Relevant bibliographies by topics / Amyotrophic lateral sclerosis – Treatment – Australia

Academic literature on the topic 'Amyotrophic lateral sclerosis – Treatment – Australia'

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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 – Treatment – Australia"

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Urbi, Berzenn, Simon Broadley, Richard Bedlack, Ethan Russo, and Arman Sabet. "Study protocol for a randomised, double-blind, placebo-controlled study evaluating the Efficacy of cannabis-based Medicine Extract in slowing the disease pRogression of Amyotrophic Lateral sclerosis or motor neurone Disease: the EMERALD trial." BMJ Open 9, no. 11 (November 2019): e029449. http://dx.doi.org/10.1136/bmjopen-2019-029449.

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IntroductionAmyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder with no known cure and with an average life expectancy of 3–5 years post diagnosis. The use of complementary medicine such as medicinal cannabis in search for a potential treatment or cure is common in ALS. Preclinical studies have demonstrated the efficacy of cannabinoids in extending the survival and slowing of disease progression in animal models with ALS. There are anecdotal reports of cannabis slowing disease progression in persons with ALS (pALS) and that cannabis alleviated the symptoms of spasticity and pain. However, a clinical trial in pALS with these objectives has not been conducted.Methods and analysisThe Efficacy of cannabis-based Medicine Extract in slowing the disease pRogression of Amyotrophic Lateral sclerosis or motor neurone Disease trial is a randomised, double-blind, placebo-controlled cannabis trial in pALS conducted at the Gold Coast University Hospital, Australia. The investigational product will be a cannabis-based medicine extract (CBME) supplied by CannTrust Inc., Canada, with a high-cannabidiol-low-tetrahydrocannabinol concentration. A total of 30 pALS with probable or definite ALS diagnosis based on the El Escorial criteria, with a symptom duration of <2 years, age between 25 and 75years and with at least 70% forced vital capacity (FVC) will be treated for 6 months. The primary objective of the study is to evaluate the efficacy of CBME compared with placebo in slowing the disease progression measured by differences in mean ALS Functional Rating Scale-Revised and FVC score between the groups at the end of treatment. The secondary objectives are to evaluate the safety and tolerability of CBME by summarising adverse events, the effects of CBME on spasticity, pain, weight loss and quality of life assessed by the differences in mean Numeric Rating Scale for spasticity and Numeric Rating Scale for pain, percentage of total weight loss and ALS specific quality of life-Revised questionnaire.Ethics and disseminationThe study has been approved by the local Institutional Review Board. The results of this study will be published in a peer-reviewed journal.Trial registration numberNCT03690791
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Vucic, Steve, Matthew C. Kiernan, Parvathi Menon, William Huynh, Austin Rynders, Karen S. Ho, Robert Glanzman, and Michael T. Hotchkin. "Study protocol of RESCUE-ALS: A Phase 2, randomised, double-blind, placebo-controlled study in early symptomatic amyotrophic lateral sclerosis patients to assess bioenergetic catalysis with CNM-Au8 as a mechanism to slow disease progression." BMJ Open 11, no. 1 (January 2021): e041479. http://dx.doi.org/10.1136/bmjopen-2020-041479.

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IntroductionAmyotrophic lateral sclerosis (ALS) is an adult-onset, progressive and universally fatal neurodegenerative disorder. In Europe, Australia and Canada, riluzole is the only approved therapeutic agent for the treatment of ALS, while in the USA, riluzole and edaravone have been approved by the Food and Drug Administration (FDA) . Neither riluzole nor edaravone treatment has resulted in substantial disease-modifying effects. There is, therefore, an urgent need for drugs that result in safe and effective treatment. Here, we present the design and rationale for the phase 2 RESCUE-ALS study, investigating the novel nanocatalytic drug, CNM-Au8, as a therapeutic intervention that enhances the metabolic and energetic capacity of motor neurones. CNM-Au8 is an aqueous suspension of clean-surfaced, faceted gold nanocrystals that have extraordinary catalytic capabilities, that enhance efficiencies of key metabolic reactions, while simultaneously reducing levels of reactive oxygen species. This trial utilises a novel design by employing motor unit number index (MUNIX), measured by electromyography, as a quantitative measure of lower motor neurone loss and as an early marker of ALS disease progression.Methods and analysisThis is a multicentre, randomised, double-blind, parallel group, placebo-controlled study of the efficacy, safety, pharmacokinetics and pharmacodynamics of CNM-Au8 in ALS patients. Patients will be randomised 1:1 to either receive 30 mg of CNM-Au8 once daily or matching placebo over a 36-week double-blind treatment period. Efficacy will be assessed as the change in motor neurone loss as measured by electromyography (eg, MUNIX, the primary endpoint; and secondary endpoints including MScanFit, motor unit size index, Split Hand Index, Neurophysiology Index). Exploratory endpoints include standard clinical and quality of life assessments.Ethics and disseminationRESCUE-ALS was approved by the Western Sydney Local Health District Human Research Ethics Committee (Ethics Ref: 2019/ETH12107). Results of the study will be submitted for publication in a peer-reviewed journal.Trial registration numberNCT04098406
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Eisen, Andrew, and Markus Weber. "Treatment of Amyotrophic Lateral Sclerosis." Drugs & Aging 14, no. 3 (1999): 173–96. http://dx.doi.org/10.2165/00002512-199914030-00003.

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Färkkilä, M. A., M. V. Iivanainen, L. Bergström, R. O. Roine, R. Laaksonen, M.-L. Niemi, and K. Cantell. "Interferon treatment in amyotrophic lateral sclerosis." Acta Neurologica Scandinavica 69, S98 (January 29, 2009): 184–85. http://dx.doi.org/10.1111/j.1600-0404.1984.tb02429.x.

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Mandrioli, Jessica, Roberto D’Amico, Elisabetta Zucchi, Annalisa Gessani, Nicola Fini, Antonio Fasano, Claudia Caponnetto, et al. "Rapamycin treatment for amyotrophic lateral sclerosis." Medicine 97, no. 24 (June 2018): e11119. http://dx.doi.org/10.1097/md.0000000000011119.

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Simpson, Ericka P. "Antioxidant treatment for amyotrophic lateral sclerosis." Lancet Neurology 4, no. 5 (May 2005): 266. http://dx.doi.org/10.1016/s1474-4422(05)70052-1.

