Academic literature on the topic 'Parkinson Diseases'
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Journal articles on the topic "Parkinson Diseases"
Zhunina, Olga A., Nikita G. Yabbarov, Andrey V. Grechko, Shaw-Fang Yet, Igor A. Sobenin, and Alexander N. Orekhov. "Neurodegenerative Diseases Associated with Mitochondrial DNA Mutations." Current Pharmaceutical Design 26, no. 1 (February 25, 2020): 103–9. http://dx.doi.org/10.2174/1381612825666191122091320.
Full textLeupold, Dieter, Lukasz Szyc, Goran Stankovic, Sabrina Strobel, Hans-Ullrich Völker, Ulrike Fleck, Thomas Müller, Matthias Scholz, Peter Riederer, and Camelia-Maria Monoranu. "Melanin and Neuromelanin Fluorescence Studies Focusing on Parkinson’s Disease and Its Inherent Risk for Melanoma." Cells 8, no. 6 (June 15, 2019): 592. http://dx.doi.org/10.3390/cells8060592.
Full textRogaeva, E., and J. Hardy. "Gaucher and Parkinson diseases: Unexpectedly related." Neurology 70, no. 24 (June 9, 2008): 2272–73. http://dx.doi.org/10.1212/01.wnl.0000314657.92762.0f.
Full textSingleton, A. "What does PINK1 mean for Parkinson diseases?" Neurology 63, no. 8 (October 25, 2004): 1350–51. http://dx.doi.org/10.1212/01.wnl.0000144272.53634.49.
Full textNUNOMURA, AKIHIKO, GEORGE PERRY, JING ZHANG, THOMAS J. MONTINE, ATSUSHI TAKEDA, SHIGERU CHIBA, and MARK A. SMITH. "RNA Oxidation in Alzheimer and Parkinson Diseases." Journal of Anti-Aging Medicine 2, no. 3 (January 1999): 227–30. http://dx.doi.org/10.1089/rej.1.1999.2.227.
Full textOkun, M. S., M. R. DeLong, J. Hanfelt, M. Gearing, and A. Levey. "Plasma testosterone levels in Alzheimer and Parkinson diseases." Neurology 62, no. 3 (February 9, 2004): 411–13. http://dx.doi.org/10.1212/01.wnl.0000106840.72938.84.
Full textZhang, Jing, Izabela Sokal, Elaine R. Peskind, Joseph F. Quinn, Joseph Jankovic, Christopher Kenney, Kathryn A. Chung, Steven P. Millard, John G. Nutt, and Thomas J. Montine. "CSF Multianalyte Profile Distinguishes Alzheimer and Parkinson Diseases." American Journal of Clinical Pathology 129, no. 4 (April 2008): 526–29. http://dx.doi.org/10.1309/w01y0b808emeh12l.
Full textTennigkeit, Jenny, Tim Feige, Maria Haak, Carina Hellqvist, Ümran S. Seven, Elke Kalbe, Jaqueline Schwarz, et al. "Structured Care and Self-Management Education for Persons with Parkinson’s Disease: Why the First Does Not Go without the Second—Systematic Review, Experiences and Implementation Concepts from Sweden and Germany." Journal of Clinical Medicine 9, no. 9 (August 28, 2020): 2787. http://dx.doi.org/10.3390/jcm9092787.
Full textOJ, Castejón, Carrero Gonzalez CM, and Lastre G. "Diabetes and Neurologic Diseases in a Developing Country." Journal of Clinical Case Studies Reviews & Reports 2, no. 4 (August 31, 2020): 1–7. http://dx.doi.org/10.47363/jccsr/2020(2)141.
Full textToovey, Stephen, Susan S. Jick, and Christoph R. Meier. "Parkinson’s disease or Parkinson symptoms following seasonal influenza." Influenza and Other Respiratory Viruses 5, no. 5 (March 21, 2011): 328–33. http://dx.doi.org/10.1111/j.1750-2659.2011.00232.x.
Full textDissertations / Theses on the topic "Parkinson Diseases"
Franco, Iborra Sandra. "Mitochondrial quality control in neurodegenerative diseases: focus on Parkinson’s disease and Huntington’s disease." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/565668.
