All Relations between Amyotrophic Lateral Sclerosis and sod1

Publication Sentence Publish Date Extraction Date Species
Silvia Silva-Hucha, M Estrella Fernández de Sevilla, Kirsty M Humphreys, Fiona E Benson, Jaime M Franco, David Pozo, Angel M Pastor, Sara Morcuend. VEGF expression disparities in brainstem motor neurons of the SOD1 Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics. 2024-03-12. PMID:38472048. vegf expression disparities in brainstem motor neurons of the sod1 amyotrophic lateral sclerosis (als) is a rare neuromuscular disease characterized by severe muscle weakness mainly due to degeneration and death of motor neurons. 2024-03-12 2024-03-15 Not clear
Natalia Nowicka, Kamila Zglejc-Waszak, Judyta Juranek, Agnieszka Korytko, Krzysztof Wąsowicz, Małgorzata Chmielewska-Krzesińska, Joanna Wojtkiewic. Novel insights into RAGE signaling pathways during the progression of amyotrophic lateral sclerosis in RAGE-deficient SOD1 G93A mice. PloS one. vol 19. issue 3. 2024-03-08. PMID:38457412. novel insights into rage signaling pathways during the progression of amyotrophic lateral sclerosis in rage-deficient sod1 g93a mice. 2024-03-08 2024-03-11 mouse
Chunling Duan, Moorim Kang, Xiaojie Pan, Zubao Gan, Vera Huang, Guanlin Li, Robert F Place, Long-Cheng L. Intrathecal administration of a novel siRNA modality extends survival and improves motor function in the SOD1 Molecular therapy. Nucleic acids. vol 35. issue 1. 2024-03-04. PMID:38435120. intrathecal administration of a novel sirna modality extends survival and improves motor function in the sod1 antisense oligonucleotides (asos) were the first modality to pioneer targeted gene knockdown in the treatment of amyotrophic lateral sclerosis (als) caused by mutant superoxide dismutase 1 (sod1). 2024-03-04 2024-03-06 human
Liam M Koehn, Joel R Steele, Ralf B Schittenhelm, Bradley J Turner, Joseph A Nicolazz. Sex-Dependent Changes to the Intestinal and Hepatic Abundance of Drug Transporters and Metabolizing Enzymes in the SOD1 Molecular pharmaceutics. 2024-02-28. PMID:38415587. sex-dependent changes to the intestinal and hepatic abundance of drug transporters and metabolizing enzymes in the sod1 amyotrophic lateral sclerosis (als) is characterized by death and dysfunction of motor neurons that result in a rapidly progressing loss of motor function. 2024-02-28 2024-03-01 Not clear
Xin-Xin Wang, Wen-Zhi Chen, Cheng Li, Ren-Shi X. Current potential pathogenic mechanisms of copper-zinc superoxide dismutase 1 (SOD1) in amyotrophic lateral sclerosis. Reviews in the neurosciences. 2024-02-21. PMID:38381656. current potential pathogenic mechanisms of copper-zinc superoxide dismutase 1 (sod1) in amyotrophic lateral sclerosis. 2024-02-21 2024-02-24 Not clear
Tzyy-Nan Huang, Yu-Tzu Shih, Tzu-Li Yen, Yi-Ping Hsue. Vcp overexpression and leucine supplementation extend lifespan and ameliorate neuromuscular junction phenotypes of a SOD1G93A-ALS mouse model. Human molecular genetics. 2024-02-21. PMID:38382647. many genes with distinct molecular functions have been linked to genetically heterogeneous amyotrophic lateral sclerosis (als), including superoxide dismutase 1 (sod1) and valosin-containing protein (vcp). 2024-02-21 2024-02-24 mouse
Zikai Xin, Cheng Xin, Jia Huo, Qi Liu, Hui Dong, Rui Li, Yaling Li. Neuroprotective Effect of a Multistrain Probiotic Mixture in SOD1 Molecular neurobiology. 2024-02-13. PMID:38349516. neuroprotective effect of a multistrain probiotic mixture in sod1 amyotrophic lateral sclerosis (als) is a devastating neurodegenerative disease characterized by the selective loss of motor neurons. 2024-02-13 2024-02-15 Not clear