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Benditt, Joshua O., and Louis Boitano. "Respiratory Treatment of Amyotrophic Lateral Sclerosis." Physical Medicine and Rehabilitation Clinics of North America 19, no. 3 (August 2008): 559–72. http://dx.doi.org/10.1016/j.pmr.2008.02.007.

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Cwik, Valerie A. "Pharmaceutical Treatment of Amyotrophic Lateral Sclerosis." Perspectives on Neurophysiology and Neurogenic Speech and Language Disorders 10, no. 2 (June 2000): 11–16. http://dx.doi.org/10.1044/nnsld10.2.11.

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Li, Lian, Jie Liu, and Hua She. "Targeting Macrophage for the Treatment of Amyotrophic Lateral Sclerosis." CNS & Neurological Disorders - Drug Targets 18, no. 5 (September 23, 2019): 366–71. http://dx.doi.org/10.2174/1871527318666190409103831.

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Background & Objective: Amyotrophic lateral sclerosis is a progressive neurodegenerative disease that specifically affects motor neurons in the brain and in the spinal cord. Patients with amyotrophic lateral sclerosis usually die from respiratory failure within 3 to 5 years from when the symptoms first appear. Currently, there is no cure for amyotrophic lateral sclerosis. Accumulating evidence suggests that dismantling of neuromuscular junction is an early event in the pathogenesis of amyotrophic lateral sclerosis. Conclusion: It is starting to realized that macrophage malfunction contributes to the disruption of neuromuscular junction. Modulation of macrophage activation states may stabilize neuromuscular junction and provide protection against motor neuron degeneration in amyotrophic lateral sclerosis.
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Marcus, Revital. "What Is Amyotrophic Lateral Sclerosis?" JAMA 328, no. 24 (December 27, 2022): 2466. http://dx.doi.org/10.1001/jama.2022.19305.

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Dissertations / Theses on the topic "Amyotrophic lateral sclerosis – Treatment – Australia"

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Mòdol, Caballero Guillem. "Gene therapy targeting neuregulins for the treatment of amyotrophic lateral sclerosis." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/667869.

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L’esclerosi lateral amiotròfica (ELA) és una malaltia neurodegenerativa devastadora sense cap tractament efectiu disponible. Els mecanismes moleculars involucrats en la mort de les motoneurones (MN) són complexos i inclouen nombroses disfuncions d’aquestes, on les cèl·lules del voltant com els astròcits i la micròglia hi poden contribuir. La Neuregulina 1 (NRG1) és un factor neurotròfic expressat en les MNs i les unions neuromusculars que ajuda en el desenvolupament neuromuscular i axonal i en el seu manteniment. Estudis recens suggereixen un rol crucial de la NRG1 i dels seus receptors ErbB en l’ELA, particularment per la isoforma I (NRG1-I) en el procés de reinnervació colateral, i per la isoforma III (NRG1-III) en la preservació de les MNs, obrint un nou camp per desenvolupar noves teràpies per l’ELA. Tanmateix, per clarificar el rol de la via NRG1-ErbB en la supervivència de les MNs és necessari fer més estudis i així provar la seva eficàcia terapèutica. En la present tesis, hem avaluat l’efecte terapèutic de la sobreexpressió de la NRG1 en el sistema nerviós central i perifèric. D’aquesta manera, primer van caracteritzar el rol de la NRG1 exògena utilitzant un model in vitro de cultius organotípics de medul·la espinal subjectes a una excitotoxicitat crònica causada per l’àcid DL-threo-β-hydroxaspàrtic. Els nostres resultats mostren que l’addició en el medi de la NRG1 recombinant humana (rhNRG1) va incrementar significativament la supervivència de les MNs a través de l’activació dels receptors ErbB. Aquest efecte va ser bloquejat quan vam afegir el lapatinib, un inhibidor dels ErbB. El tractament amb la rhNRG1 també va reduir la reactivitat microglial superant els efectes causats per l’excitotoxicitat, i va activar la via de supervivència PI3K/AKT, a més de restaurar el flux autofàgic normal en el cultiu. A més a més l’addició de la rhNRG1 al medi va promoure el creixement neurític motor i sensorial. A continuació vàrem decidir d’utilitzar teràpies gèniques basades en vectors adeno-associats per sobreexpressar la NRG1-I en el múscul esquelètic, i la NRG1-III en la medul·la espinal per preservar les MNs en un model in vivo d’ELA, els ratolins SOD1G93A. Els resultats obtinguts van indicar que ambdues teràpies gèniques van ser capaces de preservar la funció neuromuscular dels músculs de les extremitats, van millorar la locomoció, van incrementar el nombre de MNs supervivents, i van reduir la reactivitat astrocitària i microglial en les femelles SOD1G93A tractades a l’estadi final de la malaltia. A més a més, en la medul·la espinal l’eix NRG1-III/ErbB4 regula l’excitabilitat de la MN a través del transportador KCC2 i redueix l’expressió del marcador de vulnerabilitat de MN MMP-9. La NRG1-I expressada en el múscul esquelètic va senyalitzar amb els receptors ErbB2 i 3 presents en les cèl·lules de Schwann terminals, per promoure reinnervació axonal. Malgrat això, quan vàrem combinar ambdues teràpies gèniques no vam trobar un efecte sinèrgic. Conjuntament, els nostres resultats indiquen que les isoformes de la NRG1 juguen un rol important en la supervivència de les MN i que la sobreexpressió viral pot ser considerada com una nova teràpia per tractar l’ELA.
Amyotrophic Lateral Sclerosis (ALS) is a devastating neurodegenerative disorder with no effective treatment currently available. The molecular mechanisms that are involved in the motoneuron (MN) death are complex and include several MN dysfunctions, and contribution of surrounding cells such as microglia and astrocytes. Neuregulin 1 (NRG1) is a neurotrophic factor highly expressed in MNs and neuromuscular junctions that supports axonal and neuromuscular development and maintenance. Recent studies have suggested a crucial role for NRG1 and their ErbB receptors in ALS, particularly for isoform I (NRG1-I) in the collateral reinnervation process, and isoform III (NRG1-III) in the preservation of the MNs, opening a new window for developing novel ALS therapies. However, further studies are needed to clarify the role of the NRG1-ErbB pathway on MN survival and to provide the proof of concept of its therapeutical efficacy. In the present thesis we have evaluated the therapeutic effect of NRG1 overexpression in the central and the peripheral nervous system. For this purpose, we first characterized the role of exogenous NRG1 using an in vitro model of spinal cord organotypic cultures (SCOC) subject to chronic excitotoxicity caused by DL-threo-β-hydroxyaspartic acid. Our results revealed that addition of recombinant human NRG1 (rhNRG1) to the medium significantly increased MN survival through the activation of ErbB receptors, which was blocked by addition of lapatinib, an ErbB inhibitor, and reduced microglial reactivity overcoming the excitotoxicity effects. rhNRG1 activated the pro-survival PI3K/AKT pathway and restored the autophagic flux in the spinal cord culture. Furthermore, addition of rhNRG1 to the medium promoted motor and sensory neurite outgrowth. We have then directed gene therapies based on adeno-associated viruses to overexpress NRG1-I in the skeletal muscles, and NRG1-III in the spinal cord to preserve the MNs in the in vivo model of ALS, the SOD1G93A mice. Our results indicate that both gene therapies were able to preserve the neuromuscular function of the hindlimb muscles, improve the locomotor performance, increase the number of surviving MNs and reduce the astrocyte and microglial reactivity in the treated female SOD1G93A mice at the end-stage of the disease. Furthermore, in the spinal cord the NRG1-III/ErbB4 axis regulates MN excitability through the KCC2 transporter and reduces the expression of the MN vulnerability marker MMP-9. NRG1-I expressed in the skeletal muscle signals with ErbB2 and 3 receptors present in terminal Schwann cells to promote axonal reinnervation. However, when we aimed to combine both viral-mediated therapies we did not find a synergic effect. Altogether, our results indicate that NRG1 isoforms play an important role on MN survival and that a viral-mediated overexpression may be considered as a potential novel therapy to treat ALS.
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Kyllo, Hannah Marie, and Hannah Marie Kyllo. "Multifactorial Gene Therapy as a Novel Approach for the Treatment of Mutant Superoxide Dismutase-1 Linked Familial Amyotrophic Lateral Sclerosis." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625029.

