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Статті в журналах з теми "Cerebral neurodegenerative disease"
Bass, Nancy. "Cerebral palsy and neurodegenerative disease." Current Opinion in Pediatrics 11, no. 6 (December 1999): 504–7. http://dx.doi.org/10.1097/00008480-199912000-00005.
Повний текст джерелаMaruyama, Hirofumi. "Cerebral blood flow of neurodegenerative disease." Cerebral Blood Flow and Metabolism (Japanese journal of cerebral blood flow and metabolism) 28, no. 2 (2017): 337–39. http://dx.doi.org/10.16977/cbfm.28.2_337.
Повний текст джерелаDusek, Petr, Tim Hofer, Jan Alexander, Per M. Roos, and Jan O. Aaseth. "Cerebral Iron Deposition in Neurodegeneration." Biomolecules 12, no. 5 (May 17, 2022): 714. http://dx.doi.org/10.3390/biom12050714.
Повний текст джерелаTrujillo-Estrada, Laura, Angela Gomez-Arboledas, Stefânia Forner, Alessandra Cadete Martini, Antonia Gutierrez, David Baglietto-Vargas, and Frank M. LaFerla. "Astrocytes: From the Physiology to the Disease." Current Alzheimer Research 16, no. 8 (October 11, 2019): 675–98. http://dx.doi.org/10.2174/1567205016666190830110152.
Повний текст джерелаTurturici, Giuseppina, Gabriella Sconzo, and Fabiana Geraci. "Hsp70 and Its Molecular Role in Nervous System Diseases." Biochemistry Research International 2011 (2011): 1–18. http://dx.doi.org/10.1155/2011/618127.
Повний текст джерелаSalvadori, Claudia, Laura Lossi, Mario Arispici, and Carlo Cantile. "Spongiform neurodegenerative disease in a Persian kitten." Journal of Feline Medicine and Surgery 9, no. 3 (June 2007): 242–45. http://dx.doi.org/10.1016/j.jfms.2006.12.001.
Повний текст джерелаBeaman, Charles, Krystyna Kozii, Saima Hilal, Minghua Liu, Anthony J. Spagnolo-Allende, Guillermo Polanco-Serra, Christopher Chen, et al. "Cerebral Microbleeds, Cerebral Amyloid Angiopathy, and Their Relationships to Quantitative Markers of Neurodegeneration." Neurology 98, no. 16 (February 28, 2022): e1605-e1616. http://dx.doi.org/10.1212/wnl.0000000000200142.
Повний текст джерелаYadav, Dharmendra Kumar. "Potential Therapeutic Strategies of Phytochemicals in Neurodegenerative Disorders." Current Topics in Medicinal Chemistry 21, no. 31 (December 23, 2021): 2814–38. http://dx.doi.org/10.2174/1568026621666211201150217.
Повний текст джерелаRibe, Elena M., Esther Serrano-Saiz, Nsikan Akpan, and Carol M. Troy. "Mechanisms of neuronal death in disease: defining the models and the players." Biochemical Journal 415, no. 2 (September 25, 2008): 165–82. http://dx.doi.org/10.1042/bj20081118.
Повний текст джерелаAccogli, Andrea, Kether Guerrero, Maria Daniela D’Agostino, Luan Tran, Cécile Cieuta-Walti, Isabelle Thiffault, Sébastien Chénier, Jeremy Schwartzentruber, Jacek Majewski, and Geneviève Bernard. "Biallelic Loss-of-Function Variants in AIMP1 Cause a Rare Neurodegenerative Disease." Journal of Child Neurology 34, no. 2 (November 28, 2018): 74–80. http://dx.doi.org/10.1177/0883073818811223.
Повний текст джерелаДисертації з теми "Cerebral neurodegenerative disease"
Augé, Marí Elisabet. "Categorització dels cossos de poliglucosà cerebrals basada en la presència de neoepítops reconeguts per IgMs naturals." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/586351.
