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Artículos de revistas sobre el tema "FAMILIAL AMYOTROPHIC LATERAL SCLEROSIS"

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Autor: Grafiati
Publicado: 11 de septiembre de 2023

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1

Eestnes, Arnulf y Svein Ivar Mellgren. "Familial amyotrophic lateral sclerosis". Acta Neurologica Scandinavica 61, n.º 3 (29 de enero de 2009): 192–99. http://dx.doi.org/10.1111/j.1600-0404.1980.tb01482.x.

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2

Boylan, Kevin. "Familial Amyotrophic Lateral Sclerosis". Neurologic Clinics 33, n.º 4 (noviembre de 2015): 807–30. http://dx.doi.org/10.1016/j.ncl.2015.07.001.

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3

Hand, Collette K. y Guy A. Rouleau. "Familial amyotrophic lateral sclerosis". Muscle & Nerve 25, n.º 2 (febrero de 2002): 135–59. http://dx.doi.org/10.1002/mus.10001.

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4

Millichap, J. Gordon. "Juvenile Familial Amyotrophic Lateral Sclerosis". Pediatric Neurology Briefs 12, n.º 7 (1 de julio de 1998): 56. http://dx.doi.org/10.15844/pedneurbriefs-12-7-15.

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5

Savinova, A. V., N. A. Shnayder y R. F. Nasyrova. "Genetics of familial amyotrophic lateral sclerosis". Bulletin of Siberian Medicine 20, n.º 3 (22 de octubre de 2021): 193–202. http://dx.doi.org/10.20538/1682-0363-2021-3-193-202.

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To analyze results of the studies covering modern scientific views on the genetics of familial amyotrophic lateral sclerosis (FALS).We searched for full-text publications containing the key words “amyotrophic lateral sclerosis”, “FALS”, and “genetics” in the literature for the past 10 years in both Russian and English in eLibrary, PubMed, Web of Science, and OMIM databases. In addition, the review includes earlier publications of historical interest.This review summarizes all existing information on four most widespread genes associated with FALS: SOD1, TARDBP, FUS, and C9ORF72. The review also describes the functions of these genes and possible pathogenetic mechanisms of motor neuron death in amyotrophic lateral sclerosis (ALS), such as mitochondrial dysfunction, oxidative stress, glutamate excitotoxicity, damage to axonal transport components, and pathological neurofilament aggregation.As modern methods of molecular genetic diagnostics evolve, our knowledge about multifactorial FALS genetics expands. This information should be taken into consideration in clinical practice of neurologists. Information about the genes associated with ALS and understanding of particular pathogenetic mechanisms of the disease play a key role in the development of effective therapeutic strategies.
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6

Freischmidt, Axel, Kathrin Müller, Lisa Zondler, Patrick Weydt, Alexander E. Volk, Anže Lošdorfer Božič, Michael Walter et al. "Serum microRNAs in patients with genetic amyotrophic lateral sclerosis and pre-manifest mutation carriers". Brain 137, n.º 11 (5 de septiembre de 2014): 2938–50. http://dx.doi.org/10.1093/brain/awu249.

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Abstract Knowledge about the nature of pathomolecular alterations preceding onset of symptoms in amyotrophic lateral sclerosis is largely lacking. It could not only pave the way for the discovery of valuable therapeutic targets but might also govern future concepts of pre-manifest disease modifying treatments. MicroRNAs are central regulators of transcriptome plasticity and participate in pathogenic cascades and/or mirror cellular adaptation to insults. We obtained comprehensive expression profiles of microRNAs in the serum of patients with familial amyotrophic lateral sclerosis, asymptomatic mutation carriers and healthy control subjects. We observed a strikingly homogenous microRNA profile in patients with familial amyotrophic lateral sclerosis that was largely independent from the underlying disease gene. Moreover, we identified 24 significantly downregulated microRNAs in pre-manifest amyotrophic lateral sclerosis mutation carriers up to two decades or more before the estimated time window of disease onset; 91.7% of the downregulated microRNAs in mutation carriers overlapped with the patients with familial amyotrophic lateral sclerosis. Bioinformatic analysis revealed a consensus sequence motif present in the vast majority of downregulated microRNAs identified in this study. Our data thus suggest specific common denominators regarding molecular pathogenesis of different amyotrophic lateral sclerosis genes. We describe the earliest pathomolecular alterations in amyotrophic lateral sclerosis mutation carriers known to date, which provide a basis for the discovery of novel therapeutic targets and strongly argue for studies evaluating presymptomatic disease-modifying treatment in amyotrophic lateral sclerosis.
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7

