Relevant bibliographies by topics / Amyotrophic lateral sclerosis – Pathophysiology

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

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Published: 10 December 2022
Last updated: 29 January 2023

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

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Voitenkov, Vladislav B., and E. V. Ekusheva. "Pain in amyotrophic lateral sclerosis." Journal of Clinical Practice 10, no. 2 (August 17, 2019): 66–73. http://dx.doi.org/10.17816/clinpract10266-73.

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In this review, we discuss different aspects of pain syndrome in patients with amyotrophic lateral sclerosis: etiology, incidence, pathophysiology and main clinical features. Also we review the modern approaches to the treatment of pain in amyotrophic lateral sclerosis. Pain is actually not rare in this condition: it appears in 80% of patients, affecting their quality of life and functional activity, leading to the development of depressive and anxiety disorders. Pain in amyotrophic lateral sclerosis is often overlooked by clinicians, since their attention may focus on the motor symptoms of the disease. Thus, a more careful approach is needed to diagnose and treat pain in amyotrophic lateral sclerosis.
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Fawad, Laiba, and Mehrab Tahir. "Emerging Therapies in Amyotrophic Lateral Sclerosis." Molecular Medicine Communications 2, no. 01 (June 30, 2022): 31–42. http://dx.doi.org/10.55627/mmc.002.001.0041.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the loss of cortical and spinal motor neurons, leading to weakness, muscle atrophy, and, in a substantial number of patients, cognitive impairment. Most patients die within 2 to 5 years of diagnosis. The disease initiates from the death of upper and lower motor neurons leading to a degeneration of motor pathways and the paralytic effects of the disease. The disease has huge economic costs as well. FDA has approved two drugs, riluzole, and edaravone for the treatment of ALS. However, these drugs provide modest benefits in mortality and/or function. Recent developments in the understanding of the underlying pathophysiologic processes that contribute to ALS have led to the development of numerous investigational therapies, with several now in phase 3 trials. This article highlights the epidemiology, pathophysiology, and several current and emerging treatment options for ALS including stem cell therapy.
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Vucic, Steve, and Matthew Kiernan. "Pathophysiology of Neurodegeneration in Familial Amyotrophic Lateral Sclerosis." Current Molecular Medicine 9, no. 3 (April 1, 2009): 255–72. http://dx.doi.org/10.2174/156652409787847173.

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Coupé, Christophe, and Paul H. Gordon. "Amyotrophic Lateral Sclerosis – Clinical Features, Pathophysiology and Management." European Neurological Review 8, no. 1 (2012): 38. http://dx.doi.org/10.17925/enr.2013.08.01.38.

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Amyotrophic lateral sclerosis (ALS), first described by Jean-Martin Charcot 145 years ago, is an age-related neurodegenerative disorder that leads to destruction of motor neurons. The disease begins focally in the central nervous system then spreads inexorably. The clinical diagnosis, defined by progressive upper and lower motor neuron findings, is confirmed by electromyogram. Additional testing excludes other conditions. The disease is heterogeneous, but most patients die of progressive weakness and respiratory failure less than 3 years from symptom onset. Like other neurodegenerative diseases, ALS is thought to have genetic and environmental causes. Five to 10 % of cases are inherited. Genetic factors, age, tobacco use and athleticism may contribute to sporadic ALS, but major causes are unidentified for most patients. Complex pathophysiological processes, including mitochondrial dysfunction, aggregation of misfolded protein, oxidative stress, excitotoxicity, inflammation and apoptosis, involve both motor neurons and surrounding glial cells. There is clinical and pathological overlap with other neurodegenerative diseases, particularly frontotemporal dementia. One medication, riluzole, which was approved in 1996, prolongs survival by several months. Numerous ensuing clinical trials have been negative. Researchers currently aim to slow disease progression by targeting known pathophysiological pathways. Approaches under examination are directed at muscle protein, energetic balance, cell replacement and protein aggregation. Until the causes and more robust neuroprotective agents are identified, symptomatic therapies can help improve expectancy and quality of life. Palliative care ensures dignity in advanced stages.
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Dilliott, Allison A., Catherine M. Andary, Meaghan Stoltz, Andrey A. Petropavlovskiy, Sali M. K. Farhan, and Martin L. Duennwald. "DnaJC7 in Amyotrophic Lateral Sclerosis." International Journal of Molecular Sciences 23, no. 8 (April 7, 2022): 4076. http://dx.doi.org/10.3390/ijms23084076.

