Relevant bibliographies by topics / Motor neuron disease

Academic literature on the topic 'Motor neuron disease'

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Published: 4 June 2021
Last updated: 26 July 2024

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Journal articles on the topic "Motor neuron disease"

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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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Kristensen, O., and B. Melgaard. "MOTOR NEURON DISEASE." Acta Neurologica Scandinavica 56, no. 4 (January 29, 2009): 299–308. http://dx.doi.org/10.1111/j.1600-0404.1977.tb01437.x.

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Sonoo, Masahiro. "Motor Neuron Disease." Spinal Surgery 25, no. 3 (2011): 234–41. http://dx.doi.org/10.2531/spinalsurg.25.234.

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Talbot, Kevin. "Motor neuron disease." Medicine 32, no. 11 (November 2004): 105–7. http://dx.doi.org/10.1383/medc.32.11.105.53361.

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Mills, K. R. "Motor neuron disease." Brain 118, no. 4 (1995): 971–82. http://dx.doi.org/10.1093/brain/118.4.971.

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Liveson, Jay. "Motor Neuron Disease." New England Journal of Medicine 334, no. 18 (May 2, 1996): 1203. http://dx.doi.org/10.1056/nejm199605023341818.

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Mitchell, J. D. "Motor neuron disease." Neuromuscular Disorders 6, no. 2 (March 1996): 141. http://dx.doi.org/10.1016/s0960-8966(96)90024-3.

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Leigh, P. N., and K. Ray-Chaudhuri. "Motor neuron disease." Journal of Neurology, Neurosurgery & Psychiatry 57, no. 8 (August 1, 1994): 886–96. http://dx.doi.org/10.1136/jnnp.57.8.886.

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Westarp, M. E., and H. H. Kornhuber. "Motor neuron disease." Journal of Neurology, Neurosurgery & Psychiatry 58, no. 2 (February 1, 1995): 269. http://dx.doi.org/10.1136/jnnp.58.2.269.

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Dimachkie, Mazen M., and Richard J. Barohn. "Motor Neuron Disease." Neurologic Clinics 33, no. 4 (November 2015): i. http://dx.doi.org/10.1016/s0733-8619(15)00090-0.

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Dissertations / Theses on the topic "Motor 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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Williams, David Bruce. "Genetic factors in motor neuron disease." Thesis, The University of Sydney, 1989. https://hdl.handle.net/2123/26235.

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The term motor neuron disease is used by different authors to designate one or more of a wide variety of disorders whose principal common feature is dysfunction of the motor neuron (MN) or anterior horn cell (AHC). In one convention, the term motor neuron disease is used to denote all such disorders, including both infantile- and juvenile-onset forms of spinal muscular atrophy, and corticospinal degenerations in which the upper motor neuron is prominently affected. At other times the term motor neuron disease refers only to the relatively common and presumably more homogeneous condition which is idiopathic, has its onset in late adult life and is almost inevitably fatal. Often the distinction between these two uses is not clearly stated and must be inferred. In another more recent, but not yet universal convention, the term motor neuron disease designates all disorders of the anterior horn cell and associated motor system, and amyotrophic lateral sclerosis (ALS) is used to indicate the commonest disorder. This is also potentially confusing, as by definition the term ALS is the clinical presentation of a patient with combined upper and lower motor neuron signs in either or both of the bulbar and spinal regions. Therefore its use may implicitly exclude patients with the clinical features of progressive bulbar palsy (PBP) (exclusive lower motor neuron involvement in the bulbar region) or progressive muscular atrophy (PMA) (exclusive lower motor neuron involvement in the spinal region, (also called progressive spinal muscular atrophy (PSMA))). Some authors suggest that PMA has a sufficiently different clinical presentation and prognosis to define it is a different disease (Norris et al, 1978). However, there is poor correlation between the clinical and pathological features of clinically defined cases of ALS and PMA (Chou, 1978), the electrophysiological abnormalities are indistinguishable (Hansen and Ballantyne, 1978), and one clinical form may change into another (Friedman and Freedman, 1950). When patients with either pure PMA or pure PBP are examined repeatedly during the course of their illness, they are often found to develop upper motor neuron signs, so exclusive lower motor neuron syndromes confirmed at autopsy are probably quite rare (cf the Mayo Clinic patients in Juergens et al, 1980). Therefore, a reasonable inference is that ALS, PBP and PMA are clinical variants of one disease. By contrast, most authors are cautious to discuss pure upper motor neuron degeneration, or primary lateral sclerosis (PLS), as a separate entity (Stark and Moersch, 1945; Younger et al, 1988). In this thesis, the uncapitalised phrase 'motor neuron diseases' will refer to all disorders where loss or degeneration of the AHC is the principal salient feature. The abbreviation MND/ALS will be this author's term for the idiopathic, adult-onset disease which may have the variety of clinical presentations (ALS, PBP, PMA) described above. The terms MND or ALS will be used alone when they refer to a patient or group of patients described by a specific author, so that then the reference will be to the definition utilised by that author. Clinical presentations will be called the ALS, PMA or PBP 'form' of MND/ALS.
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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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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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Long, Zhe. "Frontotemporal Dementia-Motor Neuron Disease: disease continuum or distinct entity?" Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/23012.