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Amyotrophic lateral sclerosis is a rapidly progressing disease characterized by the degeneration and death of upper and lower motor neurons, and it is associated with a lifetime risk of 1 in 1000. The disease not only involves damage to the motor neurons themselves but also to neighboring glial cells. Since the characterization of the disease roughly a century and a half ago, few successes have been seen in the development of a treatment plan that yields viable results and prevents neurodegeneration. The shortcomings of past therapies have been attributed to the narrow focus of treatment plans, targeting a single aspect of the disease pathology. The pathophysiology is complex and multifactorial, integrating aspects such as aberrant reactive oxygen species formation, excitotoxicty, a reduced antioxidant response, and dysfunction of the endoplasmic reticulum and mitochondria. Recent research employing a multifactorial approach to treatment has yielded success in mice engineered with the mutant SOD1 gene, a mutation which mimics the disease progression and pathophysiology seen in ALS patients. Current clinical research for ALS has focused on using gene therapy techniques to introduce therapeutic genes coding functional proteins into affected cells in the hopes of addressing several of the pathological aspects of the neurodegenerative disease.
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Fridh, Katarina, and Sofia Persson. "Att avsluta ventilatorsbehandling för personer med amyotrofisk lateralskleros : en kvalitativ intervjustudie som beskriver sjuksköterskors erfarenheter." Thesis, Sophiahemmet Högskola, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:shh:diva-3416.

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Palliativ vård innebär att förbättra livskvalitet för personer med livshotande kronisk sjukdom och dess närstående. De fyra hörnstenar som den palliativa vården vilar på är symtomkontroll, kommunikation, teamarbete och närståendestöd. Sjuksköterskor inom palliativ vård har till uppgift att tillsammans med teamet förebygga, observera, behandla och lindra symtom för både patient och närstående. Amyotrofisk lateralskleros är en motorneuronsjukdom som påverkar kroppens alla muskler. Nedsatt andningsfunktionen hos personer med ALS leder till hypoventilation vilket kan behandlas med ventilatorstöd med noninvasiv ventilator via näseller helmask och trakeostomiansluten invasiv ventilator. Sjuksköterskan har ett ansvar att stödja personen med ALS att bevara sin autonomi, värdighet och livskvalitet samt stödja närstående som ofta även är vårdare. Behandling för att ersätta livsnödvändiga funktioner, såsom andning, som ges i syfte att bevara liv vid ett livshotande tillstånd innebär en livsuppehållande behandling. Rätten att neka behandling är lagstadgad i Sverige likaväl som rätten att avsäga sig pågående behandling. Studiens resultat diskuteras mot Katie Erikssons teorier om vårdlidande. Syftet med studien var att undersöka sjuksköterskors erfarenheter av avslutande av ventilatorbehandling för personer med amyotrofisk lateralskleros inom palliativ vård Metoden som använts var en intervjustudie med kvalitativ ansats. Tio sjuksköterskor intervjuades med avseende på deras erfarenheter av att avsluta ventilatorbehandling. En kvalitativ analys med induktiv ansats användes för att få fram både latent och manifest data. Resultatet presenteras under två teman. I temat att göra resan från oro och rädsla till trygghet beskrivs att sjuksköterskorna inför att avsluta ventilatorbehandling kunde känna rädsla och oro men att avslutet i de allra flesta fall uppfattades ett värdigt avslut där sjuksköterskan lindrade lidande. Vidare presenteras faktorer som kan minska erfarenheten av oro och rädsla. Under detta tema återfinns kategorierna att praktiskt förbereda inför avslut, att stänga av ventilatorbehandling samt förberedelse och bearbetning. I temat att balansera de egna känslorna som uppstår framkommer sjuksköterskans känslor av ansvar och hur de förhöll sig till detta ansvar. I detta tema belyser sjuksköterskorna vad de upplever är vårdens helhetsansvar, att det finns ett informationsansvar samt att de känner ett personligt ansvar mot personen som vill avsluta ventilatorbehandling. Under detta tema finns kategorierna teamarbete på olika nivåer, att förhålla sig till ansvar och målet med vården. Slutsatser som kan dras är bland annat; att närvara vid avslut av livsuppehållande ventilatorbehandling kan skapa känslor av oro och rädsla men förberedelser och planering kan göra erfarenheten positiv. Det finns en trygghet i rutiner och att använda redan befintlig erfarenhet för att sjuksköterskor ska känna sig trygga i avslutssituationen.
Palliative care means to improve quality of life for people with a life-threatening chronic illness and their family. The four cornerstones on which palliative care rests are symptom control, communication, team work and support for family. Nurses in palliative care have the task, together with the palliative team, to prevent, observe, treat and alleviate symptoms for both patient and their family members. The need for palliative care to be adapted for people with neurological disease, which includes amyotrophic lateral sclerosis (ALS), has only been noticed in recent years. For people with ALS, there can be advantages with an early contact with palliative care providers. Nurses in palliative care has a challenge to support the person with ALS in order to preserve autonomy, dignity and quality of life, and to support relatives. Amyotrophic lateral sclerosis is a collective term for several motor neuronal diseases where the most common form is classical amyotrophic lateral sclerosis. Reduced respiratory function in people with ALS lead to hypoventilation, which van be treated with ventilator support. Treatment may be either non-invasive ventilator via nasal or whole mask and with invasive ventilation via tracheostomy. Life-sustaining treatment means to replace vital functions, such as breathing, to preserve life in a life-threatening condition. The right to refuse treatment is statutory in Sweden as well as the right to renounce ongoing treatment. The results of the study are discussed against Katie Eriksson's theories of suffering of care. The aim of the study was to investigate nurses' experiences of withdrawal of ventilator treatment for patients with amyotrophic lateral sclerosis in palliative care. The method used was an interview study with qualitative approach. Ten nurses were interviewed for their experience regarding withdrawal of ventilator treatment. A qualitative analysis with inductive approach was used to obtain both latent and manifest data. The result is presented under two themes. In the theme of making the journey from worry and fear to security, it is described that the nurses before withdrawal of ventilator treatment could feel fear and anxiety, but that in most cases the conclusion was perceived as a worthy termination of treatment where the nurse alleviated suffering. Furthermore, factors are presented that can reduce the experience of concern and fear. Under this theme are the categories to practically prepare for withdrawal, to turn off ventilator treatment and preparation and processing. In the theme of balancing their own feelings that arise, the nurse's feelings of responsibility emerge and how they relate to this responsibility. In this theme, the nurses highlight what they feel is the overall responsibility of caregivers, that there is an information responsibility and that they feel a personal responsibility towards the person who wants to terminate the ventilator treatment. Under this theme are the categories team work at different levels, to relate to responsibility and the aim of the care. Conclusions that can be drawn include; attending withdrawal of life-sustaining ventilator treatment can create feelings of concern and fear, but preparation and planning can make the experience positive. Security can be found in routines and using already existing experience, which can make nurses feel safe in the withdrawal situation.
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Drbal, Abed Alnaser A. A. "Studies on Bioactive Lipid Mediators Involved in Brain Function and Neurodegenerative Disorders. The effect of ¿-3PUFA supplementation and lithium treatment on rat brain sphingomyelin species and endocannabinoids formation; changes in oxysterol profiles in blood of ALS patients and animal models of ALS." Thesis, University of Bradford, 2013. http://hdl.handle.net/10454/6285.

