Relevant bibliographies by topics / Motoer Neuron Disease

Academic literature on the topic 'Motoer Neuron Disease'

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Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Motoer Neuron Disease"

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Genc, Baris, Oge Gozutok, Nuran Kocak, and P. Hande Ozdinler. "The Timing and Extent of Motor Neuron Vulnerability in ALS Correlates with Accumulation of Misfolded SOD1 Protein in the Cortex and in the Spinal Cord." Cells 9, no. 2 (February 22, 2020): 502. http://dx.doi.org/10.3390/cells9020502.

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Understanding the cellular and molecular basis of selective vulnerability has been challenging, especially for motor neuron diseases. Developing drugs that improve the health of neurons that display selective vulnerability relies on in vivo cell-based models and quantitative readout measures that translate to patient outcome. We initially developed and characterized UCHL1-eGFP mice, in which motor neurons are labeled with eGFP that is stable and long-lasting. By crossing UCHL1-eGFP to amyotrophic lateral sclerosis (ALS) disease models, we generated ALS mouse models with fluorescently labeled motor neurons. Their examination over time began to reveal the cellular basis of selective vulnerability even within the related motor neuron pools. Accumulation of misfolded SOD1 protein both in the corticospinal and spinal motor neurons over time correlated with the timing and extent of degeneration. This further proved simultaneous degeneration of both upper and lower motor neurons, and the requirement to consider both upper and lower motor neuron populations in drug discovery efforts. Demonstration of the direct correlation between misfolded SOD1 accumulation and motor neuron degeneration in both cortex and spinal cord is important for building cell-based assays in vivo. Our report sets the stage for shifting focus from mice to diseased neurons for drug discovery efforts, especially for motor neuron diseases.
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Cork, Linda C. "Hereditary Canine Spinal Muscular Atrophy: An Animal Model of Motor Neuron Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 18, S3 (August 1991): 432–34. http://dx.doi.org/10.1017/s0317167100032613.

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ABSTRACT:Motor neuron diseases selectively produce degeneration and death of motor neurons; the pathogenesis of these disorders and the specificity for this population of neurons are unknown. Hereditary Canine Spinal Muscular Atrophy produces a lower motor neuron disease which is clinically and pathologically similar to human motor neuron disease: motor neurons dysfunction and degenerate. The canine model provides an opportunity to investigate early stages of disease when there are viable motor neurons still present and might be responsive to a variety of therapeutic interventions. The canine disease, like the human disease, is inherited as an autosomal dominant. The extensive canine pedigree of more than 200 characterized individuals permits genetic analysis using syntenic linkage techniques which may identify a marker for the canine trait and provide insights into homologous regions for study in human kindreds.
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Dr.U.J.JanI, Dr U. J. JanI, Dr Ashwin Patil, Dr Mitesh J. Makawana, Dr KalpeshH Patel, Dr Dignesh Vasava, and Dr TejasChaudhari Dr.TejasChaudhari. "Madras Variant Motor Neuron Disease - A Rare Presentation." International Journal of Scientific Research 3, no. 2 (June 1, 2012): 355–56. http://dx.doi.org/10.15373/22778179/feb2014/114.

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Souza, Paulo Victor Sgobbi de, Wladimir Bocca Vieira de Rezende Pinto, Flávio Moura Rezende Filho, and Acary Souza Bulle Oliveira. "Far beyond the motor neuron: the role of glial cells in amyotrophic lateral sclerosis." Arquivos de Neuro-Psiquiatria 74, no. 10 (October 2016): 849–54. http://dx.doi.org/10.1590/0004-282x20160117.

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ABSTRACT Motor neuron disease is one of the major groups of neurodegenerative diseases, mainly represented by amyotrophic lateral sclerosis. Despite wide genetic and biochemical data regarding its pathophysiological mechanisms, motor neuron disease develops under a complex network of mechanisms not restricted to the unique functions of the alpha motor neurons but which actually involve diverse functions of glial cell interaction. This review aims to expose some of the leading roles of glial cells in the physiological mechanisms of neuron-glial cell interactions and the mechanisms related to motor neuron survival linked to glial cell functions.
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Shannon, P., D. Chitayat, K. Chong, C. Dunham, and C. Fallet-Bianco. "Motor neuron disease presenting with fetal akinesia." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, S1 (May 2018): S4. http://dx.doi.org/10.1017/cjn.2018.44.