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Frontotemporal dementia-motor neuron disease (FTD-MND) is a rare disease characterised by the simultaneous occurrence of FTD and MND. Clinical, pathological, and genetic investigations have highlighted the association between FTD and MND, but much remains unclear. The experimental studies of this thesis comprehensively and systematically investigate the natural history of cognition and behaviour in FTD-MND and explore whether FTD-MND is distinct from well-recognised FTD phenotypes using clinical, neuropsychological and multimodal neuroimaging analyses. Results arising from two separate studies (Chapters 3 and 4) reveal that the majority of FTD-MND presents with variable combinations of behaviour, language and motor deficits initially, and fulfil FTD-MND diagnosis within 24 months from symptom onset. Heterogenous deficits persist even after meeting FTD-MND diagnostic criteria. Clinical heterogeneity in FTD-MND, highlighted by using a data-driven approach, may reflect variable white matter tract involvement. Language impairment in FTD-MND is highly prevalent, and more mixed than in FTD language phenotypes. The frequency and severity of behavioural and language deficits in FTD-MND lie between that of FTD phenotypes. Over time (Chapter 5), cognition and language deficits progress more rapidly in FTD-MND than bvFTD. Progression in FTD-MND may be driven by left inferior frontal gyrus and anterior temporal lobe involvemeny. Survival in FTD-MND is much shorter than in FTD, despite a similar age at onset. Motor neuron dysfunction may be highly specific for frontotemporal lobar degeneration TAR DNA binding protein 43 kDa (FTLD-TDP, Chapter 6), but the current FTLD-TDP pathological staging scheme may not correlate with clinical progression. These findings demonstrate that FTD-MND is distinct from, rather than simply a later clinical stage of, FTD.
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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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Stephens, Benjamin. "Pathology of spinal interneurons in motor neuron disease." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251759.

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Blackburn, Daniel J. "The role of glial cells in motor neuron disease." Thesis, University of Sheffield, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531123.

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Shum, Carole Yick Lam. "Modelling motor neuron disease using induced pluripotent stem cells." Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/modelling-motor-neuron-disease-using-induced-pluripotent-stem-cells(1686136a-d045-4edc-9439-1028b0ea47db).html.