Full textIn the past years, several important advances have expanded our understanding of the pathways that lead to cell dysfunction and death in Parkinson’s disease (PD) and Huntington’s disease (HD). Both diseases are movement disorders characterized by the loss of a specific subset of neurons within the basal ganglia, dopaminergic neurons in the substantia nigra pars compacta (SNpc), in the case of PD, and medium spiny neurons in the striatum, in the case of HD,. Despite distinct clinical and pathological features, these two neurodegenerative disorders share critical underlying pathogenic mechanisms such as the presence of misfolded and/or aggregated proteins, oxidative stress and mitochondrial anomalies. Mitochondria are the prime energy source in most eukaryotic cells, but these highly dynamic organelles are also involved in a multitude of cellular events. Disruption of mitochondrial homeostasis and the subsequent mitochondrial dysfunction plays a key role in the pathophysiology of neurodegenerative diseases. Therefore, maintenance of mitochondrial integrity through different surveillance mechanisms is critical for neuronal survival. In this thesis I have studied in depth some mitochondrial quality control mechanisms in the context of PD and HD, in order to broaden the knowledge about the pathomechanisms leading to cell death. In the first chapter I have studied mitochondrial protein import in in vitro and in vivo models of PD. In vitro, complex I inhibition, a characteristic pathological hallmark in PD, impaired mitochondrial protein import. This was associated with OXPHOS protein downregulation, accumulation of aggregated proteins inside mitochondria and downregulation of mitochondrial chaperones. Therefore, we aimed to reestablish the mitochondrial protein import by overexpressing two key components of the system: translocase of the outer membrane 20 (TOM20) and translocase of the inner membrane 23 (TIM23). Overexpression of TOM20 and TIM23 in vitro restored protein import into mitochondria and ameliorated mitochondrial dysfunction and cell death. Complex I inhibition also impaired mitochondrial protein import and led to dopaminergic neurodegeneration in vivo. Overexpression of TIM23 partially rescued protein import into mitochondria and slightly protected dopaminergic neurons in the SNpc. On the contrary, TOM20 overexpression did not rescue protein import into mitochondria and exacerbated neurodegeneration in both SNpc and striatum. These results highlight mitochondrial protein import dysfunction and the distinct role of two of their components in the pathogenesis of PD and suggest the need for future studies to target other elements in the system. In the second chapter, I have studied the role of huntingtin in mitophagy and how the polyglutamine expansion present in mutant huntingtin can affect its function. For such, I worked with differentiated striatal ST-Q7 (as control) and ST-Q111 (as mutant) cells, expressing full length huntingtin. In these conditions, induced mitophagy was not mediated by Parkin recruitment into depolarized mitochondria. Mutant huntingtin impaired induced mitophagy by altering wildtype huntingtin scaffolding activity at different steps of mitophagy process: (i) ULK1 activation through its release from the mTORC1, (ii) Beclin1-Vps15 complex formation, (iii) interaction of the mitophagy adapters OPTN and NDP52 with huntingtin and (iv) with LC3. As a result, mitochondria from ST-Q111 cells exhibited increased damage and altered mitochondrial respiration. These results uncover impaired mitophagy as a potential pathological mechanism linked with HD. In conclusion, we have discovered new mitochondrial targets for PD and HD emphasizing the important role that mitochondrial quality control plays in neurodegeneration
Luchesi, Karen Fontes 1984. "Dyphagia in amyotrophic lateral sclerosis and in parkinson¿s disease = A disfagia na esclerose lateral amiotrófica e na doença de Parkinson." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311989.
