors que se développent les premiers essais thérapeutiques, par une approche longitudinale avec IRM et TEP-FDG. Le métabolisme cérébral est réduit dans le lobe temporal latéral gauche 20 ans avant l'apparition des symptômes et, après 20 mois, dans les régions frontales et l'épaisseur corticale dans les régions temporales gauche. Le lobe temporal latéral pourrait être donc l'"épicentre " de la maladie, et le processus lésionnel pourrait, secondairement, progresser vers les régions frontales. J'ai également contribué à définir les phénotypes associés aux mutations de gènes plus rares de DLFT/DLFT-SLA. TARDBP est associé à un large spectre phénotypique; TBK1 est caractérisé par une démence sémantique ou aphasie non fluent associés à l'atteinte de la corne antérieure. Cette étude importante souligne le rôle de ces mutations dans le spectre clinique des DLFT
Frontotemporal lobar degeneration (FTLD) are rare neurodegenerative dementias. 30-50% of FTLD has a genetic cause, most are mutations in C9orf72 and in progranulin gene (GRN). The aim of the thesis was to expand the mutational and phenotypic spectrum of GRN mutations. We identified the first partial deletions of GRN gene in patients with low plasmatic progranulin (the plasmatic progranulin is low in case of mutation), but without mutation detected by sequencing. We contributed to expand the clinical spectrum of the disease by describing a posterior cortical atrophy phenotype and lesions of the cerebral white matter in GRN patients, evocative feature of this genetic form. Finally, we studied the presymptomatic stage of the disease, while the first clinical trials develop, for a longitudinal approach with MRI and FDG-PET. The cerebral metabolism is reduced in the left temporal lobe 20 years before clinical onset and, after 20 months, the metabolism is reduced in the frontal regions and the cortical thickness in the left temporal regions. The lateral temporal lobe could thus be the "epicenter" of the disease, and the lesional process could secondarily progress towards the frontal regions. I also contributed to define the phenotypes associated with rare gene mutations in FTLD/FTLD-ALS. TARDBP is associated with a wide phenotypic spectrum; TBK1 is characterized by semantic dementia or not fluent aphasia associated with involvement of the anterior horn. This important study highlights the role of these mutations in the clinical spectrum of FTLD
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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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Books on the topic "Amyotrophic lateral sclerosis – Research"

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G, Farrell Jason, ed. New amyotrophic lateral sclerosis research. New York: Nova Biomedical Books, 2008.

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International, Congress on Therapeutic Psychological and Research Aspects of Amyotrophic Lateral Sclerosis (1985 Varese Italy). Amyotrophic lateral sclerosis: Therapeutic, psychological, and research aspects. New York, N.Y: Plenum Press, 1987.

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Eisen, Andrew. Amythrophic lateral sclerosis: A synthesis of research and clinical practice. Cambridge: Cambridge University Press, 1998.

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1921-, Tsubaki Tadao, and Yase Yoshirō, eds. Amyotrophic lateral sclerosis: Recent advances in research and treatment : proceedings of the International Conference on Amyotrophic Lateral Sclerosis, Kyoto, Japan, 29-31, October 1987. Amsterdam: Excerpta Medica, 1988.

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Gajdusek, D. Carleton. Interference with axonal transport of neurofilament as the common etiology and pathogenesis of neurofibrillary tangles, amyotrophic lateral sclerosis, parkinsonism-dementia, and many other degenerations of the CNS: A series of hypotheses, perspectives for research. Bethesda, Md: U.S. Dept. of Health and Human Services, National Institutes of Health, Laboratory of Central Nervous System Studies, National Institute of Neurological and Communicative Disorders and Stroke, 1985.

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Imaharu, Nakano, and Hirano Asao 1926-, eds. Amyotrophic lateral sclerosis: Progress and perspectives in basic research and clinical application : proceedings of the 11th Tokyo Metropolitan Institute for Neuroscience (TMIN) International Symposium, Tokyo, October 25-27, 1995. Amsterdam: Elsevier Science, 1996.