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Amyotrophic Lateral Sclerosis (ALS) is the most common adult motor neuron disease. The majority of ALS cases are sporadic (SALS), but 10% of patients have a familial form of ALS (FALS). Mutations in Fused in Sarcoma (FUS) occur in approximately 4% of FALS and less than 1% of SALS. A hallmark feature of ALS is the degeneration of upper and lower motor neurons in the brain and spinal cord; however, the mechanism underlying this loss is not known. Studies of degenerative mechanisms have been impeded by the inaccessibility of human neural tissue. A possible solution is to use induced pluripotent stem cells (iPSCs) derived from patients, which may be differentiated into the cell types affected by disease. To test whether patient-specific stem cells can be used to model aspects of ALS pathogenesis, iPSC lines were generated from a patient carrying the pathogenic FUS R521C mutation. FUS iPSCs derived from patient fibroblasts and WT iPSCs derived from fibroblasts from two healthy controls were differentiated into neural progenitors and motor neurons. FUS iPSC-derived neuronal cells recapitulate key aspects of FUSassociated ALS, including mislocalisation of FUS protein, the redistribution of FUS protein into cytoplasmic stress granules, and increased apoptotic cell death. The second study uses this iPSC model to investigate the effects of mutant FUS on dendritic morphology and synaptic regulation. FUS iPSC-derived neurons display abnormal dendritic morphology, such as reduced neurite outgrowth and reduced density of dendritic protrusions. FUS iPSC-derived neurons also show differences in the localisation of synaptic proteins. This study suggests that physiological levels of mutant FUS protein affect the morphology and synaptic structure of human neurons. These studies validate the stem cell approach to disease modelling and provide support for the use of patient-specific stem cells for the study of disease mechanisms.
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Books on the topic "Motor neuron disease"

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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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C, Williams A., ed. Motor neuron disease. London: New York, 1994.

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

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W, Kuncl Ralph, ed. Motor neuron disease. London: W.B. Saunders, 2002.

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

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

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J, Strong Michael, ed. Dementia and motor neuron disease. Abingdon [England]: Informa UK Ltd., 2006.

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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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Book chapters on the topic "Motor neuron disease"

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Rabin, Bruce A., and David R. Borchelt. "Motor Neuron Disease." In Cell Death and Diseases of the Nervous System, 429–43. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-4612-1602-5_20.

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Roy, Bhaskar, and Basil T. Darras. "Motor Neuron Disease." In Pediatric Electromyography, 199–220. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-61361-1_16.

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Sivak, Mark A. "Motor Neuron Disease." In Mount Sinai Expert Guides, 393–402. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118621042.ch35.

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Brooks, Benjamin Rix, Roxanne Depaul, Yan De Tan, Mohammed Sanjak, Robert L. Sufit, and Joanne Robbins. "Motor Neuron Disease." In Foundations of Neurology, 249–81. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1495-0_18.

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Anderson, Janice R. "Motor Neuron Disease." In Atlas of Skeletal Muscle Pathology, 37–43. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4866-2_4.

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Joshua, Abraham M., and Zulkifli Misri. "Motor Neuron Disease." In Physiotherapy for Adult Neurological Conditions, 539–62. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-0209-3_8.

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Oette, Mark, Marvin J. Stone, Hendrik P. N. Scholl, Peter Charbel Issa, Monika Fleckenstein, Steffen Schmitz-Valckenberg, Frank G. Holz, et al. "Motor Neuron Disease." In Encyclopedia of Molecular Mechanisms of Disease, 1351. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8992.

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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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Conference papers on the topic "Motor neuron disease"

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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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Paula, Igor Roque de, Maria Alice Dias da Costa, Danielle Antoniazzi Kirscht Auermann D'Allembert Costa Sousa, Julia Magalhães Waybe Gonçalves, Marcela Ferreira de Andrade Rangel, Kamila Silva de Mattos, and Mariana Asmar Alencar. "Motor neuronic disease starting in the elderly and young adults." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.497.