Повний текст джерелаThe term polyglucosan bodies (PGBs) refers to complex aggregates composed of relatively large glucose polymers reaching diameters of tens of micrometres. PGBs have been reported in the central nervous system, but also in other organs and tissues. During the ageing process, human brain accumulates one type of PGBs called corpora amylacea (CA). Although CA have been studied for several years, their origin and function remain unclear. PGBs are also associated with Lafora disease, a neurodegenerative condition that is characterized by the presence of PGBs structures called Lafora bodies (LBs). On the other hand, brain ageing in mice leads to the progressive appearance and expansion of degenerative granular PGBs frequently referred to as Periodic Acid Schiff (PAS) granules. These granules, which are present mainly in the hippocampus, originate in astrocytes processes and tend to appear in clusters. Recently, our research group have reported the presence of neo-epitopes on these structures, responsible of numerous false positive staining on these bodies when immunohistochemical procedures are used. This thesis aimed to study the origin, composition and function of PGBs that appear with age and in neurodegenerative conditions such as Alzheimer’s disease and Lafora disease, focusing on the possible presence of neo-epitopes on these structures. The results obtained in this thesis show, firstly, that CA are structures similar to PAS granules from mice brain and that CA also contain neo-epitopes. In both cases, the neo-epitopes can be recognized by natural IgM antibodies, suggesting a new relation between PGBs and the natural immune system. This fact explains the controversial results previously described about the presence of some components in CA. In this work, some of these components have been discarded. Secondly, malin deficient mice, a mouse model of Lafora disease, present distinct types of PGBs: PAS granules or CA-like granules, originated in astrocytes, and neuronal LBs. This last type of PGBs is specific of this condition and does not contain neo-epitopes. Overall results suggest that CA are PGBs related to the aggregation of non-degradable products produced during ageing process and increased in neurodegenerative conditions, whereas LBs are pathogenic structures responsible of the neurodegeneration observed in Lafora disease.
Simões, Ana Carolina Viana. "Avaliação do efeito neuroprotetor do canabidiol em mitocôndrias isolados de córtex cerebral de rato." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/60/60134/tde-29062011-202616/.
Повний текст джерелаNeurodegenerative diseases (ND) are among the leading causes of mortality and morbidity in Western countries. There is not a definitive treatment for these neuropathies, but studies have indicated mechanisms of toxicity which include mitochondrial dysfunction, oxidative stress and apoptosis. Therefore, mitochondria are important targets for future neuroprotective strategies to treat, prevent or even slow the neurodegeneration. In this context, cannabidiol (CBD), a constituent of non-psychoactive Cannabis sativa and whose neuroprotective property has been suggested by different studies, emerges as a promising alternative. Different molecular mechanisms may be involved in the neuroprotection exerted by CBD. Although the potential beneficial effects of cannabidiol in relation to neurodegenerative diseases has already been suggested, there are no studies addressing specifically the mechanisms of protection against mitochondrial toxicity brain, a key event in the neurodegenerative process. This study aimed to investigate the effects of CBD on rat brain mitochondria, as well as the mechanisms of neuroprotection. The following parameters were evaluated: mitochondrial function, mitochondrial oxidative stress and permeability transition of the mitochondrial membrane (MPT). The results suggest that cannabidiol can protect brain mitochondria against: the osmotic swelling induced by calcium/phosphate, the production of H2O2 induced by tert-butyl hydroperoxide and the lipid peroxidation induced by Fe2+ and citrate. The mitochondrial calcium uptake and phosphorylative capacity were not affected.
Melton, Lisa M. "Neuropathological studies of glial activation in experimental head injury and a novel model of chronic cerebral inflammation." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339406.
Повний текст джерелаSalvadores, Bersezio Natalia. "Amyloid-β and chronic cerebral hypoperfusion in the early pathogenesis of Alzheimer's disease". Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23388.
Повний текст джерелаBufill, Soler Enric. "Cambios heterocrónicos en la evolución cerebral humana y su implicación en la enfermedad de alzheimer y otras enfermedades neurodegenerativas." Doctoral thesis, Universitat Rovira i Virgili, 2016. http://hdl.handle.net/10803/399143.