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Protein misfolding is a common basis of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Misfolded proteins, such as TDP-43, FUS, Matrin3, and SOD1, mislocalize and form the hallmark cytoplasmic and nuclear inclusions in neurons of ALS patients. Cellular protein quality control prevents protein misfolding under normal conditions and, particularly, when cells experience protein folding stress due to the fact of increased levels of reactive oxygen species, genetic mutations, or aging. Molecular chaperones can prevent protein misfolding, refold misfolded proteins, or triage misfolded proteins for degradation by the ubiquitin–proteasome system or autophagy. DnaJC7 is an evolutionarily conserved molecular chaperone that contains both a J-domain for the interaction with Hsp70s and tetratricopeptide domains for interaction with Hsp90, thus joining these two major chaperones’ machines. Genetic analyses reveal that pathogenic variants in the gene encoding DnaJC7 cause familial and sporadic ALS. Yet, the underlying ALS-associated molecular pathophysiology and many basic features of DnaJC7 function remain largely unexplored. Here, we review aspects of DnaJC7 expression, interaction, and function to propose a loss-of-function mechanism by which pathogenic variants in DNAJC7 contribute to defects in DnaJC7-mediated chaperoning that might ultimately contribute to neurodegeneration in ALS.
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Parakh, Sonam, Damian M. Spencer, Mark A. Halloran, Kai Y. Soo, and Julie D. Atkin. "Redox Regulation in Amyotrophic Lateral Sclerosis." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/408681.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that results from the death of upper and lower motor neurons. Due to a lack of effective treatment, it is imperative to understand the underlying mechanisms and processes involved in disease progression. Regulations in cellular reduction/oxidation (redox) processes are being increasingly implicated in disease. Here we discuss the possible involvement of redox dysregulation in the pathophysiology of ALS, either as a cause of cellular abnormalities or a consequence. We focus on its possible role in oxidative stress, protein misfolding, glutamate excitotoxicity, lipid peroxidation and cholesterol esterification, mitochondrial dysfunction, impaired axonal transport and neurofilament aggregation, autophagic stress, and endoplasmic reticulum (ER) stress. We also speculate that an ER chaperone protein disulphide isomerase (PDI) could play a key role in this dysregulation. PDI is essential for normal protein folding by oxidation and reduction of disulphide bonds, and hence any disruption to this process may have consequences for motor neurons. Addressing the mechanism underlying redox regulation and dysregulation may therefore help to unravel the molecular mechanism involved in ALS.
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Sanghai, Nitesh, and Geoffrey K. Tranmer. "Hydrogen Peroxide and Amyotrophic Lateral Sclerosis: From Biochemistry to Pathophysiology." Antioxidants 11, no. 1 (December 27, 2021): 52. http://dx.doi.org/10.3390/antiox11010052.

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Free radicals are unstable chemical reactive species produced during Redox dyshomeostasis (RDH) inside living cells and are implicated in the pathogenesis of various neurodegenerative diseases. One of the most complicated and life-threatening motor neurodegenerative diseases (MND) is amyotrophic lateral sclerosis (ALS) because of the poor understanding of its pathophysiology and absence of an effective treatment for its cure. During the last 25 years, researchers around the globe have focused their interest on copper/zinc superoxide dismutase (Cu/Zn SOD, SOD1) protein after the landmark discovery of mutant SOD1 (mSOD1) gene as a risk factor for ALS. Substantial evidence suggests that toxic gain of function due to redox disturbance caused by reactive oxygen species (ROS) changes the biophysical properties of native SOD1 protein thus, instigating its fibrillization and misfolding. These abnormal misfolding aggregates or inclusions of SOD1 play a role in the pathogenesis of both forms of ALS, i.e., Sporadic ALS (sALS) and familial ALS (fALS). However, what leads to a decrease in the stability and misfolding of SOD1 is still in question and our scientific knowledge is scarce. A large number of studies have been conducted in this area to explore the biochemical mechanistic pathway of SOD1 aggregation. Several studies, over the past two decades, have shown that the SOD1-catalyzed biochemical reaction product hydrogen peroxide (H2O2) at a pathological concentration act as a substrate to trigger the misfolding trajectories and toxicity of SOD1 in the pathogenesis of ALS. These toxic aggregates of SOD1 also cause aberrant localization of TAR-DNA binding protein 43 (TDP-43), which is characteristic of neuronal cytoplasmic inclusions (NCI) found in ALS. Here in this review, we present the evidence implicating the pivotal role of H2O2 in modulating the toxicity of SOD1 in the pathophysiology of the incurable and highly complex disease ALS. Also, highlighting the role of H2O2 in ALS, we believe will encourage scientists to target pathological concentrations of H2O2 thereby halting the misfolding of SOD1.
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Rothstein, Jeffrey D. "TDP-43 in amyotrophic lateral sclerosis: Pathophysiology or patho-babel?" Annals of Neurology 61, no. 5 (2007): 382–84. http://dx.doi.org/10.1002/ana.21155.