Brenner, David, Kathrin Müller, Thomas Wieland, Patrick Weydt, Sarah Böhm, Dorothée Lulé, Annemarie Hübers et al. "NEK1mutations in familial amyotrophic lateral sclerosis". Brain 139, n.º 5 (5 de marzo de 2016): e28-e28. http://dx.doi.org/10.1093/brain/aww033.

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8

Valdmanis, P. N. y G. A. Rouleau. "Genetics of familial amyotrophic lateral sclerosis". Neurology 70, n.º 2 (7 de enero de 2008): 144–52. http://dx.doi.org/10.1212/01.wnl.0000296811.19811.db.

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9

Fang, Fang, Freya Kamel, Paul Lichtenstein, Rino Bellocco, Pär Sparén, Dale P. Sandler y Weimin Ye. "Familial aggregation of amyotrophic lateral sclerosis". Annals of Neurology 66, n.º 1 (julio de 2009): 94–99. http://dx.doi.org/10.1002/ana.21580.

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10

Byrne, Susan y Orla Hardiman. "Familial aggregation in amyotrophic lateral sclerosis". Annals of Neurology 67, n.º 4 (2 de octubre de 2009): 554. http://dx.doi.org/10.1002/ana.21883.

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11

Byrne, Susan, Peter Bede, Marwa Elamin, Kevin Kenna, Catherine Lynch, Russell McLaughlin y Orla Hardiman. "Proposed criteria for familial amyotrophic lateral sclerosis". Amyotrophic Lateral Sclerosis 12, n.º 3 (5 de enero de 2011): 157–59. http://dx.doi.org/10.3109/17482968.2010.545420.

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12

Pfister, Ted, Ramnik Sekhon, Mitchell White, Patrick Scott, Susan Munro, Megan Johnston, Sanjay Kalra y Lawrence Korngut. "Familial amyotrophic lateral sclerosis in Alberta, Canada". Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration 14, n.º 4 (4 de enero de 2013): 273–77. http://dx.doi.org/10.3109/21678421.2012.754044.

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13

Siddique, T., M. A. Pericak-Vance, B. R. Brooks, R. P. Roos, W. Y. Hung, J. P. Antel, T. L. Munsat et al. "Linkage analysis in familial amyotrophic lateral sclerosis". Neurology 39, n.º 7 (1 de julio de 1989): 919. http://dx.doi.org/10.1212/wnl.39.7.919.

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14

Özge, Aynur, Hakan Kaleagas, Cengiz Tataroglu y Özgür ünal. "Juvenile familial amyotrophic lateral sclerosis: Two siblings". Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders 3, n.º 3 (enero de 2002): 163–64. http://dx.doi.org/10.1080/146608202760834184.

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15

Yokoseki, Akio, Atsushi Shiga, Chun-Feng Tan, Asako Tagawa, Hiroyuki Kaneko, Akihide Koyama, Hiroto Eguchi et al. "TDP-43mutation in familial amyotrophic lateral sclerosis". Annals of Neurology 63, n.º 4 (abril de 2008): 538–42. http://dx.doi.org/10.1002/ana.21392.

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16

Faes, Liesbeth y Geert Callewaert. "Mitochondrial dysfunction in familial amyotrophic lateral sclerosis". Journal of Bioenergetics and Biomembranes 43, n.º 6 (10 de noviembre de 2011): 587–92. http://dx.doi.org/10.1007/s10863-011-9393-0.