Hongmei Zhu, Urvashi Dalvi, William Cazenave, Daniel Cattaert, Pascal Brancherea. Excitatory action of low frequency depolarizing GABA/glycine synaptic inputs is prevalent in prenatal spinal SOD1 The Journal of physiology. 2024-02-12. PMID:38345477. excitatory action of low frequency depolarizing gaba/glycine synaptic inputs is prevalent in prenatal spinal sod1 amyotrophic lateral sclerosis (als) is a fatal adult-onset neurodegenerative disease characterized by progressive motor neuron degeneration and muscle paralysis. 2024-02-12 2024-02-15 Not clear
Sara Costa-Pinto, Joana Gonçalves-Ribeiro, Joana Tedim-Moreira, Renato Socodato, João B Relvas, Ana M Sebastião, Sandra H Va. Communication defects with astroglia contribute to early impairments in the motor cortex plasticity of SOD1 Neurobiology of disease. 2024-02-09. PMID:38336279. communication defects with astroglia contribute to early impairments in the motor cortex plasticity of sod1 amyotrophic lateral sclerosis (als) is a neurodegenerative disease, involving the selective degeneration of cortical upper synapses in the primary motor cortex (m1). 2024-02-09 2024-02-12 Not clear
Maria Teresa Golia, Roberto Frigerio, Susanna Pucci, Francesca Sironi, Cassandra Margotta, Laura Pasetto, Camilla Testori, Elena Berrone, Francesco Ingravalle, Marcella Chiari, Alessandro Gori, Roberto Duchi, Andrea Perota, Luca Bergamaschi, Antonio D'Angelo, Giulia Cagnotti, Cesare Galli, Cristiano Corona, Valentina Bonetto, Caterina Bendotti, Marina Cretich, Sara Francesca Colombo, Claudia Verderi. Changes in glial cell activation and extracellular vesicles production precede the onset of disease symptoms in transgenic hSOD1 Experimental neurology. 2024-02-08. PMID:38331161. changes in glial cell activation and extracellular vesicles production precede the onset of disease symptoms in transgenic hsod1 sod1 gene is associated with progressive motor neuron degeneration in the familiar forms of amyotrophic lateral sclerosis. 2024-02-08 2024-02-11 human
Sagar Verma, Abhishek Vats, Vanshika Ahuja, Kavita Vats, Shiffali Khurana, Yuvraj Vats, Mandaville Gourie-Devi, Saima Wajid, Nirmal Kumar Ganguly, Pradip Chakraborti, Vibha Tanej. Functional consequences of familial ALS-associated SOD1 FASEB journal : official publication of the Federation of American Societies for Experimental Biology. vol 38. issue 3. 2024-02-06. PMID:38317639. functional consequences of familial als-associated sod1 amyotrophic lateral sclerosis is a fatal neurodegenerative disorder characterized by progressive skeletal muscle denervation and loss of motor neurons that results in muscle atrophy and eventual death due to respiratory failure. 2024-02-06 2024-02-09 Not clear
Luis C Fernández-Beltrán, Zeinab Ali, Angélica Larrad-Sanz, Juan I Lopez-Carbonero, Juan M Godoy-Corchuelo, Irene Jimenez-Coca, Irene Garcia-Toledo, Liz Bentley, Ulises Gomez-Pinedo, Jordi A Matias-Guiu, Maria Jose Gil-Moreno, Jorge Matias-Guiu, Silvia Corrochan. Leptin haploinsufficiency exerts sex-dependent partial protection in SOD1 Scientific reports. vol 14. issue 1. 2024-02-01. PMID:38302474. leptin haploinsufficiency exerts sex-dependent partial protection in sod1 amyotrophic lateral sclerosis (als) is a fatal neurodegenerative disorder characterized by significant metabolic disruptions, including weight loss and hypermetabolism in both patients and animal models. 2024-02-01 2024-02-04 mouse
Md Amin Hossain, Richa Sarin, Daniel P Donnelly, Brandon C Miller, Alexandra Weiss, Luke McAlary, Svetlana V Antonyuk, Joseph P Salisbury, Jakal Amin, Jeremy B Conway, Samantha S Watson, Jenifer N Winters, Yu Xu, Novera Alam, Rutali R Brahme, Haneyeh Shahbazian, Durgalakshmi Sivasankar, Swathi Padmakumar, Aziza Sattarova, Aparna C Ponmudiyan, Tanvi Gawde, David E Verrill, Wensheng Yang, Sunanda Kannapadi, Leigh D Plant, Jared R Auclair, Lee Makowski, Gregory A Petsko, Dagmar Ringe, Nathalie Y R Agar, David J Greenblatt, Mary Jo Ondrechen, Yunqiu Chen, Justin J Yerbury, Roman Manetsch, S Samar Hasnain, Robert H Brown, Jeffrey N Aga. Evaluating protein cross-linking as a therapeutic strategy to stabilize SOD1 variants in a mouse model of familial ALS. PLoS biology. vol 22. issue 1. 2024-01-30. PMID:38289969. mutations in the gene encoding cu-zn superoxide dismutase 1 (sod1) cause a subset of familial amyotrophic lateral sclerosis (fals) cases. 2024-01-30 2024-02-02 mouse
