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Relevant bibliographies by topics / Amyotrophic Lateral Sclerosis – therapy

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Dissertations / Theses

Academic literature on the topic 'Amyotrophic Lateral Sclerosis – therapy'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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Dissertations / Theses on the topic "Amyotrophic Lateral Sclerosis – therapy"

1

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 e

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2

Highlander, Morgan Michelle. "Electroceutical Therapy in Amyotrophic Lateral Sclerosis: A Novel Preliminary Study." Wright State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=wright1530099548144113.

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3

Lemoignan, Josée. "Decision-making for assisted ventilation in amyotrophic lateral sclerosis." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101862.

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Amyotrophic lateral sclerosis (ALS) is a progressive neurological disease that leads to respiratory compromise and eventually death within two to five years. Even though people with ALS must make many treatment decisions, none has such a significant impact on quality of life and survival as the one pertaining to assisted ventilation. A qualitative research study was undertaken to elicit factors that are pertinent to this decision-making process. Ten individual, semi-structured interviews were conducted with individuals with ALS. Six main themes emerged from the interviews. These are: meaning o

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4

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

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5

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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6

Nanou, Aikaterini. "Gene therapy approaches to evaluate neuroprotection from oxidation stress in experimental models of amyotrophic lateral sclerosis." Thesis, University of Sheffield, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.575749.

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Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by the loss of upper and lower motor neurons, with no effective treatment to date. Only 5-10% of ALS cases are familial, of which 20% are caused by missense mutations in the gene encoding Cu/Zn superoxide dismutase 1 (SOD I). Although ALS has a multi-factorial aetiology, oxidative stress is hypothesized to be one of the key pathogenic mechanisms. It is thus proposed that manipulation of the expression of anti- oxidant genes may serve as a therapeutic strategy for the protection of motor neurons. It ha

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7

Kim, Soo Hyun. "Gene therapy demonstrates that muscle is not a primary target for non-cell autonomous toxicity in familial ALS." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1164829314.

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8

Luchesi, Karen Fontes 1984. "Dyphagia in amyotrophic lateral sclerosis and in parkinson¿s disease = A disfagia na esclerose lateral amiotrófica e na doença de Parkinson." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311989.

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Orientador: Satoshi Kitamura<br>Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>Made available in DSpace on 2018-08-22T11:47:36Z (GMT). No. of bitstreams: 1 Luchesi_KarenFontes_D.pdf: 2231982 bytes, checksum: 2f5ef1dbfa543808275311de510df643 (MD5) Previous issue date: 2013<br>Resumo: A Doença de Parkinson (DP) é uma das doenças neurodegenerativas mundialmente mais prevalentes. Dentre as doenças do neurônio motor, a Esclerose Lateral Amiotrófica (ELA) é a mais frequente. A qualidade de vida e o prolongamento da expectativa de vida dos sujeitos com doença

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9

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

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Amyotrophic lateral sclerosis (ALS) is a terminal neurodegenerative disease that affects motor neurons causing progressive muscle weakness and respiratory failure. In 2011, the presence of a hexanucleotide repeat expansion within chromosome 9 open reading frame 72(C9ORF72) was identified in ALS patient samples, becoming the major known genetic cause for ALS and frontotemporal dementia (FTD). Carriers of this mutation present reduced levels of C9ORF72 mRNA, RNA foci produced by the aggregating expansion and toxic dipeptides generated through repeat-associated non-ATG translation. These findings

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10

Scarrott, Joseph. "Investigating the specificity of RNAi molecules in human gene therapy for SOD1-linked familial amyotrophic lateral sclerosis." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22558/.

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20% of familial amyotrophic lateral sclerosis (fALS) cases are caused by mutations in the gene encoding the cytosolic protein human Cu/Zn superoxide dismutase 1 (hSOD1). RNA interference (RNAi) technology offers the therapeutic potential for the treatment of SOD-linked fALS by reducing the burden of pathogenic mutant SOD1 protein. Translation of this gene therapy strategy to the clinic requires the development of vectors that are free of significant off-target effects and with reliable biomarkers to determine treatment efficacy, successful target gene reduction, and correct dosing. Using self-

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