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Lipids are important for structural and physiological functions of neuronal cell membranes. They exhibit a range of biological effects many are bioactive lipid mediators derived from polyunsaturated fatty acids such as sphingolipids, fatty acid ethanolamides (FA-EA) and endocannabinoids (EC). These lipid mediators and oxysterols elicit potent bioactive functions in many physiological and pathological processes of the brain and neuronal tissues. They have been investigated for biomarker discovery of ageing, neuroinflammation and neurodegenerative disorders. The n-3 fatty acids EPA and DPA are thought to exhibit a range of neuroprotective effects many of which are mediated through production of such lipid mediators. The aims of this study were to evaluate the effects of n-3 EPA and n-3 DPA supplementation on RBC membranes and in this way assess dietary compliance and to investigate brain sphingomyelin species of adult and aged rats supplemented with n-3 EPA and n-3 DPA to evaluate the effects and benefits on age-related changes in the brain. Furthermore, to study the effects of lithium on the brain FA-EAs and ECs to further understand the neuroprotective effects of lithium neuroprotective action on neuroinflammation as induced by LPS. Finally to examine if circulating oxysterols are linked to the prevalence of ALS and whether RBC fatty acids are markers of this action in relation to age and disease stages. These analytes were extracted from tissue samples and analysed with GC, LC/ESI-MS/MS and GC-MS. It was found that aged rats exhibited a significant increase in brain AA and decrease in ¿n-3 and ¿n-6 PUFAs when compared to adult animals. The observed increase of brain AA was reversed following n-3 EPA and n-3 DPA supplementation. Sphingomyelin was significantly increased when aged animals were supplemented with n-3 DPA. LPS treatment following lithium supplementation increased LA-EA and ALA-EA, while it decreased DHA-EA. Both oxysterols 24-OH and 27-OH increased in ALS patients and SOD1-mice. Eicosadienoic acid was different in ASL-patients compared to aged SOD1-mice. These studies demonstrated that dietary intake of n-3 EPA and n-3DPA significantly altered RBC fatty acids and sphingolipids in rat brain. They suggest that n-3 DPA can be a potential storage form for EPA, as shown by retro-conversion of n-3 DPA into EPA in erythrocyte membranes, ensuring supply of n-3 EPA. Also, n-3 EPA and n-3 DPA supplementation can contribute to an increase in brain sphingomyelin species with implications for age effects and regulation of brain development. Effects of lithium highlight novel anti-neuroinflammatory treatment pathways. Both 24-hydroxycholesterol and eicosadienoic acid may be used as biomarkers in ALS thereby possibly helping to manage the progressive stages of disease.
Libyan Government
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Drbal, Abed Alnaser Anter Amer. "Studies on bioactive lipid mediators involved in brain function and neurodegenerative disorders : the effect of ω-3PUFA supplementation and lithium treatment on rat brain sphingomyelin species and endocannabinoids formation : changes in oxysterol profiles in blood of ALS patients and animal models of ALS." Thesis, University of Bradford, 2013. http://hdl.handle.net/10454/6285.