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Souza, Paulo Victor Sgobbi de, Wladimir Bocca Vieira de Rezende Pinto, Marco Antônio Troccoli Chieia, and Acary Souza Bulle Oliveira. "Clinical and genetic basis of familial amyotrophic lateral sclerosis." Arquivos de Neuro-Psiquiatria 73, no. 12 (October 13, 2015): 1026–37. http://dx.doi.org/10.1590/0004-282x20150161.

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Amyotrophic lateral sclerosis represents the most common neurodegenerative disease leading to upper and lower motor neuron compromise. Although the vast majority of cases are sporadic, substantial gain has been observed in the knowledge of the genetic forms of the disease, especially of familial forms. There is a direct correlation between the profile of the mutated genes in sporadic and familial forms, highlighting the main role ofC9orf72 gene in the clinical forms associated with frontotemporal dementia spectrum. The different genes related to familial and sporadic forms represent an important advance on the pathophysiology of the disease and genetic therapeutic perspectives, such as antisense therapy. The objective of this review is to signal and summarize clinical and genetic data related to familial forms of amyotrophic lateral sclerosis.
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Renga, Vijay. "Brain Connectivity and Network Analysis in Amyotrophic Lateral Sclerosis." Neurology Research International 2022 (February 7, 2022): 1–20. http://dx.doi.org/10.1155/2022/1838682.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with no effective treatment or cure. ALS is characterized by the death of lower motor neurons (LMNs) in the spinal cord and upper motor neurons (UMNs) in the brain and their networks. Since the lower motor neurons are under the control of UMN and the networks, cortical degeneration may play a vital role in the pathophysiology of ALS. These changes that are not apparent on routine imaging with CT scans or MRI brain can be identified using modalities such as diffusion tensor imaging, functional MRI, arterial spin labelling (ASL), electroencephalogram (EEG), magnetoencephalogram (MEG), functional near-infrared spectroscopy (fNIRS), and positron emission tomography (PET) scan. They can help us generate a representation of brain networks and connectivity that can be visualized and parsed out to characterize and quantify the underlying pathophysiology in ALS. In addition, network analysis using graph measures provides a novel way of understanding the complex network changes occurring in the brain. These have the potential to become biomarker for the diagnosis and treatment of ALS. This article is a systematic review and overview of the various connectivity and network-based studies in ALS.
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Dissertations / Theses on the topic "Amyotrophic lateral sclerosis – Pathophysiology"

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Ragancokova, Daniela. "The role of synaptic transmission in the pathophysiology and therapy of neurodegenerative disease, amyotrophic lateral sclerosis." Hannover Bibliothek der Tierärztlichen Hochschule Hannover, 2009. http://d-nb.info/1000125661/34.

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Harandi, Vahid M. "A Muscle Perspective on the Pathophysiology of Amyotrophic Lateral Sclerosis : Differences between extraocular and limb muscles." Doctoral thesis, Umeå universitet, Anatomi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-120219.