Повний текст джерелаLa enfermedad de Alzheimer es frecuente en los seres humanos y extremadamente infrecuente en otros mamíferos. Por lo tanto, algunos de los cambios ocurridos durante la evolución cerebral humana podrían tener relación con esta enfermedad. Durante la evolución cerebral humana se han producido cambios heterocrónicos, consistentes en la retención de caracteres juveniles en la edad adulta, como una elevada plasticidad sináptica, en algunas áreas cerebrales (neotenia neuronal). Las lesiones propias de la enfermedad de Alzheimer coinciden con las áreas en que se ha producido una neotenia neuronal. Dichas áreas se caracterizan por un elevado turn-over sináptico. Las proteínas que forman parte de la vía de señalización de la reelina intervienen en la plasticidad sináptica. Hemos encontrado tres genes que participan en dicha vía que presentan polimorfismos de nucleótido único que pueden aumentar o disminuir significativamente el riesgo de presentar Alzheimer o deterioro cognitivo leve. Dichos genotipos son RELN (rs 528528 y rs 2299356), PLK2 (rs 15009 y rs 702723) y CAMK2A (rs 3756577 y rs 3822606). Tres de los genotipos encontrados están en la región promotora del gen, lo que sugiere que en la enfermedad de Alzheimer podrían intervenir cambios epigenéticos que alteren la expresión de determinados genes relacionados con la plasticidad sináptica.
Alzheimer's disease is very common in the humans and extremely rare in other mammals. Therefore, some of the changes that have occurred during human brain evolution may be related with this disease. During the human brain evolution heterocronic changes have occurred, consisting in the retention of juvenile characters in adulthood, as a high synaptic plasticity in some brain areas (neuronal neoteniy). The characteristic lesions of Alzheimer's disease coincide with the areas in which there has been a neuronal neoteny. These areas are characterized by a high synaptic turn-over . The proteins that form part of the reelin signaling pathway are involved in the synaptic plasticity.We found three genes that participate in the reelin signaling pathway that present single nucleotide polymorphisms that may increase or decrease significantly the risk of presenting Alzheimer or mild cognitive impairment. These genotypes are RELN (*rs 528528 and *rs 2299356), PLK2 (*rs 15009 and *rs 702723) and CAMK2To (*rs 3756577 and *rs 3822606). Three of the genotypes are found in the promoter region of the gene, which suggests that in Alzheimer's disease could intervene epigenetic changes that alter the expression of certain genes related with the synaptic plasticity.
Coutinho, Artur Martins Novaes. "Análise de alterações volumétricas e metabólicas cerebrais nos diferentes subtipos de comprometimento cognitivo leve." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5151/tde-12012016-084122/.
Повний текст джерелаIntroduction: Mild cognitive impairment (MCI) is presumably a transitional stage between normal aging and dementia, particularly Alzheimer\'s disease (AD). Non-amnestic subtypes (naMCI) present with executive, attention, visuospatial and language dysfunctions. They have a lower conversion rate to dementia compared to amnestic subtypes (aMCI). Investigations regarding biomarker profiles of naMCI as an independent group are scarce. To our knowledge there is no study investigating the brain volumetric and metabolic features, as well as the profile of cerebrospinal fluid (CSF) biomarkers of naMCI patients as a single group in comparison to aMCI and cognitively normal elderly patients (control group - CG). Objective: to investigate the brain volumetric and metabolic changes in individuals presenting amnestic and non-amnestic MCI subtypes in comparison to elderly volunteers without cognitive impairment, aiming to verify if there are agreements between these changes. Possible associations between the imaging profile of these groups and classical patterns of high risk for developing AD were also evaluated, as well as possible correlations between imaging biomarkers, CSF biomarkers and clinical data. Methods: a hundred and fourteen (114) patients were included in three different groups: naMCIg (N = 38), aMCIg (N = 46) and CG (N = 30). Patients underwent brain MRI (in order to exclude other causes of the cognitive impairment but also for VBM analysis) and [18F]FDG-PET. A subsample (naMCIg = 33, aMCIg = 38) also underwent a lumbar puncture in order to assess the profile of amyloid-ß peptide, tau and phosphorylated tau protein levels in the CSF. Results: There was no difference in CSF biomarkers, education years, age, gender and cardiovascular risk factors between the naMCI and aMCI groups, except for a higher prevalence of dyslipidemia in aMCI. The amnestic MCI group had lower rBGM in relation to control group