Vera M Masegosa, Xavier Navarro, Mireia Herrando-Grabulos. ICA-27243 improves neuromuscular function and preserves motoneurons in the transgenic SOD1 Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics. vol 21. issue 2. 2024-01-23. PMID:38262101. ica-27243 improves neuromuscular function and preserves motoneurons in the transgenic sod1 amyotrophic lateral sclerosis (als) is a progressive neurodegenerative disease characterized by the death of upper and lower motor neurons (mns). 2024-01-23 2024-01-26 Not clear
Kazuki Adachi, Kota Miyata, Yukino Chida, Mikako Hirose, Yuta Morisaki, Koji Yamanaka, Hidemi Misaw. Depletion of perivascular macrophages delays ALS disease progression by ameliorating blood-spinal cord barrier impairment in SOD1 Frontiers in cellular neuroscience. vol 17. 2023-12-11. PMID:38077951. depletion of perivascular macrophages delays als disease progression by ameliorating blood-spinal cord barrier impairment in sod1 amyotrophic lateral sclerosis (als) is a fatal motor neuron disease in which non-cell-autonomous processes have been proposed as its cause. 2023-12-11 2023-12-17 Not clear
Ying Guo, Teng Guan, Qiang Yu, Nitesh Sanghai, Kashfia Shafiq, Meiyu Li, Xin Jiao, Donghui Na, Guohui Zhang, Jiming Kon. ALS-linked SOD1 mutations impair mitochondrial-derived vesicle formation and accelerate aging. Redox biology. vol 69. 2023-12-06. PMID:38056310. this study investigates the role of oxidized sod1 derived from amyotrophic lateral sclerosis (als) linked sod1 mutations in cell senescence and aging. 2023-12-06 2023-12-10 human
Marta Sequeira, Filipe Godinho, João Lourenç. Amyotrophic Lateral Sclerosis with SOD1 Mutation Presenting with Progressive Cerebellar Ataxia. Cerebellum (London, England). 2023-12-04. PMID:38049694. amyotrophic lateral sclerosis with sod1 mutation presenting with progressive cerebellar ataxia. 2023-12-04 2023-12-10 Not clear
Shaherin Basith, Balachandran Manavalan, Gwang Le. Unveiling local and global conformational changes and allosteric communications in SOD1 systems using molecular dynamics simulation and network analyses. Computers in biology and medicine. vol 168. 2023-11-21. PMID:37988788. amyotrophic lateral sclerosis (als) is a serious neurodegenerative disorder affecting nerve cells in the brain and spinal cord that is caused by mutations in the superoxide dismutase 1 (sod1) enzyme. 2023-11-21 2023-11-29 Not clear
Seyed Mostafa Noorbakhsh Varnosfaderani, Melika Sadat Haeri, Ali Sam Arian, Ali Yousefi Rad, Mohammad Yazdanpour, Fatemeh Mojahedian, Mohammad Yaghoubzad-Maleki, Hamidreza Zalpoor, Payam Baziyar, Mohsen Nabi-Afjad. Fighting against amyotrophic lateral sclerosis (ALS) with flavonoids: a computational approach to inhibit superoxide dismutase (SOD1) mutant aggregation. Journal of biomolecular structure & dynamics. 2023-11-17. PMID:37975411. fighting against amyotrophic lateral sclerosis (als) with flavonoids: a computational approach to inhibit superoxide dismutase (sod1) mutant aggregation. 2023-11-17 2023-11-20 human
Shukkwan K Chen, Zachary C E Hawley, Maria I Zavodszky, Sam Hana, Daniel Ferretti, Branka Grubor, Michael Hawes, Shanqin Xu, Stefan Hamann, Galina Marsh, Patrick Cullen, Ravi Challa, Thomas M Carlile, Hang Zhang, Wan-Hung Lee, Andrea Peralta, Pete Clarner, Cong Wei, Kathryn Koszka, Feng Gao, Shih-Ching L. Efficacy and safety of a SOD1-targeting artificial miRNA delivered by AAV9 in mice are impacted by miRNA scaffold selection. Molecular therapy. Nucleic acids. vol 34. 2023-11-06. PMID:37928442. toxic gain-of-function mutations in superoxide dismutase 1 (sod1) contribute to approximately 2%-3% of all amyotrophic lateral sclerosis (als) cases. 2023-11-06 2023-11-08 mouse