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By contrast to infantile spinal muscular atrophy, which usually links to deletions in the SMN genes, fetal onset motor neuron disease is poorly reported. We collected a series of twelve cases of fetal arthrogryposis (16-31 weeks gestational age) with fetal motor neuron disease and excluded infectious diseases, lysosomal storage disease and neuroaxonal dystrophy. Of these twelve, 3 were thought to be ischemic in nature with microvascular alterations and systemic or central nervous system ischemic injury. The remaining 9 all displayed marked reduction in anterior horn motor neurons. Of these 9, four demonstrated mineralised neurons, four demonstrated either neuronal loss or cavitation in the globus pallidus, and in two, degenerating neurons were detectable in the brainstem or globus pallidus. Specific sequencing of SMN1 was performed in 6 of 9 and was reported as normal. Whole exome sequencing was performed in 4 without definitive diagnosis. We conclude that fetal motor neuron disease can be distinguished from ischemic injury, is morphologically heterogeneous, may affect the globus pallidus and is rarely linked to SMN1 mutations.
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Karpe, Yashashree, Zhenyu Chen, and Xue-Jun Li. "Stem Cell Models and Gene Targeting for Human Motor Neuron Diseases." Pharmaceuticals 14, no. 6 (June 12, 2021): 565. http://dx.doi.org/10.3390/ph14060565.

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Motor neurons are large projection neurons classified into upper and lower motor neurons responsible for controlling the movement of muscles. Degeneration of motor neurons results in progressive muscle weakness, which underlies several debilitating neurological disorders including amyotrophic lateral sclerosis (ALS), hereditary spastic paraplegias (HSP), and spinal muscular atrophy (SMA). With the development of induced pluripotent stem cell (iPSC) technology, human iPSCs can be derived from patients and further differentiated into motor neurons. Motor neuron disease models can also be generated by genetically modifying human pluripotent stem cells. The efficiency of gene targeting in human cells had been very low, but is greatly improved with recent gene editing technologies such as zinc-finger nucleases (ZFN), transcription activator-like effector nucleases (TALEN), and CRISPR-Cas9. The combination of human stem cell-based models and gene editing tools provides unique paradigms to dissect pathogenic mechanisms and to explore therapeutics for these devastating diseases. Owing to the critical role of several genes in the etiology of motor neuron diseases, targeted gene therapies have been developed, including antisense oligonucleotides, viral-based gene delivery, and in situ gene editing. This review summarizes recent advancements in these areas and discusses future challenges toward the development of transformative medicines for motor neuron diseases.
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Rubinowicz-Zasada, Maja, Aneta Orczyk, Marek Orczyk, and Jarosław Pasek. "Боковой амиотрофический склероз – болезнь двигательных нейронов. Клинический случай." Paediatrics & Family Medicine 2, no. 1 (March 31, 2015): 109–16. http://dx.doi.org/10.15557/pfm.2015.0011.

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Coppedè, Fabio. "An Overview of DNA Repair in Amyotrophic Lateral Sclerosis." Scientific World JOURNAL 11 (2011): 1679–91. http://dx.doi.org/10.1100/2011/853474.

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Amyotrophic lateral sclerosis (ALS), also known as motor neuron disease (MND), is an adult onset neurodegenerative disorder characterised by the degeneration of cortical and spinal cord motor neurons, resulting in progressive muscular weakness and death. Increasing evidence supports mitochondrial dysfunction and oxidative DNA damage in ALS motor neurons. Several DNA repair enzymes are activated following DNA damage to restore genome integrity, and impairments in DNA repair capabilities could contribute to motor neuron degeneration. After a brief description of the evidence of DNA damage in ALS, this paper focuses on the available data on DNA repair activity in ALS neuronal tissue and disease animal models. Moreover, biochemical and genetic data on DNA repair in ALS are discussed in light of similar findings in other neurodegenerative diseases.
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Ozyurt, Tunch, and Mukesh Gautam. "Differential Epigenetic Signature of Corticospinal Motor Neurons in ALS." Brain Sciences 11, no. 6 (June 7, 2021): 754. http://dx.doi.org/10.3390/brainsci11060754.