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17

Praline, Julien, Anne-Marie Guennoc, Patrick Vourc'h, Bertrand De Toffol y Philippe Corcia. "Primary lateral sclerosis may occur within familial amyotrophic lateral sclerosis pedigrees". Amyotrophic Lateral Sclerosis 11, n.º 1-2 (enero de 2010): 154–56. http://dx.doi.org/10.3109/17482960802483038.

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18

Souza, Paulo Victor Sgobbi de, Wladimir Bocca Vieira de Rezende Pinto, Marco Antônio Troccoli Chieia y Acary Souza Bulle Oliveira. "Clinical and genetic basis of familial amyotrophic lateral sclerosis". Arquivos de Neuro-Psiquiatria 73, n.º 12 (13 de octubre de 2015): 1026–37. http://dx.doi.org/10.1590/0004-282x20150161.

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Amyotrophic lateral sclerosis represents the most common neurodegenerative disease leading to upper and lower motor neuron compromise. Although the vast majority of cases are sporadic, substantial gain has been observed in the knowledge of the genetic forms of the disease, especially of familial forms. There is a direct correlation between the profile of the mutated genes in sporadic and familial forms, highlighting the main role ofC9orf72 gene in the clinical forms associated with frontotemporal dementia spectrum. The different genes related to familial and sporadic forms represent an important advance on the pathophysiology of the disease and genetic therapeutic perspectives, such as antisense therapy. The objective of this review is to signal and summarize clinical and genetic data related to familial forms of amyotrophic lateral sclerosis.
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19

Vucic, Steve y Matthew Kiernan. "Pathophysiology of Neurodegeneration in Familial Amyotrophic Lateral Sclerosis". Current Molecular Medicine 9, n.º 3 (1 de abril de 2009): 255–72. http://dx.doi.org/10.2174/156652409787847173.

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20

Nalini, A., G. Yeshraj y M. Veerendrakumar. "Familial amyotrophic lateral sclerosis: First report from India". Neurology India 54, n.º 3 (2006): 304. http://dx.doi.org/10.4103/0028-3886.27161.

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21

Vucic, Steve, Garth A. Nicholson, Adriano Chio y Matthew C. Kiernan. "Apparent anticipation in SOD1 familial amyotrophic lateral sclerosis". Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration 14, n.º 5-6 (15 de febrero de 2013): 452–56. http://dx.doi.org/10.3109/21678421.2013.764569.

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22

Finsterer, J. y B. Mamoli. "Liquorpheresis (CSF filtration) in familial amyotrophic lateral sclerosis". Spinal Cord 37, n.º 8 (agosto de 1999): 592–93. http://dx.doi.org/10.1038/sj.sc.3100857.

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23

Leone, M. "Parental sex effect in familial amyotrophic lateral sclerosis". Neurology 41, n.º 8 (1 de agosto de 1991): 1292. http://dx.doi.org/10.1212/wnl.41.8.1292.

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24

Beaujeux, T. P., E. L. Schofield, P. J. Shaw y J. D. Wood. "SOD1 aggregation in familial amyotrophic lateral sclerosis (FALS)". Biochemical Society Transactions 30, n.º 3 (1 de junio de 2002): A85. http://dx.doi.org/10.1042/bst030a085b.

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25

Maurelli, M., E. Marchioni, D. Bosone, S. Boni, W. Bolzani, R. Cerretano, F. Simonetti y F. Savoldi. "Familial adult amyotrophic lateral sclerosis: report of cases". Italian Journal of Neurological Sciences 13, n.º 1 (febrero de 1992): 75–79. http://dx.doi.org/10.1007/bf02222892.

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26

Swash, Michael y Nigel Leigh. "Criteria for Diagnosis of Familial Amyotrophic Lateral Sclerosis". Neuromuscular Disorders 2, n.º 1 (enero de 1992): 7–9. http://dx.doi.org/10.1016/0960-8966(92)90020-7.

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27

Mulder, D., L. Kurland, K. Offord y C. Beard. "Familial adult motor neuron disease: amyotrophic lateral sclerosis". Neurology 36, n.º 4 (1 de abril de 1986): 511–17. http://dx.doi.org/10.1212/wnl.36.4.511.