in the precuneus, posterior cingulate and left medium temporal gyrus. Compared to aMCIg, naMCIg presented with bilateral prefrontal cortex hypometabolism, but without metabolic changes in relation to CG after correction for partial volume effect. Amnestic MCI group had bilateral temporal lobe volume reduction in comparison to naMCI and CG, particularly in the polar and mesial parts of the temporal lobe. Non-amnestic MCI presented with discrete volumetric reductions in comparison to CG, Conclusion: Volumetric and metabolic alterations were different and essentially discordant between aMCI and naMCI groups in comparison to CG. Amnestic MCI showed metabolic and volumetric profiles classically related to MCI due to AD, while naMCI group presented with less-significant areas of volumetric and metabolic reductions in relation to control group. Our non-amnestic MCI group probably represents a heterogeneous group with a different pattern of neurodegeneration than the classical MCI due to AD
Martínez, Moreno Margot. "Efecte de l'activació del canal K(ATP) al perfil d'expressió microglial durant la neurodegeneració a l'hipocamp de la rata." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/121511.
Повний текст джерелаIn this thesis we have studied the effect of the activation of the potassium channetl ATP-dependent (KATP channel) with the drug diazoxida, a KCO (potassium channel opener), over the phenotypic expression profile of microglial cells. We did it with two different approaches: an in vitro model with the murine cell line BV2; and an in vivo model of excitotòxic lesion in rat hippocampus. We have also studied how this modulation affects the progression of the damage of the excitotòxic lesion and the hipocampal neurogènesis associated. Finally, we have described the presence of voltage-gated calcium channels (VGCC) in microglia and how its regulation also affects to the activity of microglia in vivo and in vitro.
Chou, Chia-Mei, and 周嘉玫. "Molecular pathogenesis of experimental cerebral toxocariasis progress into neurodegenerative diseases." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/dt7fd8.
Повний текст джерела臺北醫學大學
醫學科學研究所
106
Toxocariasis is a worldwide parasitic zoonosis and mainly caused by Toxocara canis. Long-term residence of T. canis larvae in a paratenic host’s brain can cause cerebral toxocariasis (CT). In human CT and mouse model of CT, T. canis larval brain invasion can cause cerebral damage and neuroinflammation, further contributing to several neurological symptoms and neurodegenerative disorders. Hippocampus is characterized for synaptic plasticity and spatial learning and memory; however parasitic invasion of hippocampus may trigger neuroinflammatory and neurodegenerative disorders. Astrocytes are the most abundant glia cells manipulating the host’s defense in the brain; moreover, they are proposed to pathologically involve in neurodegenerative disorders, including Alzheimer’s disease. The present study intended to assess pathological changes, expressions of neurodegeneration-associated factors (NDAFs) and ubiquitin-proteasome system (UPS) function in hippocampus and associated cognitive behavior in ICR mice orally inoculated with a high, medium or low-dose of T. canis embryonated ova during a 20-week investigation. Secondly, the cytotoxic effects of T. canis larval excretory-secretory antigens (TcES Ag) on astrocytes were assessed by apoptosis and autophagy expressions in vitro. Our results indicated there were insignificant differences in learning and memory function between the experimental and uninfected control mice, possibly because the site where T. canis larvae invaded was the surrounding area but not the hippocampus per se. Nevertheless, enhanced expressions of NDAF, persistent UPS impairment and excess amyloid β (Aβ) accumulation concomitantly emerged in the experimental mice hippocampus at 8, 16 and 20 weeks post-infection. In addition, TcES Ag treatment reduced cell viability and caused morphological changes. Expressions of autophagy associated proteins including Beclin 1, phosphor-mTOR and LC3-Ⅱ were not significantly changed; however, p62 as well as the cell survival protein, mTOR, was concomitantly decreased in TcES Ag treatment. Significantly accelerated cleaved caspase-3 and cytochrome c expression as well as enhanced caspase-9 and caspase-8 activation were found in astrocytes with TcES Ag treatment. Caspase-3 activity and apoptotic cells numbers were also increased as detected by fluorescence microscopy, implying that TcES Ag may trigger astrocytes apoptosis predominantly through intrinsic and extrinsic pathways rather autophagy to further contribute to the disease progression of CT. This study provides a comprehensive role in the pathogenesis of CT progress into neurodegenerative diseases.