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L, Mancini Raffaele, ed. Motor neuron disease research progress. New York: Nova Biomedical Books, 2008.

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Research, Institute for Career. Careers in medical research: Finding cures for paralysis : spinal cord injuries, stroke, multiple sclerosis, cerebral palsy, amyotrophic lateral sclerosis : unlocking the mysteries of the brain and fixing a broken body. [Chicago, Ill.]: Institute for Career Research, 2003.

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Parker, Philip M., and James N. Parker. Sclerosis: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2003.

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United, States Congress Senate Committee on Appropriations Subcommittee on Departments of Labor Health and Human Services Education and Related Agencies. Amyotrophic lateral sclerosis (ALS): Hearing before a subcommittee of the Committee on Appropriations, United States Senate, One Hundred Ninth Congress, first session, special hearing, May 11, 2005, Washington, DC. Washington: U.S. G.P.O., 2006.

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Book chapters on the topic "Amyotrophic lateral sclerosis – Research"

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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.

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Krüger, Thomas. "Biomarker for Amyotrophic Lateral Sclerosis." In General Methods in Biomarker Research and their Applications, 1–18. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-7740-8_7-1.

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Ramdial, Kristina, Fabian H. Rossi, Maria Clara Franco, and Alvaro G. Estevez. "Amyotrophic Lateral Sclerosis: Present Understanding of the Role of SOD." In Oxidative Stress in Applied Basic Research and Clinical Practice, 597–603. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30705-3_26.

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Hubens, Wouter, and Ayako Okado-Matsumoto. "Redox Regulation and Misfolding of SOD1: Therapeutic Strategies for Amyotrophic Lateral Sclerosis." In Oxidative Stress in Applied Basic Research and Clinical Practice, 605–26. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30705-3_27.

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Mir, Nighat, Akila Sarirete, Jehad Hejres, and Manar Al Omairi. "Use of EEG Technology with Based Brain-Computer Interface to Address Amyotrophic Lateral Sclerosis—ALS." In Research & Innovation Forum 2019, 433–39. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-30809-4_39.

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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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Conference papers on the topic "Amyotrophic lateral sclerosis – Research"

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Marquardt, Matheus, Antônio Serpa do Amaral Neto, Eduardo Martins Leal, Gabriel de Deus Vieira, André Dias de Oliveira, and Gisele Espindola. "Amyotrophic lateral sclerosis associated with parkinsonism: an atypical manifestation." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.608.

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Context: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease, characterized by progressive muscle weakness. The diagnosis is not always easy, and may have atypical initial manifestations. Case report: O.S.M, female, 62 years old, started in 2016 with bradykinesia and left lower limb tremor, associated with frequent falls. Iniciated research for parkinsonism in 2017, SPECT demonstrated decreased dopamine transporter binding potential density in both striatum. Levodopa was started, with partial improvement of symptoms. In 2018, she developed dysphagia, associated with slight alterations in phonation. In 2019, in addition to the left lower limb tremor and bradykinesia, the patient developed limb paresis, also affecting the right upper limb, with proximal atrophy and fasciculations. Added to the therapeutic regimen pramipexole, without improvement in symptoms. Over the months the case progressed with axial weakness, the need for a wheelchair for walking. Patient hospitalized in April 2020, electroneuromyography performed which showed signs of active disinvervation in the bulbar, cervical, thoracic and lumbosacral segments and signs of chronic disinervation in the cervical and lumbosacral segments, with no signs of sensory or motor polyneuropathy. Such findings suggest impairment of the Lower motor neuron, and can be found in the Diseases of the Motor Neuron. With the diagnosis of ALS, Riluzole was started, with a reduction in the speed of disease progression. Conclusions: the reported case draws attention to the importance of always thinking about differential diagnoses in neurological diseases. We should always look for new symptoms, so that more rare diseases do not go unnoticed.
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Albuquerque, Pedro José Honório de, Laura Guerra Lopes, Jordy Silva de Carvalho, Luzilene Pereira de Lima, and Marina Galdino da Rocha Pitta. "Emerging therapies for amyotrophic lateral sclerosis applied to drug discovery." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.021.