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Introduction: Motor neuron diseases (MND) are degenerative disorders that affect motor neurons, leading to disability and dependence throughout their course. The onset of symptoms is variable and can occur in adults(A) and elderly(E), however little is known about the characteristics of the disease in different age groups. Objective: To investigate the characteristics and the difference between clinical and functional factors considering the onset of MND in the elderly and young adults. Method: There were 26 young adults and 26 elderly (≥60 years) evaluated, matched by gender and length of disease, treated at HC/UFMG. The following were investigated: demographic and clinical, using specific instruments (ALSFRS-R/BR and ALSAQ-40); fatigue (FSS); manual muscle strength; mobility and balance (SPPB). Analysis was performed descriptive and comparison (student t test, Mann-Whitney or X2), using SPSS, significance level of 0.05. Results: Differences were observed significant as to the place of onset of symptoms (p=0.034), presence of pain (p=0.034) and use of ambu (p=0.023). No significant differences were verified for the others: occurrence of falls (p=0.254), presence of comorbidities (p=0.158) and use of Riluzole (p=0.548), sit and stand (p=0.931), turn over in bed (p=0.402) and walk (p=0.740), total ALSFRS-R (p=0.656), MND severity level (p=0.307)strength muscular (p=0.940), SPPB (p=0.296), quality of life (p=0.686). Conclusion: The clinical and functional characteristics were similar between individuals who started the disease in the elderly and adult phase. However, it was observed a higher prevalence among the elderly with bulbar onset, which is thebeginning of the worst prognosis of disease progression.
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Pitta, Marina Galdino da Rocha, Jordy Silva de Carvalho, Luzilene Pereira de Lima, and Ivan da Rocha Pitta. "iPSC therapies applied to rehabilitation in parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.022.

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Background: Parkinson’s disease (PD) is a neurological disorder that affects movement, mainly due to damage and degeneration of the nigrostriatal dopaminergic pathway. The diagnosis is made through a clinical neurological analysis where motor characteristics are considered. There is still no cure, and treatment strategies are focused on symptoms control. Cell replacement therapies emerge as an alternative. Objective: This review focused on current techniques of induced pluripotent stem cells (iPSCs). Methods: The search terms used were: “Parkinson’s Disease”, “Stem cells” and “iPSC”. Open articles written in English, from 2016-21 were selected in the Pubmed database, 10 publications were identified. Results: With the modernization of iPSC, it was possible to reprogram pluripotent human somatic cells and generate dopaminergic neurons and individual-specific glial cells. To understand the molecular basis, cell and animal models of neurons and organelles are currently being employed. Organoids are derived from stem cells in a three-dimensional matrix, such as matrigel or hydrogels derived from animals. The neuronal models are: α-synuclein (SNCA), leucine-rich repeat kinase2 (LRRK2), PARK2, putative kinase1 induced by phosphatase and tensin homolog (PINK1), DJ-1. Both models offer opportunities to investigate pathogenic mechanisms of PD and test compounds on human neurons. Conclusions: Cell replacement therapy is promising and has great capacity for the treatment of neurodegenerative diseases. Studies using iPSC neuron and PD organoid modeling is highly valuable in elucidating relevants neuronal pathways and therapeutic targets, moreover providing important models for testing future therapies.
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Pyarali, F., S. Allen, S. Frank, R. Lewis, and A. Elsayegh. "Incidence of Venous Thromboembolism in Motor Neuron Disease: A Retrospective Analysis." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1983.

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Pereira, Camila Alves, Alana Strucker Barbosa, Vanessa de Freitas Moreira, Igor Braga Farias, Paulo de Lima Serrano, Bruno de Mattos Lombardi Badia, Hélvia Bertoldo de Oliveira, et al. "Case report: motor neurone symptoms as initial clinical manifestation in a patient with Creutzfeldt-Jakob disease." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.590.