Full textTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A Doença de Parkinson (DP) é uma das doenças neurodegenerativas mundialmente mais prevalentes. Dentre as doenças do neurônio motor, a Esclerose Lateral Amiotrófica (ELA) é a mais frequente. A qualidade de vida e o prolongamento da expectativa de vida dos sujeitos com doenças neurodegenerativas, como ELA e DP, são foco da intervenção fonoaudiológica, visto que uma das maiores causas de morte são as pneumonias aspirativas. Esta pesquisa teve por objetivo analisar e descrever aspectos relacionados à disfagia e à sua progressão em sujeitos diagnosticados com ELA e DP. Ao todo, participaram 49 sujeitos com ELA e 24 sujeitos com DP. Todos foram avaliados e acompanhados no ambulatório de Otorrinolaringologia/Disfagia do Hospital de Clínicas da Universidade Estadual de Campinas. Foram incluídos no estudo, apenas os sujeitos que estavam em acompanhamento periódico no ambulatório de neurologia do referido hospital e em tratamento medicamentoso. Foram excluídos os sujeitos sem queixa de deglutição ou que apresentassem outras doenças que pudessem causar alteração na deglutição. Todos foram submetidos à entrevista estruturada, videoendoscopia da deglutição, avaliação clínica da deglutição e intervenção fonoaudiológica, além de terem a funcionalidade de ingestão oral classificada pela Functional Oral Intake Scale. Foi realizada uma análise descritiva dos dados com apresentação de frequência das variáveis categóricas e medidas de tendência central e dispersão das variáveis numéricas. Na análise exploratória foram utilizados: Regressão de Cox, teste Exato de Fisher, teste de Kruskal-Wallis, Qui-quadrado, teste de Mann-Whitney e análise de sobrevivência de Kaplan-Meier. As análises foram realizadas por meio do software SPSS versão 13.0 para Windows, tendo sido adotado o nível de significância para os testes estatísticos de 0,05. Na ELA, foi identificado como fator associado à disfagia moderada ou grave, a odinofagia (p=0,01). Foram identificados como fatores que influenciaram na progressão da disfagia na ELA a idade de início da doença (p=0,02) e o início bulbar (p=0,04). A idade de início avançada (p=0,03) e o menor tempo de doença até a primeira avaliação (p=0,004) foram identificados como fatores que levaram à necessidade de indicação de uma via alternativa de alimentação em menor tempo na ELA. Não foram identificados fatores que influenciassem a progressão da disfagia na DP. Observou-se melhora e estabilização da função de deglutição na maioria dos sujeitos com DP estudados. Conclui-se que a idade de início e o início bulbar da ELA são fatores associados à piora rápida da disfagia. Não houve fatores associados à progressão da disfagia na PD e a funcionalidade na deglutição destes pacientes foi caracterizada por melhora e manutenção
Abstract: Parkinson's disease (PD) is one of the most prevalent neurodegenerative diseases worldwide. Among the motor neuron diseases, the Amyotrophic Lateral Sclerosis (ALS) is the most common. The quality of life and longer life expectancy for these individuals with neurodegenerative diseases are the purpose of speech-language therapy, as the leading cause of death are aspirative pneumonias. The objective of this study was to analyze and describe aspects related to dysphagia and its progression in patients diagnosed with ALS and PD. Altogether, 49 patients with ALS and 24 patients with PD participated in the study. All patients were evaluated and followed by at the Otolaryngology/Dysphagia services of the Clinical Hospital of the University of Campinas. The study included only patients who have been regularly monitored at the neurology service and undergoing drug treatment. Patients who had other conditions that could cause changes in swallowing or with no complaints concerning swallowing were excluded. All patients underwent a structured interview, Fiberoptic Endoscopic Evaluation of Swallowing, clinical evaluation of swallowing and swallowing management. Furthermore, they had the swallowing functionality classified by the Functional Oral Intake Scale. We performed a descriptive analysis with presenting the frequency of categorical variables, central measures tendency and dispersion of numerical variables. In exploratory data analysis were applied Cox Regression, Kruskal-Wallis, Chi-square, Mann-Whitney and survival analysis of Kaplan-Meier. The analyses were performed using SPSS version 13.0 for Windows and the significance level for statistical tests was 5%. Odynophagia was identified as an associated factor with moderate or severe dysphagia in ALS. The onset age of ALS (p = 0.02) and the bulbar onset ALS (p = 0.04) were identified as factors that influence the progression of dysphagia in ALS. Advanced onset age (p = 0.03) and shorter disease duration (p = 0.004) were identified as factors that lead to sooner need for non-oral feeding. We did not identify any associated factors with the progression of dysphagia in PD. We noticed an improvement and stabilization of the swallowing function in most patients with PD. We conclude that the onset age and bulbar onset of ALS are factors associated with rapid worsened dysphagia
Doutorado
Epidemiologia
Doutora em Saúde Coletiva
Vilas, Rolán Dolores. "Caracterización clínica, bioquímica y de neuroimagen de la enfermedad de Parkinson asociada a mutaciones del gen LRRK2 y de su fase prodrómica." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/397743.