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28

Gurney, Mark E. "Transgenic animal models of familial amyotrophic lateral sclerosis". Journal of Neurology 244, S2 (mayo de 1997): S15—S20. http://dx.doi.org/10.1007/bf03160575.

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29

Gros-Louis, Francois, Claudia Gaspar y Guy A. Rouleau. "Genetics of familial and sporadic amyotrophic lateral sclerosis". Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1762, n.º 11-12 (noviembre de 2006): 956–72. http://dx.doi.org/10.1016/j.bbadis.2006.01.004.

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30

Dilliott, Allison A., Catherine M. Andary, Meaghan Stoltz, Andrey A. Petropavlovskiy, Sali M. K. Farhan y Martin L. Duennwald. "DnaJC7 in Amyotrophic Lateral Sclerosis". International Journal of Molecular Sciences 23, n.º 8 (7 de abril de 2022): 4076. http://dx.doi.org/10.3390/ijms23084076.

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Protein misfolding is a common basis of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Misfolded proteins, such as TDP-43, FUS, Matrin3, and SOD1, mislocalize and form the hallmark cytoplasmic and nuclear inclusions in neurons of ALS patients. Cellular protein quality control prevents protein misfolding under normal conditions and, particularly, when cells experience protein folding stress due to the fact of increased levels of reactive oxygen species, genetic mutations, or aging. Molecular chaperones can prevent protein misfolding, refold misfolded proteins, or triage misfolded proteins for degradation by the ubiquitin–proteasome system or autophagy. DnaJC7 is an evolutionarily conserved molecular chaperone that contains both a J-domain for the interaction with Hsp70s and tetratricopeptide domains for interaction with Hsp90, thus joining these two major chaperones’ machines. Genetic analyses reveal that pathogenic variants in the gene encoding DnaJC7 cause familial and sporadic ALS. Yet, the underlying ALS-associated molecular pathophysiology and many basic features of DnaJC7 function remain largely unexplored. Here, we review aspects of DnaJC7 expression, interaction, and function to propose a loss-of-function mechanism by which pathogenic variants in DNAJC7 contribute to defects in DnaJC7-mediated chaperoning that might ultimately contribute to neurodegeneration in ALS.
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31

Frecker, M. F., F. C. Fraser, E. Andermann y W. E. M. Pryse-Phillips. "Association Between Alzheimer Disease and Amyotrophic Lateral Sclerosis?" Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 17, n.º 1 (febrero de 1990): 12–14. http://dx.doi.org/10.1017/s0317167100029942.

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ABSTRACT:We report two cases of Alzheimer disease (AD) — one of them familial — in which the patient also had amyotrophic lateral sclerosis (ALS), and one patient with familial AD who had a son with ALS. Three further cases of probable ALS were found in pedigrees of AD reported from the literature. It is proposed that this association is not coincidental, but may suggest an etiological factor in common.
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32

Lehky, Tanya y Christopher Grunseich. "Juvenile Amyotrophic Lateral Sclerosis: A Review". Genes 12, n.º 12 (30 de noviembre de 2021): 1935. http://dx.doi.org/10.3390/genes12121935.

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Juvenile amyotrophic lateral sclerosis (JALS) is a rare group of motor neuron disorders with gene association in 40% of cases. JALS is defined as onset before age 25. We conducted a literature review of JALS and gene mutations associated with JALS. Results of the literature review show that the most common gene mutations associated with JALS are FUS, SETX, and ALS2. In familial cases, the gene mutations are mostly inherited in an autosomal recessive pattern and mutations in SETX are inherited in an autosomal dominant fashion. Disease prognosis varies from rapidly progressive to an indolent course. Distinct clinical features may emerge with specific gene mutations in addition to the clinical finding of combined upper and lower motor neuron degeneration. In conclusion, patients presenting with combined upper and lower motor neuron disorders before age 25 should be carefully examined for genetic mutations. Hereditary patterns and coexisting features may be useful in determining prognosis.
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33

Navarro, Etiane y Charles J. Golden. "A-151 Cognitive Impairment in Amyotrophic Lateral Sclerosis". Archives of Clinical Neuropsychology 36, n.º 6 (30 de agosto de 2021): 1205. http://dx.doi.org/10.1093/arclin/acab062.169.