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Lipids are important for structural and physiological functions of neuronal cell membranes. They exhibit a range of biological effects many are bioactive lipid mediators derived from polyunsaturated fatty acids such as sphingolipids, fatty acid ethanolamides (FA-EA) and endocannabinoids (EC). These lipid mediators and oxysterols elicit potent bioactive functions in many physiological and pathological processes of the brain and neuronal tissues. They have been investigated for biomarker discovery of ageing, neuroinflammation and neurodegenerative disorders. The n-3 fatty acids EPA and DPA are thought to exhibit a range of neuroprotective effects many of which are mediated through production of such lipid mediators. The aims of this study were to evaluate the effects of n-3 EPA and n-3 DPA supplementation on RBC membranes and in this way assess dietary compliance and to investigate brain sphingomyelin species of adult and aged rats supplemented with n-3 EPA and n-3 DPA to evaluate the effects and benefits on age-related changes in the brain. Furthermore, to study the effects of lithium on the brain FA-EAs and ECs to further understand the neuroprotective effects of lithium neuroprotective action on neuroinflammation as induced by LPS. Finally to examine if circulating oxysterols are linked to the prevalence of ALS and whether RBC fatty acids are markers of this action in relation to age and disease stages. These analytes were extracted from tissue samples and analysed with GC, LC/ESI-MS/MS and GC-MS. It was found that aged rats exhibited a significant increase in brain AA and decrease in Σn-3 and Σn-6 PUFAs when compared to adult animals. The observed increase of brain AA was reversed following n-3 EPA and n-3 DPA supplementation. Sphingomyelin was significantly increased when aged animals were supplemented with n-3 DPA. LPS treatment following lithium supplementation increased LA-EA and ALA-EA, while it decreased DHA-EA. Both oxysterols 24-OH and 27-OH increased in ALS patients and SOD1-mice. Eicosadienoic acid was different in ASL-patients compared to aged SOD1-mice. These studies demonstrated that dietary intake of n-3 EPA and n-3DPA significantly altered RBC fatty acids and sphingolipids in rat brain. They suggest that n-3 DPA can be a potential storage form for EPA, as shown by retro-conversion of n-3 DPA into EPA in erythrocyte membranes, ensuring supply of n-3 EPA. Also, n-3 EPA and n-3 DPA supplementation can contribute to an increase in brain sphingomyelin species with implications for age effects and regulation of brain development. Effects of lithium highlight novel anti-neuroinflammatory treatment pathways. Both 24-hydroxycholesterol and eicosadienoic acid may be used as biomarkers in ALS thereby possibly helping to manage the progressive stages of disease.
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Lind, Anne-Li. "Biomarkers for Better Understanding of the Pathophysiology and Treatment of Chronic Pain : Investigations of Human Biofluids." Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-326180.

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Chronic pain affects 20 % of the global population, causes suffering, is difficult to treat, and constitutes a large economic burden for society. So far, the characterization of molecular mechanisms of chronic pain-like behaviors in animal models has not translated into effective treatments. In this thesis, consisting of five studies, pain patient biofluids were analyzed with modern proteomic methods to identify biomarker candidates that can be used to improve our understanding of the pathophysiology chronic pain and lead to more effective treatments. Paper I is a proof of concept study, where a multiplex solid phase-proximity ligation assay (SP-PLA) was applied to cerebrospinal fluid (CSF) for the first time. CSF reference protein levels and four biomarker candidates for ALS were presented. The investigated proteins were not altered by spinal cord stimulation (SCS) treatment for neuropathic pain. In Paper II, patient CSF was explored by dimethyl and label-free mass spectrometric (MS) proteomic methods. Twelve proteins, known for their roles in neuroprotection, nociceptive signaling, immune regulation, and synaptic plasticity, were identified to be associated with SCS treatment of neuropathic pain. In Paper III, proximity extension assay (PEA) was used to analyze levels of 92 proteins in serum from patients one year after painful disc herniation. Patients with residual pain had significantly higher serum levels of 41 inflammatory proteins. In Paper IV, levels of 55 proteins were analyzed by a 100-plex antibody suspension bead array (ASBA) in CSF samples from two neuropathic pain patient cohorts, one cohort of fibromyalgia patients and two control cohorts. CSF protein profiles consisting of levels of apolipoprotein C1, ectonucleotide pyrophosphatase/phosphodiesterase family member 2, angiotensinogen, prostaglandin-H2 D-isomerase, neurexin-1, superoxide dismutases 1 and 3 were found to be associated with neuropathic pain and fibromyalgia. In Paper V, higher CSF levels of five chemokines and LAPTGF-beta-1were detected in two patient cohorts with neuropathic pain compared with healthy controls. In conclusion, we demonstrate that combining MS proteomic and multiplex antibody-based methods for analysis of patient biofluid samples is a viable approach for discovery of biomarker candidates for the pathophysiology and treatment of chronic pain. Several biomarker candidates possibly reflecting systemic inflammation, lipid metabolism, and neuroinflammation in different pain conditions were identified for further investigation.
Uppsala Berzelii Technology Centre for Neurodiagnostics
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Elias, Ana Catarina Lopes. "Etiology and Treatment of Amyotrophic Lateral Sclerosis - A Systematic Review." Master's thesis, 2018. https://hdl.handle.net/10216/112158.

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Elias, Ana Catarina Lopes. "Etiology and Treatment of Amyotrophic Lateral Sclerosis - A Systematic Review." Dissertação, 2018. https://hdl.handle.net/10216/112158.

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"Cellular approach for the treatment of amyotrophic lateral sclerosis using adult mesenchymal stem cells." Université catholique de Louvain, 2008. http://edoc.bib.ucl.ac.be:81/ETD-db/collection/available/BelnUcetd-12102008-125817/.

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Serra, Catarina Ferreira Mendes. "Use of ipscs for the treatment of neurodegenerative diseases." Master's thesis, 2019. http://hdl.handle.net/10451/43309.