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Corticospinal motor neurons (CSMN) are an indispensable neuron population for the motor neuron circuitry. They are excitatory projection neurons, which collect information from different regions of the brain and transmit it to spinal cord targets, initiating and controlling motor function. CSMN degeneration is pronounced cellular event in motor neurons diseases, such as amyotrophic lateral sclerosis (ALS). Genetic mutations contribute to only about ten percent of ALS. Thus understanding the involvement of other factors, such as epigenetic controls, is immensely valuable. Here, we investigated epigenomic signature of CSMN that become diseased due to misfolded SOD1 toxicity and TDP-43 pathology, by performing quantitative analysis of 5-methylcytosine (5mC) and 5-hydroxymethycytosine (5hmC) expression profiles during end-stage of the disease in hSOD1G93A, and prpTDP-43A315T mice. Our analysis revealed that expression of 5mC was specifically reduced in CSMN of both hSOD1G93A and prpTDP-43A315T mice. However, 5hmC expression was increased in the CSMN that becomes diseased due to misfolded SOD1 and decreased in CSMN that degenerates due to TDP-43 pathology. These results suggest the presence of a distinct difference between different underlying causes. These differential epigenetic events might modulate the expression profiles of select genes, and ultimately contribute to the different paths that lead to CSMN vulnerability in ALS.
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Oh, Seong-il, Jin-Sung Park, Jung-Joon Sung, and Seung Hyun Kim. "Clinical Scales Used in Motor Neuron Disease." Journal of the Korean Neurological Association 39, no. 2 Suppl (May 1, 2021): 77–86. http://dx.doi.org/10.17340/jkna.2021.2.22.

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Motor neuron diseases (MND) are heterogeneous spectra of disorders that that primarily affect the motor neurons (MN) resulting in motor nerve and muscle degeneration. The pathophysiological mechanisms of MN cell death are known to be combined with disturbance of proteostasis, ribonucleostasis and exaggerated neuro-inflammation. Amyotrophic lateral sclerosis is the prototypic disease of MND followed by spinal and bulbar muscular atrophy, spinal muscular atrophy, benign focal amyotrophy and other various diseases. Although diverse spectra of these diseases share common symptoms, significant differences are known in their clinical manifestations and their clinical progression. With increasing number of new clinical trials, the importance of selecting appropriate clinical scales for the monitoring of clinical progression in different types of MNDs should be emphasized. The purpose of this review is to illustrate different types of clinical scales and demonstrate how to utilize these in the clinical research field with consensus. With these efforts, we hope to be ready to understand different kinds of clinical scales in MND in participating global standard clinical trials.
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Dissertations / Theses on the topic "Motoer Neuron Disease"

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Parton, Matthew James. "Disease-modifying factors in motor neuron disease." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289882.

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Martin, Joanne Elizabeth. "Cellular pathology of the lower motor neuron in motor neuron disease." Thesis, Queen Mary, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266426.

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Kwok, Alice. "Unfolded protein responses in models of Motor Neuron Disease." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:2f3efba7-dce1-4521-bda6-4db8ee81094d.

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Motor neuron disorders are a heterogeneous group of diseases characterized by the selective degeneration of motor neurons leading to muscle wasting and atrophy. Amyotrophic Lateral Sclerosis (ALS) is the most common amongst these disorders and is characterized by the selective loss of both upper and lower motor neurons in the brain and spinal cord. 20% of familial cases of ALS are caused by mutations in the Cu, Zn-superoxide dismutase gene (SOD1), a ubiquitously expressed enzyme responsible for scavenging superoxide radicals. The exact mechanisms underlying mutant SOD1-mediated neurotoxicity are unknown. Misfolded mutant SOD1 accumulates in the cytosol and mitochondrial intermembrane space (IMS) indicating the involvement of unfolded protein responses in ALS pathogenesis. Unfolded protein responses (UPRs) are complex signal transduction cascades which detect perturbations in protein folding and couple them to the expression of protein quality control machinery thereby allowing individual compartments to adapt to stress. In the cytosol, this study has shown that HspB8 was upregulated by SOD1 mutants, where it induced the clearance of aggregates by macroautophagy. This is a protective mechanism, as overexpression of HspB8 suppressed mutant-SOD1 mediated toxicity. In contrast, HspB8 mutants were impaired in macroautophagy and are toxic to NSC-34 cells. The mechanisms for the IMS-UPR have not been previously identified. To address this issue, a model for the accumulation of misfolded mutant SOD1 within the IMS was created and candidate proteins involved in protein quality control within the IMS were explored at the transcriptional level and at the level of protein expression. Preliminary results revealed some possible candidates that may have a role in the adaptation to mitochondrial stress. Interestingly, increased mitophagy was also found in IMS-G93A expressing cells, advocating the central role of macroautophagy in eliminating protein aggregates and damaged mitochondria in SOD1-FALS.
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Simoes, Fabio Andre Amaral Lopes. "Cytoskeleton and molecular motors in the causation of motor neuron diseases." Thesis, University of Brighton, 2018. https://research.brighton.ac.uk/en/studentTheses/2629bd8d-bbba-4360-9ba2-d77733e431ad.