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Female, 54-year-old, began with weakness in her right hand and loss of dexterity. Four months after initial symptoms, patient developed sudden onset vertigo. She progressed with difficulties in coordination, dystonic posture and involuntary movements in her right arm. Family also reported insomnia and cognitive impairment. Ten days later, she had no recognition of family members, and developed myoclonia. After two weeks, progression of ataxia rendered her unable to walk and she also had urinary incontinence. Neurological examination revealed perseveration of speech, oculomotor apraxia, severe gait and limb ataxia, intention tremors and generalized hiperrreflexia. She had marked tenar, first dorsal and palmar interosseus amyotrophy. Video-EEG showed markedly disorganized activity and generalized periodic complexes. Neuroimaging had no signs of spinal cord suffering. Electroneuromyography showed preganglionic chronic neurogenic involvement in cervical and lumbosacral myotomes, and acute denervation bilateral of C5–C7. Cerebrospinal fluid examination showed discrete hyperproteinorraquia and positivity for protein research 14-3-3. Genetic testing showed M129M variant in the PRNP gene. Brain tissue neuropathology revealed histologic spongiform encephalopathy associated with reactional gliosis and neuronal loss. Creutzfeldt-Jakob disease is a rare neurodegenerative disease caused by prion propagation. It has been mainly associated with central nervous system involvement, but lower neuron signs have been described. We report a case of motor neurone symptoms as initial clinical manifestation of Creutzfeldt-Jakob disease.
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Marquardt, Matheus, Antônio Serpa do Amaral Neto, Eduardo Martins Leal, Gabriel de Deus Vieira, André Dias de Oliveira, and Gisele Espindola. "Amyotrophic lateral sclerosis associated with parkinsonism: an atypical manifestation." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.608.

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Context: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease, characterized by progressive muscle weakness. The diagnosis is not always easy, and may have atypical initial manifestations. Case report: O.S.M, female, 62 years old, started in 2016 with bradykinesia and left lower limb tremor, associated with frequent falls. Iniciated research for parkinsonism in 2017, SPECT demonstrated decreased dopamine transporter binding potential density in both striatum. Levodopa was started, with partial improvement of symptoms. In 2018, she developed dysphagia, associated with slight alterations in phonation. In 2019, in addition to the left lower limb tremor and bradykinesia, the patient developed limb paresis, also affecting the right upper limb, with proximal atrophy and fasciculations. Added to the therapeutic regimen pramipexole, without improvement in symptoms. Over the months the case progressed with axial weakness, the need for a wheelchair for walking. Patient hospitalized in April 2020, electroneuromyography performed which showed signs of active disinvervation in the bulbar, cervical, thoracic and lumbosacral segments and signs of chronic disinervation in the cervical and lumbosacral segments, with no signs of sensory or motor polyneuropathy. Such findings suggest impairment of the Lower motor neuron, and can be found in the Diseases of the Motor Neuron. With the diagnosis of ALS, Riluzole was started, with a reduction in the speed of disease progression. Conclusions: the reported case draws attention to the importance of always thinking about differential diagnoses in neurological diseases. We should always look for new symptoms, so that more rare diseases do not go unnoticed.
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Fattah, Shaikh Anowarul, A. B. M. Sayeed Ud Doulah, Md Asif Iqbal, Celia Shahnaz, Wei-Ping Zhu, and M. Omair Ahmad. "Identification of motor neuron disease using wavelet domain features extracted from EMG signal." In 2013 IEEE International Symposium on Circuits and Systems (ISCAS). IEEE, 2013. http://dx.doi.org/10.1109/iscas.2013.6572094.

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Aslam, Zaryab, Aisha Zahid Junejo, Aarish Memon, Ali Raza, Juveria Aslam, and Liaquat Ali Thebo. "Optical Assistance for Motor Neuron Disease (MND) Patients Using Real-time Eye Tracking." In 2019 8th International Conference on Information and Communication Technologies (ICICT). IEEE, 2019. http://dx.doi.org/10.1109/icict47744.2019.9001922.