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Background: Amyotrophic lateral sclerosis (ALS) is a late-onset progressive neurodegenerative disorder. ALS has been traditionally believed to be primarily a motor neuron disease. However, accumulating data indicate that loss of contact between the axons and the muscle fibres occurs early; long before the death of motor neurons and that muscle fibres may initiate motor neuron degeneration. Thus, the view of ALS is changing focus from motor neurons alone to also include the muscle fibres and the neuromuscular junctions (NMJs). While skeletal muscles are affected in ALS, oculomotor disturbances are not dominant features of this disease and extraocular muscles (EOMs) are far less affected than limb muscles. Why oculomotor neurons and EOMs are capable to be more resistant in the pathogenetic process of ALS is still unknown. The overall goal of this thesis is to explore the pathophysiology of ALS from a muscle perspective and in particular study the expression and distribution of key neurotrophic factors (NTFs) and Wnt proteins in EOMs and limb muscles from ALS donors and from SOD1G93A transgenic mice. Comparisons were made with age-matched controls to distinguish between changes related to ALS and to ageing. Results: Brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), neurotrophin-3 (NT-3) and neurotrophin-4/5 (NT-4) were present in EOMs and limb muscles at both mRNA and protein levels in control mice. The mRNA levels of BDNF, NT-3 and NT-4 were significantly lower in EOMs than in limb muscles of early and/or late control mice, indicating an intrinsic difference in NTFs expression between EOMs and limb muscles. qRT-PCR analysis showed significantly upregulated mRNA levels of NT-3 and GDNF in EOMs but significantly downregulated mRNA levels of NT-4 in limb muscles from SOD1G93A transgenic mice at early stage. The NTFs were detected immunohistochemically in NMJs, nerve axons and muscle fibres. The expression of BDNF, GDNF and NT-4 on NMJs of limb muscles, but not of EOMs, was significantly decreased in terminal stage ALS animals as compared to the limb muscles of the age-matched controls. In contrast, NTFs expression in intramuscular nerve axons did not present significant changes in either muscle group of early or late ALS mice. NTFs, especially BDNF and NT-4 were upregulated in some small-sized muscle fibres in limb muscles of late stage ALS mice. All the four Wnt isoforms, Wnt1, Wnt3a, Wnt5a and Wnt7a were detected in most axon profiles in all human EOMs with ALS, whereas significantly fewer axon profiles were positive in the human limb muscles except for Wnt5a. Similar differential patterns were found in myofibres, except for Wnt7a, where its expression was elevated within sarcolemma of limb muscle fibres. β-catenin, a marker of the canonical Wnt pathway was activated in a subset of myofibres in the EOMs and limb muscle in all ALS patients. In the SOD1G93A mouse, all four Wnt isoforms were significantly decreased in the NMJs at the terminal stage compared to age matched controls. Conclusions: There were clear differences in NTF and Wnt expression patterns between EOM and limb muscle, suggesting that they may play a role in the distinct susceptibility of these two muscle groups to ALS. In particular, the early upregulation of GDNF and NT-3 in the EOMs might play a role in the preservation of the EOMs in ALS. Further studies are needed to determine whether these proteins and the pathways they control may be have a future potential as protecting agents for other muscles.
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Ragancokova, Daniela [Verfasser]. "The role of synaptic transmission in the pathophysiology and therapy of neurodegenerative disease, amyotrophic lateral sclerosis / Daniela Ragancokova." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2009. http://d-nb.info/1000125661/34.

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Hurtado, Caballero Erica. "Coordinated effects of synaptic activity and muscle contraction on cpkc regulation by pdk1 and bdnf/trkb signalling. An approach towards the amyotrophic lateral sclerosis pathophysiology." Doctoral thesis, Universitat Rovira i Virgili, 2017. http://hdl.handle.net/10803/457136.