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Background: Amyotrophic Lateral Sclerosis (ALS) is a progressive neuromuscular disease mainly caused by genetic disorders. This progressive disorder involves the degeneration of motor neurons at various levels. Drugs have been studied, and they show improvement in survival and reduced progression of the disease, they are riluzole and edaravone. Objectives: Investigate emerging therapies for the treatment of ALS. Methods: The Pubmed database was used to conduct the research, and the keywords were “Amyotrophic Lateral Sclerosis”, “Emerging”, “Therapies”,”Drugs”, all present in Mesh. Articles from 2016 to 2021 were used. And the survey was conducted on May 2, 2021. Results: Only two drugs have been approved yet by the Food and Drug Administration for the treatment of ALS, riluzole and edaravone, and each one offers modest benefits in mortality and/or function. On the other hand, 88 studies of clinical intervention trials are active using different drugs. Current therapies under development include oral tyrosine kinase inhibitors (masitinib, trametinib); the antisense oligonucleotide (tofersen); the human monoclonal antibody inhibitor (ravulizumab); and mesenchymal stem cells (MSC); among others (RT001, Enoxacin, Engensis, ANX005, Deferiprone). Conclusions: Due to gaps in the knowledge of the specific pathophysiology of ALS, the definitive treatment is still a mystery. The drugs currently in use, riluzole and edaravone, are the most promising in terms of delaying the progression of the disease.
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Devipriya, S., and M. S. Vijaya. "Drug Efficacy Score Prediction using Signature Based Approaches for Amyotrophic Lateral Sclerosis Disorder: A Review." In 2022 4th International Conference on Inventive Research in Computing Applications (ICIRCA). IEEE, 2022. http://dx.doi.org/10.1109/icirca54612.2022.9985468.

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Meneses-Claudio, Brian, and Avid Roman-Gonzalez. "Study of the Brain Waves for the identification of the Basic Needs of Patients with Amyotrophic Lateral Sclerosis." In 2018 Argentine Congress of Computer Science and Research Development (CACIDI). IEEE, 2018. http://dx.doi.org/10.1109/cacidi.2018.8584193.

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Fernandez, Paulo Eduardo Lahoz, Guilherme Diogo Silva, and Eduardo Genaro Mutarelli. "Studies across subspecialties of neurology (SON) report noninferiority of telemedicine (TM) compared with face-to-face intervention (FTF-I)." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.680.

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Background: Studies across subspecialties of neurology (SON) report noninferiority of telemedicine (TM) compared with face-to-face intervention (FTF-I). Clinical scales (CS) are important tools for outcome measures in clinical care. However, which CS in FTF-I can be used in teleneurology is unclear. Objectives: Define the most used CS in studies comparing TM with FTF-I in different SON. Design and Setting/Methods: We searched PubMed and Embase for randomized controlled trials, published from 2011 to April 2021, with Key words ‘’telemedicine’’ cross-referenced with ‘’neurology’’ or neurological diseases, considering the synonyms. Results: 43 eligible studies in 400 records, from 12 countries, with 5600 patients and 8 SON: stroke (10), headache (4), epilepsy (6), cognitive disorders (7), demyelinating diseases (8), movement disorders (3), neuromuscular diseases (3), and vestibular diseases (2). The most used CS: National Institute of Health Stroke Scale (NIHSS) and Modified Rankin Scale (MRS) for stroke impairment and limitation; Headache Impact Test (HIT-6) and Migraine Disability Assessment Scale (MIDAS) for headache disability; Quality Of Life in Epilepsy Inventory (QOL-31) for seizure burden; Mini-Mental State Exam (MMSE) and Zarit Burden Interview (ZBI) for cognitive function and caregiver burden in dementia care; Expanded Disability Status Scale (EDSS) and Fatigue Impact Scale (FIS) for disability and fatigue in Multiple Sclerosis; Parkinson’s disease Questionnaire (PDQ-39) and Unified Parkinson’s Disease Rating Scale (UPDRS) for QOL and disability in PD; Amyotrophic Lateral Sclerosis Functional Rating Scale Revised (ALSFRS-R) for severity in ALS; and Vertigo Symptom Scale Short form (VSS-SF) for vertigo. Conclusions: We present feasible CS usually applied in teleneurology that can be used as important tools for future findings in TM research and practice.
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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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Jugl, Sebastian, Aimalohi Okpeku, Brianna Costales, Earl Morris, Golnoosh Alipour-Harris, Juan Hincapie-Castillo, Nichole Stetten, et al. "A Mapping Literature Review of Medical Cannabis Clinical Outcomes and Quality of Evidence in Approved Conditions in the United States, from 2016 to 2019." In 2020 Virtual Scientific Meeting of the Research Society on Marijuana. Research Society on Marijuana, 2021. http://dx.doi.org/10.26828/cannabis.2021.01.000.25.