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Trabalho Final de Mestrado Integrado, Ciências Farmacêuticas, Universidade de Lisboa, Faculdade de Farmácia, 2019
As células estaminais, devido ao seu potencial de multi-diferenciação e capacidade auto-replicativa, têm sido, nos últimos anos, alvo de elevada investigação, sendo um campo de crescente conhecimento e novas descobertas. Takahashi e Yamanaka foram os primeiros a derrubar o paradigma das células indiferenciadas, ao descobrirem que fibroblastos, células diferenciadas da pele, poderiam ser revertidas em células estaminais pluripotentes induzidas (iPSCs), permitindo assim a geração de células indiferenciadas a partir de células do próprio doente. Esta notável descoberta permitiu a criação de uma plataforma alternativa para a construção de novos modelos de estudo de doenças, com a possibilidade de testar diferentes estratégias terapêuticas. Com o aumento da esperança média de vida, a população mundial tem vindo a tornar-se mais envelhecida, constituindo um desafio constante para a sociedade. Neste contexto, existe uma crescente incidência de doenças neurodegenerativas, tais como o Alzheimer, o Parkinson e a Esclerose Lateral Amiotrófica, que constituem algumas das mais difíceis doenças de estudar e para as quais é necessário desenvolver novos fármacos. Estas são, atualmente, doenças sem cura, cuja terapêutica é maioritariamente sintomática e pouco dirigida. Desta forma, o progresso científico das iPSCs possibilitou o surgimento de um rumo inovador para a terapêutica destas doenças, proporcionando o desenvolvimento de iPSCs humanas, derivadas de células dos próprios doentes, com capacidade de serem diferenciadas em neurónios motores, neurónios dopaminérgicos, oligodendrócitos, entre outros. As iPSCs constituem, desta forma, uma fonte de células relevantes de doenças, na forma 2D (bidimensional) ou 3D (tridimensional), os chamados organoides, sendo pertinentes para o desenvolvimento do fenótipo característico das patologias, capazes de gerar um modelo de estudo ‘em placa’ fidedigno. Estas células podem ser usadas para estudos de toxicidade, triagem de novos fármacos e ainda, gerar células autólogas importantes para terapêuticas regenerativas. É deste modo esperado que as iPSCs possam ultrapassar o problema da rejeição, ao serem usadas células do próprio doente, possuindo grande potencial como terapêutica de transplantação e correção genética, permitindo produzir células saudáveis passíveis de serem transplantadas. Recentemente, o número de ensaios clínicos com recurso às iPSCs tem vindo a aumentar, comprovando a evolução constante que esta tecnologia tem apresentado, desde o momento da sua descoberta. Todavia, para o seu contínuo sucesso, é imprescindível que sejam desvendados os mecanismos moleculares subjacentes à fase de reprogramação aquando da geração das iPSCs, procurando atingir a segurança absoluta desta tecnologia científica. Nesta dissertação serão discutidos os fundamentos das iPSCs e a sua promissora aplicação na área das doenças neurodegenerativas, abordando as vantagens e desafios da sua utilização.
Stem cells, due to their multi-differentiation potential, have been in these last years, a promising and growing field of study. Since Takahashi and Yamanaka’s breakthrough, investigators were granted with means to generate human induced pluripotent stem cells (iPSCs) from patient cells, providing an unparalleled platform for in vitro modelling and development of new therapeutic strategies. The increase of life expectancy leading to a worldwide aging of the population is becoming an ongoing challenge for societies. Adult-uprising of neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS), are among the most difficult human health conditions to model for drug development, lacking any curable treatment, with the present therapies being more focused on relieving the symptoms. The recent progresses in the field of iPSCs have provided a novel route of treatment for neurodegenerative diseases, with the possibility of developing human iPSCs-patient derived, which have successfully differentiated, in vitro, into motor neurons, dopaminergic neurons and oligodendrocytes, among others. This way, iPSCs can be a source of disease-relevant cells, from 2D (two dimensional) to 3D (three dimensional) organoids, suitable for the recapitulation of disease phenotypes, providing an accurate disease model ‘in a dish’. They can be used for toxicity studies, drug screening and even allow for the generation of autologous cells, for cell-replacement therapy. Recently, there has been an emergence of new clinical trials, showing the evolving state that this technology has had since its discovery. Nevertheless, for the continuous success of these experiments it will be critical to uncover the molecular mechanisms underlying the reprogramming events when generating iPSCs, focusing on the safety of this technology. In this essay it is discussed the fundaments of iPSCs technology and their very promising application in the field of neurodegenerative diseases, questioning its advantages and challenges.
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Books on the topic "Amyotrophic lateral sclerosis – Treatment – Australia"

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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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Excellence, National Institute for Clinical. Guidance on the use of Riluzole (Rilutek) for the treatment of Motor Neurone Disease. London: National Institute for Clinical Excellence, 2001.

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Lou Gehrig Disease, ALS or Amyotrophic Lateral Sclerosis explained: ALS symptoms, signs, stages, types, diagnosis, treatment, caregiver tips, aids and what to expect is all covered. [Ireland]: IMB Publishing, 2013.

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Richer, Catherine Balsdon. Occupational therapy practice guidelines for adults with neurodegenerative diseases: Multiple sclerosis, transverse myelitis, and amyotrophic lateral sclerosis. Bethesda, Md: American Occupational Therapy Association, 1999.

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United States. Congress. House. A bill to amend the Social Security Act to waive the 24-month waiting period for Medicare coverage of individuals disabled with amyotrophic lateral sclerosis (ALS), and to provide Medicare coverage of drugs used for treatment of ALS. Washington, D.C: U.S. G.P.O., 1999.

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United States. Congress. Senate. A bill to amend the Social Security Act to waive the 24-month waiting period for Medicare coverage of individuals disabled with amyotrophic lateral sclerosis (ALS), and to provide Medicare coverage of drugs and biologicals used for the treatment of ALS or for the alleviation of symptoms relating to ALS. Washington, D.C: U.S. G.P.O., 1999.

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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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Williams, Brian J. (Brian Jeremy), 1976- and American Academy of Orthopaedic Surgeons, eds. Principles of ALS care. Sudbury, Mass: Jones and Bartlett Publishers, 2011.

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Gulf War exposures: Hearing before the Subcommittee on Health of the Committee on Veterans' Affairs, U.S. House of Representatives, One Hundred Tenth Congress, first session, July 26, 2007. Washington: U.S. G.P.O., 2008.

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Brain disorders sourcebook: Basic consumer health information about acquired and traumatic brain injuries, brain tumors, cerebral palsy and other genetic and congenital brain disorders, infections of the brain, epilepsy, and degenerative neurological disorders such as dementia, huntington disease, and amyotrophic lateral sclerosis (ALS) : along with information on brain structure and function, treatment and rehabilitation options, a glossary of terms related to brain disorders, and a directory of resources for more information. 3rd ed. Detroit, MI: Omnigraphics, 2010.

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Book chapters on the topic "Amyotrophic lateral sclerosis – Treatment – Australia"

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Norris, F. H., R. A. Smith, and E. H. Denys. "The Treatment of Amyotrophic Lateral Sclerosis." In Amyotrophic Lateral Sclerosis, 175–82. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5302-7_29.

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Fallat, R. J., F. H. Norris, D. Holden, K. Kandal, and P. C. Roggero. "Respiratory Monitoring and Treatment: Objective Treatments Using Non-Invasive Measurements." In Amyotrophic Lateral Sclerosis, 191–200. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5302-7_31.