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Amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy with lower extremity predominance (SMA-LED) are motor neuron diseases defined by the loss of motor neurons. RNA metabolism and molecular transport have both become increasingly implicated in the pathogenesis of motor neuron diseases. As such, this thesis explores the role of TAR-DNA binding protein 43 (TDP-43) in the regulation of peripherin expression in ALS, and the molecular consequences of mutations in DYNC1H1, a component of the cytoplasmic dynein motor complex, in SMA-LED. TDP-43 is a DNA/RNA binding protein implicated in ALS pathogenesis. Recent evidence suggests that TDP-43 regulates peripherin, an ALS associated intermediate filament protein. Here, analysis of peripherin in the lumbar spinal cord of TDP-43+/F210I mice revealed a significant increase in the levels of Per-45, a shift towards an increase in Per-58 in the Triton X-100 soluble fraction that did not reach statistical significance, and an increase in an isoform of 50 kDa in the insoluble fraction. These changes in the expression of peripherin in TDP-43+/F210I mice may indicate a regulatory role for TDP-43 in peripherin expression, which could contribute to ALS pathology. Furthermore, there is evidence that defects in neurodevelopment are present in SMA-LED. Analysis of paxillin, a key focal adhesion protein in mouse embryonic fibroblasts from the Legs at odd angles (Loa) model of SMA-LED was performed, which indicated a reduction in its expression which may underpin the previously reported migration phenotypes in these cells. This data provides further evidence that SMA-LED may be a neurodevelopmental disorder. Furthermore, analysis revealed that the Golgi apparatus in DYNC1H1+/D338N patient fibroblasts was significantly condensed, while in BICD2+/I189F fibroblasts there was a decrease in localisation of dynein to the Golgi. The lack of dynein at the Golgi in BICD2+/I189F fibroblasts indicates that BICD2 may be necessary for the recruitment of the molecular motor to the organelle. These Golgi phenotypes may also contribute to impaired migration in disease. Importantly, analysis of DYNC1H1+/D338N patient fibroblasts and mouse embryonic fibroblasts (MEFs) from the Loa mouse strain showed a significant decrease in α-tubulin acetylation, a phenotype previously seen in another DYNC1H1 substitution. In conclusion, these data support previous data which suggested that peripherin expression is altered in the context of TDP-43 mutations, potentially contributing to ALS pathology. Additionally, Golgi phenotypes were found in both DYNC1H1+/D338N and BICD2+/I189F fibroblasts with potential consequences for cellular migration. Finally, decreased microtubule acetylation may be a common factor in SMA-LED linked with DYNC1H1 mutations. The conserved nature of this phenotype could indicate a potential target for therapeutics.
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Christou, Yiota Apostolou. "Generation of motor neurons from embryonic stem cells : application in studies of the motor neuron disease mechanism." Thesis, University of Sheffield, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505426.

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Embryonic stem cells are pluripotent cells with the potential to differentiate into any cell type in the presence of appropriate stimulatory factors and environmental cues. Their broad developmental potential has led to the proposal that in the future, the use of human embryonic stem cells or their differentiated progeny may be beneficial in regenerative medicine. In particular, a current goal in the field of clinical neurology is to use stem cells in cell-based therapies for motor neuron disease (MND) or amyotrophic lateral ~clerosis. MND is a progressive neurodegenerative disease that specifically affects upper and lower motor neurons and leads ultimately to death from respiratory failure. Stem cellderived motor neurons could conceivably be used to replace the degenerated cells, to provide authentic substrates for drug development and screening and for furthering our understanding of disease mechanisms. However, to reliably and accurately culture motor neurons, the complex pathways by which differentiation occurs in vivo must be understood and reiterated in vitro to direct embryonic stem cells towards motor neurons. This thesis presents the work I have performed on the directed differentiation of embryonic stem cells towards motor neuron fates. I describe the various experimental approaches I took in attempts to produce motor neurons in vitro. My studies reveal that it is possible to deploy the signals used during normal development to direct the differentiation of both human and mouse embryonic stem cells into neural and neuronal cells, including motor neurons. Two major limitations precluded my analysis of pure motor neuron cultures: first, the high concentrations of the ventralising morphogen, SHH, apparently required to direct embryonic stem cells towards motor neuron fates, and second, the difficulties encountered in culturing purified motor neurons. However, using a mixed culture, I obtained evidence that motor neurons and their progenitors fail to survive in medium conditioned by mutant SOD1-G93A astrocytes.
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Bäumer, Dirk. "Functional genetic analysis of motor neuron disease." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:859016f8-5eff-4a8e-bfda-48afb8695646.