Книги з теми "Cerebral neurodegenerative disease"
Cerebral plasticity: New perspectives. Cambridge, Mass: MIT Press, 2011.
Знайти повний текст джерелаAttems, Johannes, and Kurt A. Jellinger. Neuropathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0006.
Повний текст джерелаForsyth, Rob, and Richard Newton. Specific conditions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784449.003.0004.
Повний текст джерелаChalupa, Leo M., Nicoletta Berardi, Nicoletta Berardi, and Matteo Caleo. Cerebral Plasticity: New Perspectives. MIT Press, 2011.
Знайти повний текст джерелаChalupa, Leo M., Nicoletta Berardi, and Matteo Caleo. Cerebral Plasticity: New Perspectives. MIT Press, 2011.
Знайти повний текст джерелаHodges, John R. Localized Cognitive Functions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749189.003.0003.
Повний текст джерелаBenarroch, Eduardo E. Neuroscience for Clinicians. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.001.0001.
Повний текст джерела(Editor), Bruce Trembly, and William Slikker (Editor), eds. Neuroprotective Agents: Fourth International Conference (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1999.
Знайти повний текст джерелаM.D.) International Conference on Neuroprotective Agents: Clinical and Experimental Aspects (4th : 1998 : Annapolis. Neuroprotective Agents: Fourth International Conference (Annals of the New York Academy of Sciences, V. 890). New York Academy of Sciences, 1999.
Знайти повний текст джерелаЧастини книг з теми "Cerebral neurodegenerative disease"
Sahni, Jasjeet Kaur, Sihem Doggui, Lé Dao, and Charles Ramassamy. "Nanotechnology for Cerebral Delivery of Nutraceuticals for the Treatment of Neurodegenerative Diseases." In Functional Foods, Nutraceuticals, and Degenerative Disease Prevention, 263–83. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9780470960844.ch10.
Повний текст джерелаVogt, Brent A., Alex Martin, Kent E. Vrana, John R. Absher, Leslie J. Vogt, and Patrick R. Hof. "Multifocal Cortical Neurodegeneration in Alzheimer’s Disease." In Cerebral Cortex, 553–601. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4885-0_16.
Повний текст джерелаFiskum, Gary, and Robert E. Rosenthal. "Metabolic Failure, Oxidative Stress, and Neurodegeneration Following Cerebral Ischemia and Reperfusion." In Neurodegenerative Diseases, 203–9. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0209-2_26.
Повний текст джерелаFarrer, Lindsay A. "Locating Genetic Modifiers for Inherited Neurodegenerative Diseases." In Cerebral Cortex, 433–59. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4885-0_12.
Повний текст джерелаKhan, Shagufta, Aarti Belgamwar, and Pramod Yeole. "Nanopharmaceuticals for the Improved Treatment of Cerebral Stroke." In Nanobiotechnology in Neurodegenerative Diseases, 369–85. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-30930-5_15.
Повний текст джерелаMehler, Mark E. "Regional Forebrain Patterning and Neural Subtype Specification: Implications for Cerebral Cortical Functional Connectivity and the Pathogenesis of Neurodegenerative Diseases." In Results and Problems in Cell Differentiation, 157–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-540-46006-0_8.
Повний текст джерелаV., Hugh Perry. "Environmental Influences on Neurodegenerative Disease: The Impact of Systemic Inflammation." In Cerebral Plasticity, 315–24. The MIT Press, 2011. http://dx.doi.org/10.7551/mitpress/9780262015233.003.0025.