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Stecco, Alessandro, Letizia Mazzini, Mariangela Lombardi, Francesco Fabbiano, Anna Viola, Roberto Cantello, and Alessandro Carriero. "Amyotrophic Lateral Sclerosis Stem Cells Transplant." In Imaging Spine After Treatment, 287–89. Milano: Springer Milan, 2013. http://dx.doi.org/10.1007/978-88-470-5391-5_94.

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Diana, A., and P. Bongioanni. "Glutamate-Based Treatment for Amyotrophic Lateral Sclerosis/Motor Neuron Disease." In Glutamate and Neuropsychiatric Disorders, 359–80. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-87480-3_12.

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McEachin, Zachary T., Anthony Donsante, and Nicholas Boulis. "Gene Therapy for the Treatment of Neurological Disorders: Amyotrophic Lateral Sclerosis." In Gene Therapy for Neurological Disorders, 399–408. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3271-9_28.

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Dutta, Kallol, Vivek Swarup, and Jean-Pierre Julien. "Potential Therapeutic Use of Withania somnifera for Treatment of Amyotrophic Lateral Sclerosis." In Science of Ashwagandha: Preventive and Therapeutic Potentials, 389–415. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-59192-6_19.

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Plaitakis, Andreas. "Altered glutamate metabolism in amyotrophic lateral sclerosis and treatment with branched chain amino acids." In Amino Acids, 379–85. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-011-2262-7_44.

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Pinelli, P., C. Pasetti, L. Mazzini, F. Pisano, and A. Villani. "Motorneuron Sprouting and Spinal Plasticity in Amyotrophic Lateral Sclerosis: The “Window of Opportunity” for a Ganglioside Treatment." In Gangliosides and Neuronal Plasticity, 453–60. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-5309-7_37.

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Osafo, Newman, David Darko Obiri, Oduro Kofi Yeboah, and Prince Amankwah Baffour Minkah. "Amyotrophic Lateral Sclerosis." In Advances in Medical Diagnosis, Treatment, and Care, 322–46. IGI Global, 2019. http://dx.doi.org/10.4018/978-1-5225-5282-6.ch015.

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Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder (ND) that primarily comprises the neurons responsible for controlling voluntary muscle movement. The unique neuropathologic findings include anterior horn cell degeneration producing muscle atrophy or amyotrophy, degeneration, and sclerosis of the corticospinal tracts. It is a common neuromuscular disease worldwide and has been identified in people of all races. There seems to be neither identified risk factors nor family history associated with most of the documented ALS cases. There exists no treatment for ALS that can prevent neither its progression nor reverse its development. However, there are treatments available that can help control symptoms, prevent unnecessary complications, and make living with the disease easier. This chapter extensively discusses this neurodegenerative disorder based on the currently available knowledge on the condition.
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"Nutritional Treatment: Theoretical and Practical Issues." In Amyotrophic Lateral Sclerosis, 753–68. CRC Press, 2005. http://dx.doi.org/10.1201/b14133-36.

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Conference papers on the topic "Amyotrophic lateral sclerosis – Treatment – Australia"

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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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Sohler, Renato Puccioni, Gabriel Pinto Mendonça, Rodrigo Cesar Carvalho Freitas, and José Roberto Ribas. "Effectiveness of riluzole in the treatment of amyotrophic lateral sclerosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.424.

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Background: amyotrophic lateral sclerosis (ALS) is a motor neuron degenerative disease with high mortality and few therapies. One of these is riluzole, inspite of uncertainty effectiveness. Objective: the aim of this study was to evaluate the survival rate associated with the use of this medication in the treatment of ALS. Methods: The study was based on a narrative review of the scientific articles that used randomized controled trials with riluzole for ALS. We selected articles published in english during the period of January 1th, 2000 to December 31th, 2020. The MeSH terms “amyotrophic lateral sclerosis” or “motor neuron disease” and “riluzole” or “rilutek” were used in Pubmed and Lilacs databases. Studies that used only patients with advanced stage ALS were excluded. The t-Student test between sample means was applied to determine the significance of the difference between the survival time (years) of the riluzole and placebo treatment, for a 95% confidence level. Results: through the search, four articles were obtained (Table 1). Conclusion: Data analysis showed that riluzole is only effective in the first year. From the second onward, it does not exceed the results of the placebo.
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Gonçalo, Ana Clara Mota, and Kaline dos Santos Kishishita Castro. "Treatment and main complications of Amyotrophic Lateral Sclerosis: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.520.

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Background: Greek, the word sklerosis means hardening. In medicine, the term sclerosis refers to the stiffening of body tissues - scars. These scars (sclerosis), when located in motor neurons, are signs of Amyotrophic Lateral Sclerosis (ALS), a neurodegenerative disease that affects neurons located in the primary motor cortex, brain stem, spinal cord and pyramidal tract. ALS has no cure and its treatment options are currently limited. Objectives: Review on the major complications of ALS, as well as the therapeutic methods for its treatment. Methods: Study conducted trough articles found on The New English Journal of Medicine, SpringerLink and Scholar Google and dated between 2009 and 2021. Results: ALS is known for the gradual atrophy of the muscle fibers associated with muscle loss, dysarthria and dysphagia complicated by sialorrhea, depending on the condition. All forms of the disease lead to paralysis, which causes the main consequent complication for the early mortality of patients - respiratory failure. The treatment of ALS has only one specific approved drug: riluzole, which decreases motor neuron damage, reducing disease progression and increasing patient survival. New therapeutic methods are being studied, such as treatment with stem cells and STING- induced inflammation, but they remain with limited evidence. Conclusions: ALS still has extremely restricted targeted treatment. There’s evident need for further studies aimed at a greater understanding of therapies with the potential to become effective in delaying the progression of the disease.
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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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Oliveira, Victória Nunes, Mellyssa Cota Elias, Heloiza Castilhoni Belique, Gabriel Lima Martins, Bianca Soares de Sá Peixoto, Luiza Siqueira Barreto de Souza, Millena Silva dos Santos, et al. "Case of aluminium poisoning, with differential diagnosis for amyotrophic lateral sclerosis (als)." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.246.