Full textThis thesis is based on four studies that belong to the same line of research: the study of Parkinson’s disease associated with mutations in the LRRK2 gene (LRRK2-PD). First, we studied the LRRK2-PD from a clinical point of view. Secondly, we conducted a study through transcranial sonography in individuals with the G2019S mutation of the LRRK2 gene, both patients with Parkinson's disease as asymptomatic carriers. Third, we assess functional connectivity by means of magnetic resonance imaging in asymptomatic carriers of mutations in the LRRK2 gene (aLRRK2). Finally, we investigated the ability of biomarkers in cerebrospinal fluid to distinguish LRRK2 mutation carriers from noncarriers. In the manuscript Nonmotor symptoms in LRRK2 G2019S associated Parkinson's disease we found that nonmotor symptoms are frequent in LRRK2-PD and the only nonmotor symptom that differentiates LRRK2-PD and idiopathic PD is hyposmia, present in 39% of LRRK2-PD patients but in 75% of idiopathic PD patients. A significant proportion of LRRK2-PD patients perceived that several nonmotor symptoms, such as hyposmia, depression, constipation or excessive daytime sleepiness, were present before the onset of motor symptoms, suggesting that these symptoms can characterize the prodromal phase of LRRK2-PD. In the study entitled Clinical and imaging markers in premotor LRRK2 G2019S mutation carriers we observed that hyperechogenicity of the substantia nigra is frequent in LRRK2-PD and also in asymptomatic LRRK2 mutation carriers, suggesting that this sonographic finding could be a marker of the premotor phase of LRRK2-PD. In work number 3, Reduced thalamo-cortical functional connectivity in asymptomatic LRRK2 mutation carriers, we found that aLRRK2 showed a decrease in functional connectivity between the left thalamus and contralateral cortical areas, that precede structural changes. Finally, in the manuscript Cerebrospinal fluid biomarkers and clinical features in LRRK2 mutation carriers we found that levels of α-syn in CSF were similar among LRRK2-PD, aLRRK2 and noncarriers but significantly higher than in IPD patients. We found no differences between Aβ1-42, T-tau, and p-tau181 among the study groups. We did not detect differences in CSF protein among aLRRK2 and relatives without the mutation, suggesting that CSF proteins are not a good marker of the disease in asymptomatic subjects.
Gaig, Ventura Carles. "Prevalencia, fenotipo clínico y neuropatológico del parkinsonismo asociado a mutaciones en el gen LRRK2." Doctoral thesis, Universitat de Barcelona, 2011. http://hdl.handle.net/10803/51568.
Full textLRRK2 G2019S mutation is a frequent cause of Parkinson’s disease (PD). This mutation is present in 5-6% of familial PD cases and 1-2 % of sporadic PD patients. LRRK2 R1441G is frequent in PD patients from the Basque country. We hypothesize that 1) In Catalonia, the G2019S and R1441G mutations are frequent in patients with familial as well as sporadic parkinsonism. 2) Clinical features in LRRK2-related parkinsonism are heterogeneous 3) The neuropathological substrate of LRRK2-related parkinsonism is pleomorphic and determines the clinical phenotype. We aim to assess 1) The frequency of the G2019S and R1441G mutations in patients with a clinical diagnosis of PD in Barcelona 2) The clinical phenotype of PD patients carrying a LRRK2 mutation, and 3) The presence of LRRK2 G2019S and R1441G mutations in brains diagnosed of PD, other neurodegenerative parkinsonism, as well as frontotemporal lobar degeneration, and assess the clinical and neuropathological features of those cases carrying a LRRK2 mutation. Results and conclusions: 1) LRRK2 mutations are frequent in PD patients from Barcelona (5.3% of them). The G2019S mutation is more frequent (4.3%) than the R1441G mutation (0.7%). 2) LRRK2 mutations are more frequent in familial PD cases (9.6% of them) than in sporadic cases (3.4%). Family history of parkinsonism is absent in up to 43.7% of patients with LRRK2 mutations. 3) Clinical features of motor and non-motor symptoms of LRRK2-related parkinsonism is indistinguishable from those of classical PD. 4) The neuropathological phenotype of LRRK2 G2019S-related parkinsonism is heterogeneous. Although the most frequent neuropathological substrate is Lewy boby type pathology, we describe a patient with non-specific nigral degeneration and the G2019S mutation. 5) We have not been able to identify LRRK2 mutations in brains of a neurodegenerative disease other than PD (e.g Lewy bodies dementia, Progressive supranuclear palsy or Multiple system atrophy). Presence of LRRK2 mutations in these neurodegenerative diseases would be exceptional or coincidental.