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Yang, Po Sheng, Robert Henderson, and Pamela McCombe. "016 Genetic epidemiology of Motor Neuron Disease: Royal Brisbane and Women’s Hospital Cohort." In ANZAN Annual Scientific Meeting 2021 Abstracts. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/bmjno-2021-anzan.16.

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Morimoto, Nobutoshi, Tomoko Kurata, Kota Sato, Yoshio Ikeda, Koji Abe, and Shuhei Sato. "A computerized touch panel-type screening test in Patients with Motor Neuron Disease." In 2012 ICME International Conference on Complex Medical Engineering (CME). IEEE, 2012. http://dx.doi.org/10.1109/iccme.2012.6275654.

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Reports on the topic "Motor neuron disease"

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Santos, Ana Lúcia Yaeko da Silva, Deyse Mayara Rodrigues Caron, Livia Shirahige, and Abrahão Fontes Baptista. Alterations in Corticomotor Excitability in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2023. http://dx.doi.org/10.37766/inplasy2023.5.0078.

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Review question / Objective: To systematically evaluate the utility of TMS to follow up on ALS patients using neurophysiological metrics and to quantify corticomotor excitability compared to sham controls or other neuromuscular diseases. Condition being studied: Amyotrophic Lateral Sclerosis (ALS) is the third most common neurodegenerative disease (BRUNET et al., 2020). The condition is characterized by progressive muscle atrophy due to upper and lower motor neuron death (GOETZ, 2000).
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Andrades, Oscar, David Ulloa, Dario Martinez, Francisco Guede, Gustava Muñoz, Luis Javier Chirosa, and Amador García. Effect of the manipulation of the variables that configure the stimulus of strength training on motor symptoms in people with Parkinson's disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0079.

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Review question / Objective: To analyze the evidence on studies that have manipulated the variables that make up the strength training stimulus and its effects on motor symptoms in people with Parkinson's disease. Condition being studied: Parkinson's is a multisystemic neurodegenerative disease that affects the central nervous system and is caused by a loss of dopaminergic neurons in the compact part of the substantia nigra of the basal ganglia of the midbrain. People with Parkinson's disease (PEP) have non-motor and motor clinical symptoms. Classic motor symptoms are rest tremor, joint stiffness, bradykinesia, decreased balance, gait disturbances (speed, temporality, spatiality, support, and freezing) and decreased functional performance.
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Zhang, Yu, Chaoliang Sun, Hengxi Xu, Weiyang Shi, Luqi Cheng, Alain Dagher, Yuanchao Zhang, and Tianzi Jiang. Connectivity-Based Subtyping of De Novo Parkinson Disease: Biomarkers, Medication Effects and Longitudinal Progression. Progress in Neurobiology, April 2024. http://dx.doi.org/10.60124/j.pneuro.2024.10.04.

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Parkinson's disease (PD) is characterized by divergent clinical symptoms and prognosis, suggesting the presence of distinct subtypes. Identifying these subtypes is crucial for understanding the underlying pathophysiology, predicting disease progression, and developing personalized treatments. In this study, we propose a connectivity-based subtyping approach, which measures each patient's deviation from the reference structural covariance networks established in healthy controls. Using data from the Parkinson's Progression Markers Initiative, we identified two distinct subtypes of de novo PD patients: 248 patients with typical cortical-striato-thalamic dysfunctions and 41 patients showing weakened dorsal raphe nucleus (DRN)-to-cortical/striatal projections. The proposed subtyping approach demonstrated high stability in terms of random sampling of healthy or diseased population and longitudinal prediction at follow-up visits, outperforming the traditional motor phenotypes. Compared to the typical PD, patients with the DRN-predominant subtype were characterized by less server motor symptoms at baseline and distinct imaging biomarkers, including larger striatal volumes, higher concentration of cerebrospinal fluid amyloid-β and amyloid-β/t(p)-tau ratio. Subtype-specific associations and drug effects were identified that the DRN subtype exhibited more pronounced medication effects on motor symptoms, potentially regulated by DRN serotonergic modulation through striatal dopaminergic neurons. The DRN serotonergic inputs also regulated non-motor symptoms, the aggregation of CSF biomarkers and the conversion to more severe disease states. Our findings suggest that the DRN-predominant subtype represents a unique clinical and biological phenotype of PD characterized by an enhanced response to anti-parkinsonian treatment, more favorable prognosis and slower progression of dopamine depletion. This study may contribute to clinical practice of precision medicine, early invention and individualized treatments in PD and other neurodegenerative diseases.
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Wang, Xiao, Hong Shen, Yujie Liang, Yixin Wang, Meiqi Zhang, and Hongtao Ma. Effectiveness of Tango Intervention on Motor Symptoms in Patients with Parkinson's Disease: A Protocol for Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0009.