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Introduction: Essential metals in high quantities can accumulate and reach toxicity. In the CNS, they lead to neurodegeneration, causing movement and cognitive disorders. Case Report: White man, 59 years, sanitation agent, uses PPE irregularly. For 1 year presented progressive speech disorder, paresis, emaciation, dysphonia, tongue atrophy, limbs fasciculations and abnormal reflexes; normal tonus/ sensibility. Bulbar/limb electroneuromyography and serum dosage of metals in contact were requested, revealing muscles denervation, axonal diffuse polyneuropathy with postganglionic injury and elevated seric Aluminum (Al), (35,7ug/L). The management was work leave, Nortriptyline, and dietary supplementation. It evolved with reduction in seric Al (3,3ug/L); the physical examination remained unaltered. The condition stabilized after treatment. Discussion: Al exposure causes oxidative stress/neurotoxicity, leading to neuronal degeneration. Axonal sensorimotor neuropathy, progressive asthenia, emaciation, fasciculations, aphasia, ataxia, tongue atrophy, and organs injuries can be found. In this case, the clinical presentation differs from ALS because of sensibility commitment and postganglionic alteration, compatible with chronic axonal neuropathy. Conclusion: Although ALS is the most common MND, atypical cases need further investigation to diagnose and treat correctly.
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Merchant, Nandan Amol, TK Kavya, Rachana Srinivasa, Praphulla Rao, Prathibha Narayanan, and Savithri Bhat. "Ginsenoside Rg1 Nanophytosome synthesis and their characterization: An initiative towards the treatment of Amyotrophic Lateral Sclerosis." In 2021 IEEE 21st International Conference on Nanotechnology (NANO). IEEE, 2021. http://dx.doi.org/10.1109/nano51122.2021.9514358.

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Costa, Maria Alice Dias da, Danielle Antoniazzi Costa Sousa, Igor Roque de Paula, Marcela Ferreira de Andrade Rangel, and Mariana Asmar Alencar. "Fatigue presence in amiotrophic lateral sclerosis and related clinical and functional aspects." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.481.

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Background: Some symptoms are reported in Amyotrophic Lateral Sclerosis (ALS), such as fatigue, which, despite having an impact on the individual, is still poorly investigated, seeming to have a multifactorial cause and manifesting itself as tiredness. Therefore, it is necessary to investigate this symptom and check the factors associated with this condition. Objective: To investigate the presence of ALS fatigue and the correlated clinical and functional factors. Objectives: 65 people with ALS attended at the Neuromuscular Diseases Clinic of HC / UFMG participated. Demographic, clinical, functional aspects were assessed and the Fatigue Severity Scale (FSS), Functional Scale (ALSRFSR), Quality of Life Questionnaire (ALSAQ-40) and mobility were used. Results: Participants (56.6 ± 11.0 years), about 44.6% (n = 29) presented fatigue. The average intensity was 5.4 ± 1.2 and 10.4% used specific medication. The fatigue group differed from the fatigue group in terms of: gender (male n = 48.3% vs female n = 72.2% (p = 0.049)); the presentation of greater pain intensity (p= 0.026); the worst results in functionality and independence in ALSFRS-R (p =0.004); worse perception of Quality of Life (QOL) (p = 0.000). Fatigue correlated with pain (r = 0.425; p = 0.001), overall muscle strength (r = -0.356; p = 0.004), functionality (r = -0.363; p = 0.003) and QOL (r = 0.481; p = 0.000). Conclusions: Fatigue is a symptom that is correlated with worse functionality and QOL, therefore, it is necessary to investigate this symptom and adopt treatment.
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Tse, Zion Tsz Ho, Alexander Squires, and John Oshinski. "Robot for MRI-Guided ALS Spinal Therapy." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3527.

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Limited treatment options are available for treating Amyotrophic Lateral Sclerosis (ALS) (1). Small animal models have shown promise in halting neurodegeneration associated with ALS where cellular therapeutics are delivered to the ventral horn of the spinal cord (2), although this procedure is invasive and requires multi-level laminectomy and dissection of the dura mater (Fig. 1). We hypothesized that SpinoBof, a robotic needle guidance platform (Fig. 2) could deliver cellular therapeutics to the ventral horn percutaneously under MRI guidance, enhancing upon existing invasive and time-consuming techniques for targeting injection sites.
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Jorge, Frederico Mennucci de Haidar, Angela Genge, Ammar Al Chalabi, Orla Hardiman, Alice Shen, Jennifer Shoskes, and David Weinstein. "MERIDIAN: A phase 2, randomized, double-blind, placebo-controlled, multicenter study to evaluate the efficacy and safety of pegcetacoplan in patients with amyotrophic lateral sclerosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.744.

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Introduction: Inflammation underlies the pathogenesis of numerous neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). In ALS, the complement system has been implicated in the neuropathology of disease and disease progression. Pegcetacoplan, a subcutaneously administered C3 complement inhibitor, is being investigated in hematology, nephrology, and neurology. The current clinical study (NCT04579666) is investigating whether pegcetacoplan can improve survival and function in people diagnosed with apparent sporadic ALS. Objectives and Methodology: Evaluate the efficacy and safety of pegcetacoplan compared to placebo among people diagnosed with ALS in a global, multicenter, randomized, double-blind, placebo-controlled, phase 2 study. Approximately 228 patients diagnosed with apparent sporadic ALS, ≥18 years of age and with an ALS Functional Rating Scale-Revised (ALSFRS-R) score ≥30, slow vital capacity (SVC) ≥60% of the predicted value at screening, and with symptom onset within 72 weeks before screening, are eligible for enrollment. After screening, patients will be randomized 2:1 to treatment groups receiving either subcutaneous pegcetacoplan (1080 mg) or placebo twice weekly for a duration of 52 weeks. The primary efficacy endpoint is the difference in the Combined Assessment of Function and Survival (CAFS) ranked score at 52 weeks after treatment initiation. Additional, secondary functional efficacy (ALSFRS-R, percent SVC, muscle strength, quality of life, and caregiver burden) and safety endpoints will be analyzed at 52 weeks. After the placebo-controlled period, all patients will have the option to receive pegcetacoplan in an open-label period for an additional 52 weeks. Results: This ongoing study is currently enrolling participants. Conclusions: Results of this study will determine the role of complement and C3 inhibition in patients with ALS.
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MARSHANSKY, VLADIMIR. "STRUCTURAL MODEL OF A2-SUBUNIT V-ATPASE AND ITS INTERACTION WITH ARF-GEF CYTOHESIN 2: DRUG DEVELOPMENT FOR THE TREATMENT OF AMYOTROPHIC LATERAL SCLEROSIS (ALS) AND TO CONTROL THE CALORIE RESTRICTION (CR) PATHWAY." In HOMO SAPIENS LIBERATUS. TORUS PRESS, 2020. http://dx.doi.org/10.30826/homosapiens-2020-15.

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Reports on the topic "Amyotrophic lateral sclerosis – Treatment – Australia"

1

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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2

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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3

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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4

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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