Canal, de la Iglesia Mercè. "Study of pro-apoptotic protein RTP801 homeostasis and its regulation by NEDD4 in Parkinson's disease." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/398915.
Full textRTP801/REDD1 es una proteína pro-apoptótica que se encuentra aumentada en modelos celulares y animales y en muestras humanas de la enfermedad de Parkinson. RTP801 es suficiente y necesaria para promover muerte celular mediante un mecanismo de inhibición de la quinasas de supervivencia mTOR y Akt. NEDD4 es una E3 ubiquitina ligasa que ubiquitiniza proteínas señalizándolas para su posterior degradación. Esta proteína se ha relacionado recientemente con la enfermedad de Parkinson, ya que se ha visto que ubiquitiniza la proteína alfa-sinucleína. En este trabajo, se ha descrito que la RTP801 es un sustrato de la ubiquitina ligasa NEDD4. Se ha demostrado que ambas proteínas interaccionan y que NEDD4 ubiquitiniza RTP801 con cadenas de ubiquitina del tipo K63, señalizándola para su posterior degradación lisosomal. También, se ha observado que NEDD4 regula los niveles de RTP801 en sistemas neuronales, y que la pérdida de función de NEDD4 es tóxica debido al incremento de RTP801 y la consecuente inhibición de las quinasas mTOR/Akt. De forma interesante, la NEDD4 ectópica es capaz de proteger ante la toxicidad provocada por la sobreexpresión de RTP801 y ante la toxina parkinsoniana 6-OHDA. Además, la proteína NEDD4 se encuentra disminuida en neuronas nigrales de la SNpc de cerebros post mortem con la enfermedad de Parkinson. De forma consistente, el compuesto NAB2, un activador de NEDD4, disminuye los niveles de la RTP801 en neuronas. No obstante, la acción de este compuesto no es suficiente para proteger ante la toxicidad de la 6-OHDA. También, se ha identificado una posible regulación entre las E3 ligasas parkina y NEDD4, que conferiría un grado de complejidad mayor a la regulación de la RTP801. Diferentes mutantes de la proteína RTP801 han sido generados para estudiar cómo afecta la ubiquitinización a su estabilidad y función. De forma interesante, el mutante RTP801-K185R pierde la función pro-apoptótica de la RTP801, poniendo en relieve que la ubiquitinización en este residuo es crítica para su función. Finalmente, mediante estudios proteómicos se han identificado numerosos interactores de RTP801 putativos, entre los cuáles se encuentra la clatrina y la proteína adaptadora AP-2, sugiriendo un posible papel de la RTP801 en procesos relacionados con la endocitosis mediada por clatrina.
Ekstrand, Mats. "Mitochondrial dysfunction in neurodegeneration /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-204-7/.
Full textMartín, Flores Núria. "Study of the mTOR pathway in neurodegenerative diseases: from synapses to genes." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/665330.
Full textLa enfermedad de Huntington (EH) y la enfermedad de Parkinson (EP) son enfermedades neurodegenerativas devastadoras caracterizadas por la muerte de subpoblaciones neuronales selectivas. La disfunción neuronal y la muerte son consecuencia de múltiples procesos patogénicos que llevan a la alteración de cascadas de señalización. Una de las vías afectadas de forma común en los procesos neurodegenerativos es la vía mTOR. Como modulador de numerosos procesos celulares, la vía de mTOR está regulada para mantener la supervivencia neuronal y la plasticidad sináptica. Una de las proteínas que modula esta cascada de señalización es RTP801. RTP801 se induce en respuesta a factores de estrés celular y su aumento desencadena la muerte neuronal al regular negativamente la vía mTOR/Akt. La implicación de RTP801 en la EP ha sido ampliamente estudiada, sin embargo, su contribución a la patogénesis de la EH nunca antes había sido explorada. Específicamente, nuestros resultados han identificado a RTP801 como un mediador de la toxicidad inducida por huntingtina mutada. El aumento de RTP801 medía la muerte celular inducida por huntingtina mutada y contribuye a la disfunción del aprendizaje motor en el modelo murino R6/1. El silenciamiento de RTP801 en el estriado de los ratones R6/1 contribuye a preservar la plasticidad sináptica de la vía corticoestriatal, y por tanto del aprendizaje motor. Por otra parte, mostramos que los exosomas secretados por neuronas activan la vía de supervivencia mTOR/Akt en neuronas recipientes. Sin embargo, ante un estrés celular, la toxicidad de RTP801 es propagada a través de exosomas que contrarrestan la activación trófica de la vía mTOR/Akt. Finalmente, demostramos que variaciones genéticas en los componentes de la vía de mTOR modulan la susceptibilidad y la edad de inicio de la EP y, contribuyen a la aparición y severidad de la discinesia inducida por levodopa. En conjunto, nuestros hallazgos indican que la desregulación de la vía de mTOR desempeña un papel importante en la patogénesis asociada a la EP y la EH y, su correcta regulación es crucial para mantener la viabilidad y función neuronal.