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Amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) are the commonest motor neuron diseases of adult- and childhood onset. Alterations of the RNA binding protein TDP-43 are associated with most cases of ALS, while SMA is caused by deletion of the Survival Motor Neuron (SMN1) gene. SMN has been well characterised in its role in the assembly of the cellular machinery that carries out splicing of pre-mRNA, but is thought to have other functions in RNA metabolism unrelated to pre-mRNA splicing. It is conceivable that specific aspects of RNA handling are disrupted in both SMA and ALS. A variety of genetic, molecular and neuropathological approaches were applied to investigate a potential common pathway in these diseases. The spectrum of genetic mutations underlying motor neuron disorders were explored by screening patient DNA. Cell culture and mouse models were used to test the hypothesis that altered pre-mRNA splicing causes motor neuron death. Human neuropathological specimens were examined for changes in proteins involved in RNA metabolism. The results indicate that altered pre-mRNA splicing is a late occurrence in disease and more likely to be a consequence rather than the cause of motor neuron degeneration. However, the notion that RNA metabolism is highly relevant to motor neuron diseases was strengthened by the discovery of mutations in another RNA binding protein, FUS, in cases of ALS without TDP-43 pathology. Overall the findings highlight the need to consider disruption of mRNA transport and regulation of mRNA translation in future motor neuron disease research.
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Sargsyan, Siranush Anna. "Microglial activationas a potential contributor to motor neuron injury in motor neuron disease." Thesis, University of Sheffield, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444237.

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Tennant, Maria Elizabeth. "Axonal transport in motor neurone disease." Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424667.

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Aspin, Jacqueline Patricia. "Immunological studies in motor neurone disease." Thesis, University of Bath, 1986. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376335.

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Gopinath, Sumana. "Finding new genes causing motor neuron diseases." University of Sydney, 2006. http://hdl.handle.net/2123/1624.

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Doctor of Philosophy
Abstract Neurodegenerative disorders are a diverse group of disorders that affect specific subsets of neurons. Motor neuron diseases, neurodegenerative disorders of motor neurons, are seen commonly as sporadic cases and less frequently as familial disease forms. The familial forms show genetic and phenotypic heterogeneity. Clinically motor neuron diseases may be seen as rapidly progressive disorders like amyotrophic lateral sclerosis, ALS or slowly progressive disorders like hereditary motor neuropathies, HMN. The only proven causes for motor neuron diseases are gene mutations that lead to motor neuron degeneration in familial disease forms. Only some of these genes have been identified and have contributed greatly to our understanding of the neurobiology of familial and sporadic disease forms. Identification of additional disease causing genes would help enhance our knowledge of the pathophysiological mechanisms underlying all forms of motor neuron disorders, which would lead to early diagnoses, effective prophylaxis and efficient therapies for these disorders. This study aimed to find gene mutations that cause rapid and slowly progressive familial motor neuron disorders in Australian families and to determine their relevance to sporadic forms of motor neuron disease. The familial forms of ALS show reduced disease penetrance, that is, not all gene mutation carriers manifest the disease. This study examines ALS penetrance in a group of Australian families. The most frequently observed mutations in ALS families are cytosolic superoxide dismutase/SOD1 gene mutations. In a collection of ALS families in our centre, families without the common SOD1 gene mutations were genotyped for other ALS genes and loci and studied using genetic linkage and haplotype analyses. Studies in a large Australian ALS family further confirmed genetic heterogeneity in non-SOD familial ALS, all known autosomal dominant ALS genes and chromosomal loci were excluded as cause of disease in this family. Such families can be studied further to identify additional disease genes and loci mapped in other ALS families. These families represent powerful resources for identification of additional ALS genes. Identifying the pathogenic genes in families with reduced disease penetrance may be more relevant to sporadic forms of disease. dHMN is a chronic neurodegenerative disorder predominantly affecting motor neurons. In a large Australian dHMN family, all the known dHMN genes and chromosomal loci were excluded as cause of disease. A genome wide microsatellite screen was performed in this family and genetic linkage was established to a novel 12.98 Mb locus on chromosome 7q34.2-q36. Candidate genes in this large interval will be screened based on their function and expression profile. Identification of a new dHMN locus provides the basis for future identification of a novel gene involved in motor neuron degeneration. Genes in dHMN have been shown to be pathogenic in ALS and Charcot Marie Tooth syndromes. The new locus for dHMN mapped in this project would lead to identification of a novel dHMN gene, which may elucidate the pathogenesis underlying a wide range of neurodegenerative disorders.
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Books on the topic "Motoer Neuron Disease"