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Review question / Objective: Parkinson's disease (PD) is a degenerative neurological disease caused by the loss of dopaminergic neurons in the pars compacta of the substantia nigra of the brain, resulting in lesions in the basal ganglia. The main motor symptoms of PD include resting tremor, rigidity, akinesia or bradykinesia and postural instability. As an exercise intervention based on musical accompaniment, tango dance has shown positive effects on the rehabilitation of motor symptoms in PD patients in recently. In this study, we systematically reviewed the efficacy of tango intervention in alleviating the motor symptoms of patients with PD. Condition being studied: Parkinson. Information sources: The following electronic databases will be searched: PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science Core collection, and China National Knowledge Infrastructure Database (CNKI) and WanFang Database.
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Singh, Ruchi, Akhiya Nail, and Nirendra Kumar Rai. Effectiveness of Vitamin B12 Supplementation on cognitive, motor & mood instability of Parkinson’s disease patients on levodopa treatment :A Systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0066.

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Review question / Objective: The treatment of choice for patients of Parkinson's disease is levodopa. However, levodopa has been suggested to decrease Vit B12 level in these patients. Thus, the research question for this systematic review is whether vit B 12 supplementation in Parkinson's disease(PD) patients on treatment with levodopa improves vit B12 level effecting the Cognition, Motor functions and Mood instability among them in comparison to PD patients on levodopa treatment who are not supplemented with Vit B12. Condition being studied: Parkinson disease is the progressive degeneration of dopaminergic neurons present within the substantia nigra that can lead to altered movements along with the prevalence of cognitive and mood instability as a result of dopamine(neurotransmitter) deficiency. The most effective treatment for the Parkinson's disease is the administration of levodopa, a dopamine precursor . Long term treatment with levodopa causes an increase in homocysteine levels and tissue deficiency of vitamin B12 and folate may occur. Vitamin B12 supplementation is administered as after management regime, in Parkinson patient on levodopa treatment . This study aims to conduct a systematic review, of studies , randomized control trials investigating the ability of vitamin B12 supplementation to enhances the recovery/reduce the decline, if any, of the symptoms of cognitive, motor, mood impairments associated with Parkinson's disease patient on levodopa treatment.
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Zhu, Qiaochu, Jin Zhou, Hai Huang, Jie Han, Biwei Cao, Dandan Xu, Yan Zhao, and Gang Chen. Risk factors associated with amyotrophic lateral sclerosis: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0118.

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Review question / Objective: To identify and list the risk factors associated with the onset and progression of ALS. Condition being studied: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder affecting the upper and lower motor neurons in the spinal bulb, cerebral cortex, and spinal cord. The clinical processing symptoms accompany muscle atrophy, fasciculation, and fatigue of limbs, which can lead to general paralysis and death from respiratory failure within 3-5 years after the onset of this disease. Though the pathogenesis of ALS is still unclear, exploring the associations between risk factors and ALS can provide reliable evidence to find the pathogenesis in the future. This meta-analysis aims to synthesize all related risk factors on ALS, comprehensively understand this disease, and provide clues to mechanism research and clinicians.
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