Roman, Andrei. "Tau protein aggregation and α-synuclein dysfunction : development of new in vitro and in vivo models to study neurodegenerative diseases." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0281.
Full textThe histopathological hallmarks of the most common neurodegenerative diseases – Alzheimer’s disease and Parkinson’s disease are neurofibrillary tangles formed by tau protein and Lewy bodies inclusions formed by aggregated α-synuclein. The formation and accumulation of these proteins into inclusions cause functional disruptions of the cytoskeleton and leads to neuronal degeneration. The precise mechanisms of tau and synuclein misfolding and aggregation leading to those cellulare incluses, even though very studied, are not fully understood neither for tau protein nor for α-synuclein.Here we have addressed this question using both in vitro and in vivo models. Investigating tau aggregation in vitro, we have found a reversible self-assembly of tau, which depends on temperature and is induced by zinc ions, which is different from the tau aggregation in the presence of aggregation-inducers such as heparin. This process could be implicated in the first steps of tau pathological aggregation. In a second part, we have developed a mouse model for studying the α-synuclein dysfunction. We have shown that α- synuclein is directly involved in the embryonic development of the specific regions of the nervous system, and that it has modulating effect only on the populations of dopaminergic neurons of substantia nigra, which are affected in Parkinson’s disease.Results obtained in our studies of two proteins that undergo pathogenic aggregation and form intracellular inclusions contributed to understanding of molecular and cellular processes associated with neuronal degeneration, which is important for the development of new disease-modifying therapies of neurodegenerative disorders
Campello, Blasco Laura. "Expression in the mammalian retina of genes and proteins associated with Parkinson and other neurodegenerative diseases." Doctoral thesis, Universidad de Alicante, 2015. http://hdl.handle.net/10045/85191.
Full textDomuro, Soriano Carla. "Paper de la proteïna p27 en la regulació de l'expressió de l'α-sinucleïna: Implicacions en la malaltia de Parkinson." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/669150.
Full textOur group has identified different transcriptional programs regulated by the protein p27. In this work we focus on the role of p27 in the transcriptional regulation of the gene that encodes for α-synuclein (SNCA gene), a very important protein involved in Parkinson’s disease. Specifically, α-synuclein forms aggregates in specific regions of the brain. In this thesis, we found that p27-deficient cells have higher levels of α-synuclein. On the other hand, in brains of p27 KO mice we also observed an increase in α-synuclein levels in some brain regions. Additionally, using the CRISPR/Cas9 gene silencing technique we obtained KO cell lines of p27 and E2F4 and in these cell lines we also observe an increase of α-synuclein. Subsequently, through ChIP and luciferase assays, we described the transcriptional regulation of p27 of the SNCA gene in association with two different transcription factors, C/EBPδ and E2F4/p130. In both cases, p27 expression supresses SNCA expression. Furthermore, using shRNAs and the Proximity Ligation Assay (PLA) technique, we observed how the decrease of p27 and p130 protein levels also increased α-synuclein aggregation levels. We have also identified CDK5 as a kinase that phosphorylates p27 and cause it exportation to cytoplasm where it cannot function as a transcriptional regulator. Finally, using shRNAs we decreased the levels of CDK5 in these cells and with PLA we were able to see how the decrease of CDK5 levels causes an increase in α-synuclein aggregation levels. As it is described that CDK5 can interact with E2F1/pRb complexes, we have characterized the binding of p27 to E2F1 by affinity chromatography assays and we established that, as occurs with E2F4, E2F1 binds to the carboxyl moiety of p27, between aminoacids 160-170.
Books on the topic "Parkinson Diseases"
Understanding Parkinson's disease: [a self help guide]. Omaha, NB: Addicus Books, 1999.
Find full textCram, David L. Understanding Parkinson's disease: [a self help guide]. Omaha, Neb: Addicus Books, 1999.