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Talbot, Kevin. Motor neuron disease. Oxford: Oxford University Press, 2008.

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Talbot, Kevin. Motor neuron disease. Oxford: Oxford University Press, 2008.

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Leigh, P. N., and Michael Swash, eds. Motor Neuron Disease. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8.

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David, Oliver. Motor neurone disease. 2nd ed. London: Royal College of General Practitioners, 1994.

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1948-, Hunter Maggie, ed. Motor neurone disease. London: Routledge, 1998.

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Orrell, Richard William. Genetics of motor neuron disease. Manchester: University of Manchester, 1996.

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Talbot, Kevin. Motor neuron disease: A practical manual. Oxford: Oxford University Press, 2010.

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Talbot, Kevin. Motor neuron disease: A practical manual. Oxford: Oxford University Press, 2010.

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Motor neuron disease: A practical manual. Oxford: Oxford University Press, 2010.

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Association, Motor Neurone Disease. Motor neurone disease resource file. Northampton: Motor Neurone Disease Association, 2000.

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Book chapters on the topic "Motoer Neuron Disease"

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Swash, M., and M. S. Schwartz. "Motor Neuron Disease: The Clinical Syndrome." In Motor Neuron Disease, 1–17. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_1.

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Nunn, P. B. "Toxicology of Motor Systems." In Motor Neuron Disease, 201–18. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_10.

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Appel, S. H., J. I. Engelhardt, R. G. Smith, and E. Stefani. "Theories of Causation." In Motor Neuron Disease, 219–40. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_11.

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Martin, J. E. "Neurotrophic Factors and Neurodegeneration." In Motor Neuron Disease, 241–58. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_12.

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Holstege, G. "Somatic Motoneurons and Descending Motor Pathways. Limbic and Non-limbic Components." In Motor Neuron Disease, 259–330. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_13.

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Schwartz, M. S., and M. Swash. "Neurophysiological Changes in Motor Neuron Disease." In Motor Neuron Disease, 331–44. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_14.

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Guiloff, R. J. "Clinical Pharmacology of Motor Neurons." In Motor Neuron Disease, 345–73. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_15.

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Langton Hewer, R. "The Management of Motor Neuron Disease." In Motor Neuron Disease, 375–406. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_16.

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Munsat, T. L., D. Hollander, and L. Finison. "Clinical Trial Methodology." In Motor Neuron Disease, 407–17. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_17.

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Mitsumoto, H. "New Therapeutic Approaches: Rationale and Results." In Motor Neuron Disease, 419–41. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8_18.

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Conference papers on the topic "Motoer Neuron Disease"

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Crawford, Emma, Helen Stone, Ian Cliff, Karen Morrison, Hardev Pall, and Naveed Mustfa. "Hypoxic challenge testing in motor neurone disease." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2296.

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Cooper, Adam P., and Wilson Vallat. "093 CJD and motor neuron disease: a growing association." In ANZAN Annual Scientific Meeting 2021 Abstracts. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/bmjno-2021-anzan.93.

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Cliff, IJ, N. Mustfa, and H. Stone. "P140 Hypoxic challenge testing in motor neurone disease." In British Thoracic Society Winter Meeting 2017, QEII Centre Broad Sanctuary Westminster London SW1P 3EE, 6 to 8 December 2017, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2017. http://dx.doi.org/10.1136/thoraxjnl-2017-210983.282.

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Bai, Qifan, Tianyu Shen, Baoteng Xu, Qian Yu, Huijun Zhang, Chengjie Mao, Chunfeng Liu, and Shouyan Wang. "Quantification of the motor symptoms of Parkinson's disease." In 2017 8th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2017. http://dx.doi.org/10.1109/ner.2017.8008297.