Повний текст джерелаTam, J. H. K., and S. H. Pasternak. "Alzheimer’s Disease." In The Cerebral Cortex in Neurodegenerative and Neuropsychiatric Disorders, 83–118. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-801942-9.00004-5.
Повний текст джерелаKim, E. H., N. Mehrabi, L. J. Tippett, H. J. Waldvogel, and R. L. M. Faull. "Huntington Disease." In The Cerebral Cortex in Neurodegenerative and Neuropsychiatric Disorders, 195–221. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-801942-9.00008-2.
Повний текст джерелаAttems, Johannes, and Kurt A. Jellinger. "Neuropathology." In Oxford Textbook of Old Age Psychiatry, 77–98. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198807292.003.0005.
Повний текст джерелаТези доповідей конференцій з теми "Cerebral neurodegenerative disease"
Elkan, Eva-Maria, Ana-Maria Papuc, Roxana Elena Bogdan Goroftei, Elena Ariela Banu, Monica Laura Zlati, Adriana Gabriela Albeanu, and Alina Pleșea Condratovici. "DREAMING AND PARASOMNIAS FROM A CEREBRAL STRUCTURAL VIEW." In The European Conference of Psychiatry and Mental Health "Galatia". Archiv Euromedica, 2023. http://dx.doi.org/10.35630/2022/12/psy.ro.6.
Повний текст джерелаCollar, Giovanna Carello, Marco Antônio De Bastiani, and Eduardo R. Zimmer. "HUNTINGTON’S DISEASE AND EARLYONSET ALZHEIMER’S DISEASE SHARE A TRANSCRIPTOMIC SIGNATURE." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda082.
Повний текст джерелаGrah, Vitor Matias, Guilherme Sampaio Silva, Karla Viana Rezende, Ayrton Senna do Brasil Amaral Alves, Maria Inês Vaz de Oliveira, Maria Paula Banhara Rodrigues, and Juliana Carollyne Amorim. "The relationship between apolipoprotein e4 and bloodbrain barrier dysfunction in Alzheimer Disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.091.
Повний текст джерелаBarbosa, Mateus Gonçalves de Sena, Ghaspar Gomes de Oliveira Alves Francisco, Rafaela Luiza Vilela de Souza, João Marcos Alcântara de Souza, and Nicollas Nunes Rabelo. "Chronic traumatic encephalopathy in military and sportsists: a factual problem?: a systematic review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.324.
Повний текст джерелаSaito, Monalisa Moura, Dhyego Ferreira Moreira de Lacerda, Ana Claudia Marque Gouveia de Melo, Lucas Monteiro Barros Nunes, Luana Cristina Rodrigues de Oliveira Costa, and Eduarda Silvestre Ribeiro da Costa Gomes. "Neurodegeneration with cerebral iron accumulation: a case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.145.
Повний текст джерелаClemotte, Alejandro, Harbil Arregui, Miguel Ángel Velasco, Luis Unzueta, Jon Goenetxea, Unai Elordi, Eduardo Rocon, et al. "Trajectory clustering for the classification of eye-tracking users with motor disorders." In Actas de las XXXVII Jornadas de Automática 7, 8 y 9 de septiembre de 2016, Madrid. Universidade da Coruña, Servizo de Publicacións, 2022. http://dx.doi.org/10.17979/spudc.9788497498081.0150.
Повний текст джерелаMarques, Daiane Silva, Roseane Oliveira Veras, Maria Dhescyca Ingrid Silva Arruda, João Felipe Tinto Silva, and Francisco Lucas de Lima Fontes. "REPERCUSSÕES CLÍNICAS E FISIOPATOLÓGICAS DA DOENÇA DE HUNTINGTON: REVISÃO INTEGRATIVA DA LITERATURA." In II CONGRESSO ON-LINE NACIONAL DE CIÊNCIAS & SAÚDE (II CONCS). Literacia Cientifica Editora & Cursos, 2022. http://dx.doi.org/10.53524/lit.edt.978-65-84528-09-3/72.
Повний текст джерелаЗвіти організацій з теми "Cerebral neurodegenerative disease"
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.
Повний текст джерела