Find full text1953-, Gao Xiao Ke, and Schechter Steven 1961-, eds. Understanding Parkinson's disease: A patient's guide to treatment. 2nd ed. Omaha, Neb: Addicus Books, 2009.
Find full textOHOLO Conference on Basic and Therapeutic Strategies in Alzheimer's and Other Related Neuropsychiatric Disorders (30th. 1985 Elat, Israel). Alzheimer's and Parkinson's diseases: Strategies for research and development. New York: Plenum Press, 1986.
Find full textStarkstein, Sergio E. Psychiatric and cognitive disorders in Parkinson Disease. New York: Cambridge University Press, 2002.
Find full textNational, Conference on Alzheimer's Disease and Dementia: Problems Prospects and Perspectives (3rd 1988 Detroit Mich ). Alzheimer's and Parkinson's diseases: Recent advances in research and clinical management. New York: Plenum Press, 1989.
Find full textInternational Conference on Alzheimer's and Parkinson's Diseases: Basic and Therapeutic Strategies (2nd 1989 Kyoto, Japan). Basic, clinical, and therapeutic aspects of Alzheimer's and Parkinson's diseases. New York: Plenum Press, 1990.
Find full textInternational Conference on Alzheimer's and Parkinson's Diseases: Basic and Therapeutic Strategies (2nd 1989 Kyoto, Japan). Basic, clinical, and therapeutic aspects of Alzheimer's and Parkinson's diseases. New York: Plenum Press, 1990.
Find full textInternational Conference on Alzheimer's and Parkinson's Diseases: Basic and Therapeutic Strategies (2nd 1989 Kyoto, Japan). Basic, clinical, and therapeutic aspects of Alzheimer's and Parkinson's diseases. New York: Plenum Press, 1990.
Find full textDieterich, Heinz. Curar en Cuba: Descubrimientos de prevención y curación de sida, cáncer, parkinson, y otras. Tafalla: Txalaparta, 1998.
Find full textBook chapters on the topic "Parkinson Diseases"
Weis, Serge, Michael Sonnberger, Andreas Dunzinger, Eva Voglmayr, Martin Aichholzer, Raimund Kleiser, and Peter Strasser. "Neurodegenerative Diseases: Parkinson Disease." In Imaging Brain Diseases, 1001–20. Vienna: Springer Vienna, 2019. http://dx.doi.org/10.1007/978-3-7091-1544-2_37.
Full textAllen, Jacqui E., and Anna Miles. "Parkinson Disease." In Neurologic and Neurodegenerative Diseases of the Larynx, 143–59. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-28852-5_12.
Full textMiller-Patterson, Cameron, Kathryn E. Krobot, Edward A. Burton, and Libby J. Smith. "Parkinson-Plus Syndromes." In Neurologic and Neurodegenerative Diseases of the Larynx, 161–69. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-28852-5_13.
Full textJiang, Hong, Ning Song, Qian Jiao, Limin Shi, and Xixun Du. "Iron Pathophysiology in Parkinson Diseases." In Brain Iron Metabolism and CNS Diseases, 45–66. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9589-5_4.
Full textDavids, Joseph, and Hutan Ashrafian. "AIM in Neurodegenerative Diseases: Parkinson and Alzheimer." In Artificial Intelligence in Medicine, 1–15. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-58080-3_190-1.
Full textKaramat, E., J. Ilmberger, W. Poewe, and F. Gerstenbrand. "Memory dysfunction in Parkinson patients: an analysis of verbal learning processes." In Age-associated Neurological Diseases, 93–97. Vienna: Springer Vienna, 1991. http://dx.doi.org/10.1007/978-3-7091-9135-4_14.
Full textTomlinson, Julianna, Valerie Cullen, and Michael G. Schlossmacher. "Identifying Targets in α-Synuclein Metabolism to Treat Parkinson Disease and Related Disorders." In Protein Misfolding Diseases, 817–41. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470572702.ch37.
Full textDickson, Dennis W., Howard Crystal, Shu-Hui Yen, and Peter Davies. "Alzheimer - Parkinson Disease Spectrum and Diffuse Lewy Body Disease." In Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases, 385–90. Boston, MA: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4684-5844-2_79.
Full textGollob, Michael H., Rafeeq Samie, David H. Birnie, Martin S. Green, and Robert M. Gow. "The Wolff-Parkinson-White Syndrome and the Risk of Sudden Death." In Electrical Diseases of the Heart, 55–72. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4978-1_5.