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Aggarwal, Nikita, Jasleen Saini, B. S. Saini, and Savita Gupta. "Different Classification Approaches for Early Detection of Parkinson’s Disease." In International Conference on Women Researchers in Electronics and Computing. AIJR Publisher, 2021. http://dx.doi.org/10.21467/proceedings.114.12.

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Parkinson’s disease is perhaps the most well-known neurodegenerative disorder that mainly occurs due to the loss of dopamine-producing neurons and consists of motor/non-motor symptoms. The progression of the symptoms is often varying from one person to another to the diversity of the disease. The condition causes a huge burden both on those affected, as well as their families. Accurate diagnosis is critical and challenging but still, no specific diagnostic process is available. The computer-aided diagnosis techniques of signalling and imaging processing are very helpful in the prediction and classification of PD. This review gives a brief description of different methods of classification for early detection and also highlights the most profitable research directions by focusing on continuous monitoring patterns of daily activities, interactions, and routine that may provide the data on status changes, clinical management, and controlling self-correction
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Kuznetsov, Andrey V. "Modeling the Effect of Vesicle Traps on Mass Transfer and Traffic Jam Formation in Fast Axonal Transport." In 2010 14th International Heat Transfer Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/ihtc14-22169.

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This paper simulates effects of structural changes in the microtubule (MT) system on mass transfer in an axon. Understanding this process is important for understanding the underlying reasons for many neurodegenerative diseases, such as Alzheimer’s disease. In particular, it is investigated how the degree of polar mismatching in an MT swirl affects organelle trap regions in the axon and inhibiting transport of organelles down the axon. The model is based on modified Smith-Simmons equations governing molecular-motor-assisted transport in neurons. It is established that the structure that develops as a result of a region with disoriented MTs (the MT swirl) consists of two organelle traps, the trap to the left of the swirl region accumulates plus-end oriented organelles and the trap to the right of this region accumulates minus-end oriented organelles. The presence of such a structure is shown to decrease the transport of organelles toward the synapse of the axon. Four cases with a different degree of polar mismatching in the swirl region are investigated; the results are compared with simulations for a healthy axon, in which case organelle traps are absent.
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Kuznetsov, A. V., A. A. Avramenko, and D. G. Blinov. "Simulation of Traffic Jam Formation in Fast Axonal Transport." In ASME 2009 Heat Transfer Summer Conference collocated with the InterPACK09 and 3rd Energy Sustainability Conferences. ASMEDC, 2009. http://dx.doi.org/10.1115/ht2009-88345.

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Many neurodegenerative diseases, such as Alzheimer’s disease, are linked to swellings occurring in long arms of neurons. Many scientists believe that these swellings result from traffic jams caused by the failure of intracellular machinery responsible for fast axonal transport; such traffic jam can plug an axon and prevent the sufficient amount of organelles to be delivered toward the synapse of the axon. Mechanistic explanation of the formation of traffic jams in axons induced by overexpression of tau protein is based on the hypothesis that the traffic jam is caused not by the failure of molecular motors to transport organelles along individual microtubules but rather by the disruption of the microtubule system in an axon, by the formation of a swirl of disoriented microtubules at a certain location in the axon. This paper investigates whether a microtubule swirl itself, without introducing into the model microtubule discontinuities in the traffic jam region, is capable of capturing the traffic jam formation. The answer to this question can provide important insight into the mechanics of the formation of traffic jams in axons.
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Ballard, Emily, Mike Mackie, Samiha Ismail, Reegan Puthussery, Hina Pattani, Joerg Steier, Philip Marino, et al. "Ventilation in Motor Neurone Disease (MND): what happens in practice." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2177.

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McGee, Michael, and Said Shakerin. "Leg Stretcher for Rehabilitation." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-60258.

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To alleviate some of the problems associated with upper motor neuron diseases, passive movement and stretching are often prescribed. However, the patient has to make continual and frequent visits to a physical therapist, which is expensive and inconvenient. Therefore, there is a need for devices by which the patient can self-administer some of the prescribed exercise(s) at home. In this paper, the design of a portable unit for self-administered stretching of thigh muscles is presented.
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Howard, Mark, David Berlowitz, Ian Batchelder, and Chris Smith. "Day Implementation Model For Non-invasive Ventilation In Motor Neurone Disease." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3059.

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