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El sistema neuromuscular és un complex circuit interconnectat en el qual les motoneurones presinàptiques i cèl·lules de Schwann indiquen al múscul esquelètic com créixer, diferenciar-se i funcionar. D’altra banda, el múscul proporciona senyals, incloent les neurotrofines, que regulen la supervivència i les funcions de les motoneurones. En concret, la neurotrofina BDNF regulada per activitat, a l’unir-se al TrkB, pot activar diferents vies incloent les PKCs. Per tant, és important conèixer com opera l’activitat pre- i post-sinàptica en condicions fisiològiques per controlar la funció neuromuscular a través de la regulació del BDNF i PKCs. Per estudiar això, es va estimular el nervi frènic del diafragma de rata amb o sense contracció, per tal de separar els efectes de l’activitat sinàptica i la contracció muscular. A continuació es van realitzar les tècniques ELISA, Western Blot, qRT-PCR, immunofluorescència i electrofisiologia. Els resultats van mostrar que tant l’activitat sinàptica com la contracció muscular regulen la maduració i l’activació de la cPKCβI d’una manera complexa i equilibrada a través de la PDK1 y del BDNF/TrkB. Això determinarà la funcionalitat de la sinapsi ja que els resultats també van mostrar que la cPKCβI potencia l’alliberament d’acetilcolina. No obstant, què ocorre en l’esclerosi lateral amiotròfica (ELA) on l’activitat neuromuscular disminueix? Podria l’exercici físic, incrementant l’activitat neuromuscular, prevenir els símptomes? Per abordar això, es van realitzar protocols d’entrenament basats en la natació i el running i es va analitzar la via del BDNF en el múscul plantaris de ratolins SOD1-G93A mitjançant Western Blot. Els resultats van mostrar que en l’ELA, la senyalització del BDNF està alterada però es pot prevenir aquesta afectació de manera diferent en funció de la natura i/o intensitat de l’exercici físic imposat. En conjunt, aquí es mostra un plantejament mecanicista del rol coordinat entre els components pre- i post-sinàptics per preservar la funció sinàptica.
El sistema neuromuscular es un complejo circuito interconectado en el cual las motoneuronas presinápticas y células de Schwann indican al músculo esquelético cómo crecer, diferenciarse y funcionar. Por otra parte, el músculo proporciona señales, incluyendo las neurotrofinas, que regulan la supervivencia y las funciones de las motoneuronas. Concretamente, la neurotrofina BDNF regulada por actividad, al unirse a TrkB, puede activar diferentes vías incluyendo las PKCs. Por consiguiente, es importante conocer cómo opera la actividad pre- y post-sináptica en condiciones fisiológicas para controlar la función neuromuscular a través de la regulación de BDNF y PKCs. Para realizarlo, se estimuló el nervio frénico del diafragma de rata bloqueando o no la contracción, para separar los efectos de la actividad sináptica y de la contracción muscular. A continuación, se realizaron las técnicas ELISA, Western Blot, qRT-PCR, inmunofluorescencia y electrofisiología. Los resultados mostraron que tanto la actividad sináptica como la contracción muscular regulan la maduración y la activación de la cPKCβI de una manera compleja y balanceada a través de PDK1 y BDNF/TrkB. Esto determinará la funcionalidad de la sinapsis porque los resultados también mostraron que cPKCβI potencia la liberación de acetilcolina. Sin embargo, ¿qué ocurre en la esclerosis lateral amiotrófica (ELA) donde la actividad neuromuscular disminuye? ¿Podría el ejercicio físico, incrementando la actividad neuromuscular, prevenir los síntomas? Para abordar esto, se realizaron protocolos de entrenamiento basados en la natación y el running y se analizó la señalización del BDNF en el músculo plantaris de ratones SOD1-G93A mediante Western Blot. Los resultados mostraron que en ELA, la señalización del BDNF está alterada, pero se puede preservar este deterioro de diferente manera en función de la naturaleza y/o intensidad el ejercicio físico impuesto. En conjunto, aquí se muestra un planteamiento mecanicista del rol coordinado entre los componentes pre- y post-sinápticos para preservar la función sináptica.
The neuromuscular system is a complex and interconnected network in which presynaptic motoneurons and Schwann cells “tell” skeletal muscle to grow, to differentiate and how they should function. Conversely, skeletal muscle provides signals, including neurotrophins, that regulates the survival and function of motoneurons during development, maintenance and/or injury. Neurotrophins as BDNF, are regulated by activity and binding to TrkB triggers different pathways that impact on NMJ function, for example activating presynaptic PKCs. Thus, it is important to address how operates pre- and postsynaptic activities in physiological conditions to balance neuromuscular functionality through regulation of BDNF and PKC signalling. To address that, we stimulated the phrenic nerve of rat diaphragms with or without contraction to differentiate the effects of synaptic activity from that of muscle contraction. Then, we performed ELISA, Western Blot, qRT-PCR, immunofluorescence and electrophysiological techniques. Results showed that both synaptic activity and muscle contraction regulate cPKCβI maturation and activation in a complex and balanced way through PDK1 and BDNF/TrkB signalling. This regulation will determine NMJ functionality since our results also demonstrated that cPKCβI is directly involved in neurotransmission enhancing ACh release. However, what happens in a pathological context such us Amyotrophic lateral sclerosis (ALS) where neuromuscular activity is decreased? Could therapies as physical exercise, increasing activity, prevent the symptoms of ALS? To address that, we performed running and swimming-based training protocols to analyse the BDNF signalling in the plantaris muscle of SOD1-G93A mice by Western Blot. Results showed that in ALS disease where there is a loss of the connection between nerve and muscle, BDNF signalling is impaired but could be prevented in a different way depending on the nature and the intensity of the physical exercise imposed. Altogether, these results provide a mechanistic insight into the coordinated role of pre- and postsynaptic components to accurately preserve NMJ function.
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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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Books on the topic "Amyotrophic lateral sclerosis – Pathophysiology"

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

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

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1941-, Smith Richard Alan, ed. Handbook of amyotrophic lateral sclerosis. New York: Dekker, 1992.

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Motor neurone diseases: Amyotrophic lateral sclerosis. London: Chapman & Hall, 1995.

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Hiroshi, Mitsumoto, ed. Amyotrophic lateral sclerosis: A guide for patients and families. 3rd ed. New York, NY: Demos Health, 2009.

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Behind those eyes: Our journey with ALS. Renfrew, Ont: General Store Publishing House, 2013.

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Respiratory management of ALS: Amyotrophic lateral sclerosis. Sudbury, Mass: Jones and Bartlett, 2009.

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

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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 – Pathophysiology"

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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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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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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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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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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 – Pathophysiology"

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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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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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