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Abstract Objective Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease caused by degeneration of the upper and lower motor neurons. This literature review examines the recurring etiology of cognitive impairments in ALS through empirical literature. The current study explores ALS across different subtypes and potential cognitive impairments. Two classifications are primarily examined ALS, and ALS with frontotemporal dementia (ALS-FTD). Involving three categories: familial inheritance pattern, genetic mutation, or sporadic. Neuropsychological studies affirm cognitive impairments in individuals diagnosed with ALS and ALS-FTD. Data Selection Data was culled from the American Psychological Association (PsycInfo), PubMed, Google Scholar. Terms used in this literature review include cognitive impairment in ALS and ALS-FTD, executive function deficiencies in ALS, neuropsychology in ALS, neuropsychological deficits in ALS, neuropsychological assessments for ALS, cognitive impairments in familial ALS, genetic ALS, and sporadic ALS, familial ALS, sporadic ALS, genetic mutations involved in ALS. Search dates December 20–23 of 2020 and March 3–4 of 2021. A total of 40 studies were examined. Data Synthesis ALS-patients demonstrate a significant cognitive impairment. However, influencing comorbidities accompanying the disease may be contributing to these impairments. Researchers employed neuroimaging and neuropsychological batteries to further understand influencing factors involved in ALS and cognition. Conclusions Researchers now understand ALS as a multi-symptomatic disorder and acknowledge the presence of cognitive impairments at various encased levels. There are limitations in neuropsychological batteries that accommodate for executive dysfunctions observed in ALS patients. Future studies should explore neuropsychological assessments that accommodate for motor deficits and dysarthria when assessing cognitive impairment in ALS patients.
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34

Ebben, Matthew R., Mona Shahbazi, Dale J. Lange y Ana C. Krieger. "REM behavior disorder associated with familial amyotrophic lateral sclerosis". Amyotrophic Lateral Sclerosis 13, n.º 5 (7 de junio de 2012): 473–74. http://dx.doi.org/10.3109/17482968.2012.673172.

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35

Turner, Bradley y Julie Atkin. "ER Stress and UPR in Familial Amyotrophic Lateral Sclerosis". Current Molecular Medicine 6, n.º 1 (1 de febrero de 2006): 79–86. http://dx.doi.org/10.2174/156652406775574550.

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36

Talbot, K. "Familial versus sporadic amyotrophic lateral sclerosis--a false dichotomy?" Brain 134, n.º 12 (3 de noviembre de 2011): 3429–34. http://dx.doi.org/10.1093/brain/awr296.

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37

Iwasaki, Yasuo, Masao Kinoshita y Ken Ikeda. "Concurrence of familial amyotrophic lateral sclerosis with ribbing's disease". International Journal of Neuroscience 58, n.º 3-4 (enero de 1991): 289–92. http://dx.doi.org/10.3109/00207459108985445.

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38

Wang, L., B. Popko y R. P. Roos. "The unfolded protein response in familial amyotrophic lateral sclerosis". Human Molecular Genetics 20, n.º 5 (15 de diciembre de 2010): 1008–15. http://dx.doi.org/10.1093/hmg/ddq546.

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39

Orrell, RichardW, AndrewW King y JackieS deBelleroche. "Parental influence on inheritance of familial amyotrophic lateral sclerosis". Lancet 345, n.º 8946 (febrero de 1995): 391–92. http://dx.doi.org/10.1016/s0140-6736(95)90381-x.

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40

Millecamps, Stéphanie, Séverine Boillée, Elodie Chabrol, William Camu, Cécile Cazeneuve, François Salachas, Pierre-François Pradat et al. "Screening of OPTN in French familial amyotrophic lateral sclerosis". Neurobiology of Aging 32, n.º 3 (marzo de 2011): 557.e11–557.e13. http://dx.doi.org/10.1016/j.neurobiolaging.2010.11.005.