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Background: Medical cannabis is available to patients by physician order in two-thirds of the United States (U.S.) as of 2020, but remains classified as an illicit substance by federal law. States that permit medical cannabis ordered by a physician typically require a diagnosed medical condition that is considered qualifying by respective state law. Objectives: To identify and map the most recently (2016-2019) published clinical and scientific literature across approved conditions for medical cannabis, and to evaluate the quality of identified recent systematic reviews. Methods: Literature search was conducted from five databases (PubMed, Embase, Web of Science, Cochrane, and ClinicalTrials.gov), with expansion and update from the National Academies of Sciences, Engineering, and Medicine’s (NASEM) comprehensive evidence review through 2016 of the health effects of cannabis on several conditions. Following consultation with experts and stakeholders, 11 conditions were identified for evidence evaluation: amyotrophic lateral sclerosis (ALS), autism, cancer, chronic pain, Crohn’s disease, epilepsy, glaucoma, HIV/AIDS, multiple sclerosis (MS), Parkinson’s disease, and posttraumatic stress disorder (PTSD). The following exclusion criteria were imposed: preclinical focus, non-English language, abstracts only, editorials/commentary, case studies/series, and non-U.S. study setting. Data extracted from studies included: study design type, outcome, intervention, sample size, study setting, and reported effect size. Studies classified as systematic reviews with or without meta-analysis were graded using the AMSTAR-2 tool by two raters to evaluate the quality of evidence, with additional raters to resolve cases of evidence grade disagreement. Results: A total of 438 studies were included after screening. Five completed randomized controlled trials (RCTs) were identified, and an additional 11 trials were ongoing, and 1 terminated. Cancer, chronic pain, and epilepsy were the most researched topic areas, representing more than two-thirds of all reviewed studies. The quality of evidence assessment for each condition suggests that few high-quality systematic reviews are available for most conditions, with the exceptions of MS, epilepsy, and chronic pain. In those areas, findings on chronic pain are mostly in alignment with the previous literature, suggesting that cannabis or cannabinoids are potentially beneficial in treating chronic neuropathic pain. In epilepsy, findings suggest that cannabidiol is potentially effective in reducing seizures in pediatric patients with drug-resistant Dravet and Lennox-Gastaut syndromes. In MS, recent high-quality systematic reviews did not include new RCTs, and are therefore not substantially expanding the evidence base. In sum, the most recent clinical evidence suggests that for most of the conditions assessed, we identified few studies of substantial rigor and quality to contribute to the evidence base. However, there are some conditions for which significant evidence suggests that select dosage forms and routes of administration likely have favorable risk-benefit ratios (i.e., epilepsy and chronic pain), with the higher quality of evidence for epilepsy driven by FDA-approved formulations for cannabis-based seizure treatments. Conclusion: The body of evidence for medical cannabis requires more rigorous evaluation before consideration as a treatment option for many conditions and evidence necessary to inform policy and treatment guidelines is currently insufficient for many conditions.
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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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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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Reports on the topic "Amyotrophic lateral sclerosis – Research"

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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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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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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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