Full textMüller, Martijn L. T. M., and Nicolaas I. Bohnen. "In Vivo Positron Emission Tomography of Extrastriatal Non-Dopaminergic Pathology in Parkinson Disease." In The Neuroimaging of Brain Diseases, 143–70. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78926-2_7.
Full textConference papers on the topic "Parkinson Diseases"
Martins, Wanghley, and Fábio Henrique Oliveira. "Protótipo de sistema para coleta de dados inerciais com foco na doença de Parkinson." In Encontro Nacional de Computação dos Institutos Federais. Sociedade Brasileira de Computação - SBC, 2020. http://dx.doi.org/10.5753/encompif.2020.11062.
Full textBaga, Dina, Dimitrios I. Fotiadis, Spiros Konitsiotis, Sofia Tsouli, Maria Diakou, Maria Teresa Arrendondo, Juan Jacobo Estrada, Mario Pansera, and Metin Akay. "PERFORM: A platform for monitoring and management of chronic neurodegenerative diseases: The Parkinson and Amyotrophic Lateral Sclerosis case." In 2009 4th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2009. http://dx.doi.org/10.1109/ner.2009.5109220.
Full textWei, Yunyue, Bingquan Zhu, Chen Hou, Chen Zhang, and Yanan Sui. "Interactive Video Acquisition and Learning System for Motor Assessment of Parkinson's Disease." In Thirtieth International Joint Conference on Artificial Intelligence {IJCAI-21}. California: International Joint Conferences on Artificial Intelligence Organization, 2021. http://dx.doi.org/10.24963/ijcai.2021/718.
Full textCruttenden, Corey, Mahdi Ahmadi, Xiao-Hong Zhu, Wei Chen, and Rajesh Rajamani. "An MRI Compatible Brain Probe for Signal Recording and Deep Brain Stimulation." In 2018 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dmd2018-6951.
Full textLy, Khoi, Aimee Cloutier, and James Yang. "Quantitative Motor Assessment, Detection, and Suppression of Parkinson’s Disease Hand Tremor: A Literature Review." In ASME 2016 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/detc2016-59095.
Full textRudraraju, Sreekanth, and The Nguyen. "Wearable Tremor Reduction Device (TRD) for Human Hands and Arms." In 2018 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dmd2018-6918.
Full textTully, Brett, and Yiannis Ventikos. "Modelling Normal Pressure Hydrocephalus as a ‘Two-Hit’ Disease Using Multiple-Network Poroelastic Theory." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19135.
Full textZanini, Rafael Anicet, and Esther Luna Colombini. "Parkinson sEMG signal prediction and generation with Neural Networks." In Concurso de Teses e Dissertações da SBC. Sociedade Brasileira de Computação, 2021. http://dx.doi.org/10.5753/ctd.2021.15759.
Full textRanchet, Maud, Mark Tant, Abiodun E. Akinwuntan, and Hannes Devos. "Comorbidities in Drivers with Parkinson Disease." In Driving Assessment Conference. Iowa City, Iowa: University of Iowa, 2015. http://dx.doi.org/10.17077/drivingassessment.1549.
Full textKim, Jung Hwan, Thomas H. Mareci, and Malisa Sarntinoranont. "Computational Model of Interstitial Transport in the Rat Brain Using Diffusion Tensor Imaging." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176633.
Full textReports on the topic "Parkinson Diseases"
Liu, Liushu, and Zhiyou Cai. Association between cerebral small diseases and the risk of Parkinson disease: a systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0083.
Full textTrimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, November 2008. http://dx.doi.org/10.21236/ada493391.
Full textBeal, M. F. Oxidative Damage in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada434051.
Full textTrimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, November 2010. http://dx.doi.org/10.21236/ada609645.
Full textSeroogy, Kim B., and David M. Yurek. Neuregulins, Neuroprotection and Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, December 2002. http://dx.doi.org/10.21236/ada415998.
Full textBeal, M. F. Oxidative Damage in Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada416957.
Full textTrimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada609150.
Full textTrimble, Brian A. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, November 2009. http://dx.doi.org/10.21236/ada511588.
Full textNelson, Lorene M. Military Service and Parkinson's Disease. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada583477.
Full textTanner, Caroline M. Alaska Native Parkinson's Disease Registry. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada562185.
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