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41

Koppers, Max, Marka M. van Blitterswijk, Lotte Vlam, Paulina A. Rowicka, Paul W. J. van Vught, Ewout J. N. Groen, Wim G. M. Spliet et al. "VCP mutations in familial and sporadic amyotrophic lateral sclerosis". Neurobiology of Aging 33, n.º 4 (abril de 2012): 837.e7–837.e13. http://dx.doi.org/10.1016/j.neurobiolaging.2011.10.006.

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42

van Doormaal, Perry T. C., Wouter van Rheenen, Marka van Blitterswijk, Raymond D. Schellevis, Helenius J. Schelhaas, Marianne de Visser, Anneke J. van der Kooi, Jan H. Veldink y Leonard H. van den Berg. "UBQLN2 in familial amyotrophic lateral sclerosis in the Netherlands". Neurobiology of Aging 33, n.º 9 (septiembre de 2012): 2233.e7–2233.e8. http://dx.doi.org/10.1016/j.neurobiolaging.2012.02.032.

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43

Hemminki, Kari, Xinjun Li, Jan Sundquist y Kristina Sundquist. "Familial risks for amyotrophic lateral sclerosis and autoimmune diseases". neurogenetics 10, n.º 2 (17 de diciembre de 2008): 111–16. http://dx.doi.org/10.1007/s10048-008-0164-y.

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44

Köroğlu, Çiğdem, Rezzak Yılmaz, Mine Hayriye Sorgun, Seyhun Solakoğlu y Özden Şener. "GNE missense mutation in recessive familial amyotrophic lateral sclerosis". neurogenetics 18, n.º 4 (31 de octubre de 2017): 237–43. http://dx.doi.org/10.1007/s10048-017-0527-3.

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45

Shang, Yulei y Eric J. Huang. "Mechanisms of FUS mutations in familial amyotrophic lateral sclerosis". Brain Research 1647 (septiembre de 2016): 65–78. http://dx.doi.org/10.1016/j.brainres.2016.03.036.

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46

Lemmens, R., V. Race, N. Hersmus, G. Matthijs, L. Van Den Bosch, P. Van Damme, B. Dubois, S. Boonen, A. Goris y W. Robberecht. "TDP-43 M311V mutation in familial amyotrophic lateral sclerosis". Journal of Neurology, Neurosurgery & Psychiatry 80, n.º 3 (1 de marzo de 2009): 354–55. http://dx.doi.org/10.1136/jnnp.2008.157677.

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47

Wicks, P., S. Abrahams, B. Papps, A. Al-Chalabi, C. E. Shaw, P. N. Leigh y L. H. Goldstein. "SOD1 and cognitive dysfunction in familial amyotrophic lateral sclerosis". Journal of Neurology 256, n.º 2 (febrero de 2009): 234–41. http://dx.doi.org/10.1007/s00415-009-0078-0.

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48

Fecto, Faisal. "SQSTM1 Mutations in Familial and Sporadic Amyotrophic Lateral Sclerosis". Archives of Neurology 68, n.º 11 (1 de noviembre de 2011): 1440. http://dx.doi.org/10.1001/archneurol.2011.250.

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49

Rademakers, Rosa, Heather Stewart, Mariely Dejesus-Hernandez, Charles Krieger, Neill Graff-Radford, Marife Fabros, Hannah Briemberg, Neil Cashman, Andrew Eisen y Ian R. A. Mackenzie. "Fusgene mutations in familial and sporadic amyotrophic lateral sclerosis". Muscle & Nerve 42, n.º 2 (16 de abril de 2010): 170–76. http://dx.doi.org/10.1002/mus.21665.

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50

Orell, Richard W., James Habgood, Petter Rudge, Russell J. M. Lane y Jackie S. de Belleroche. "Difficulties in distinguishing sporadic from familial amyotrophic lateral sclerosis". Annals of Neurology 39, n.º 6 (junio de 1996): 810–12. http://dx.doi.org/10.1002/ana.410390620.

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