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Relevant bibliographies by topics / Alpha-Synuclein, Prion Protein, Aggregation / Dissertations / Theses

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Dissertations / Theses on the topic 'Alpha-Synuclein, Prion Protein, Aggregation'

Author: Grafiati

Published: 14 March 2023

Last updated: 27 July 2025

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1

Aulic, Suzana. "Alpha-synuclein amyloid accumulation and its interaction with prion protein." Doctoral thesis, SISSA, 2015. http://hdl.handle.net/20.500.11767/4101.

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α-Synuclein (α-syn) plays a central role in the pathogenesis of neurodegenerative disorders collectively known as “synucleinopathies” that include Parkinson’s disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Understanding the underlying molecular mechanisms of neurodegenerative diseases is indispensably important because of the prevalence of these devastating conditions in the elderly population. Several findings from cell culture and in vivo experiments suggest intercellular transfer of α-syn aggregates. The concept of intracellular α-syn pathology spread was

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2

Roostaee, Alireza. "Importance of dimerization in aggregation and neurotoxicity of Prion and [alpha]-Synuclein in prion and Parkinson's diseases." Thèse, Université de Sherbrooke, 2012. http://hdl.handle.net/11143/6650.

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Abstract: Neurodegenerative diseases are associated with progressive loss of structure or function of neurons which results in cell death. Recent evidence indicate that all neurodegenerative disorders, sporadic or transmissible, may have a common pathological mechanism at the molecular level. This common feature consists of protein aggregation and accumulation of harmful aggregates in neuronal cells resulting in cellular apoptosis and neurotoxicity. Neurodegenerative diseases can affect abstract thinking, skilled movements, emotional feelings, cognition, memory and other abilities. This divers

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3

Ryazanov, Sergey. "Oligomer modulator anle138b and related compounds in neurodegeneration and beyond." Doctoral thesis, Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2020. http://hdl.handle.net/21.11130/00-1735-0000-0005-1519-8.

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4

Fonseca, Ornelas Luis Eduardo Verfasser], Markus [Akademischer Betreuer] Zweckstetter, Tiago Fleming [Gutachter] Outeiro, et al. "Modulating the aggregation of alpha-synuclein and prion protein with small molecules. / Luis Eduardo Fonseca Ornelas ; Gutachter: Tiago Fleming Outeiro, Henning Urlaub, Kai Tittmann, Christian Griesinger, Reinhard Jahn ; Betreuer: Markus Zweckstetter." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2016. http://d-nb.info/1118846931/34.

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5

Morgan, Sophie. "The prion-like properties of assembled human alpha-synuclein." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/277553.

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The pathological hallmark of many age-related neurodegenerative diseases is the presence of proteinaceous inclusions in nerve cells and glial cells. Alpha-synuclein is the main component of the inclusions of Parkinson’s disease, dementia with Lewy bodies and multiple system atrophy, as well as of rarer diseases, collectively called synucleinopathies. For a long time, it was widely believed that neurodegenerative diseases were cell-autonomous; however, a more recent hypothesis has suggested that some misfolded proteins resemble prions. Thus, aggregated alpha-synuclein shares features of PrPSc,

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6

Iljina, Marija. "Aggregation of alpha-synuclein using single-molecule spectroscopy." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/263216.

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The aggregation of alpha-synuclein (αS) protein from soluble monomer into solid amyloid fibrils in the brain is associated with a range of devastating neurodegenerative disorders such as Parkinson’s disease. Soluble oligomers formed during the aggregation process are highly neurotoxic and are thought to play a key role in the onset and spreading of disease. Despite their importance, these species are difficult to study by conventional experimental approaches owing to their transient nature, heterogeneity, low abundance and a remarkable sensitivity of the oligomerisation process to the chosen e

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7

Tosatto, Laura. "Insights on alpha-synuclein interaction network and aggregation pattern." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3426440.

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Parkinson’s disease (PD) is the most important neurodegenerative disease which regards movement. The 1% of the population over 65 years old is affected by this disorder. The main symptoms are bradykinesia, resting tremor, postural instability, muscle rigidity and sometimes cognitive and personality problems. The cause of the disease is a selective death of dopaminergic neurons in substantia nigra pars compacta. Actually, the best therapy can help to solve only symptoms and it is based on the supply of the precursor of dopamine, which is the neurotransmitter lacking in the disease, or inhibitor

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8

Plotegher, Nicoletta. "Unraveling the mechanisms of alpha-synuclein aggregation and toxicity." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3423061.

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Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease and affects about 1% of the population over 65 years old. This disorder can be both sporadic and familial and some genetic forms are due to mutations in SNCA gene, encoding for the protein alpha-synuclein (aS). PD pathological hallmarks are the prominent death of the dopaminergic neurons in the substantia nigra pars compacta and the presence of proteins and lipid inclusions, termed Lewy’s body (LBs), in the surviving neurons in parkinsonian brains. The main constituent of LBs is an aggregated fi

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9

Goodwin, Jacob J. "The Role of Calcium in Alpha-Synuclein Aggregation: A Potential Mechanism of Neurodegeneration." Thesis, Griffith University, 2014. http://hdl.handle.net/10072/366325.

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Abnormal protein aggregation has been implicated in the pathogenesis of many neurological disorders. This study focuses on the protein alpha-synuclein (α-syn), a pre- synaptic protein that is involved in a number of diseases collectively termed alpha- synucleinopathies, which include Parkinson’s disease (PD) and Multiple System Atrophy (MSA). α-syn aggregation and microscopically-visible α-syn-positive intracellular inclusion bodies are common features of these diseases, occurring in multiple cell types and localisation throughout the central nervous system. Although gene mutati

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10

De, Franceschi Giorgia. "Alpha-Synuclein and polyunsaturated fatty acids molecular characterization of the interaction and implication in protein aggregation." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3426125.

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The project of my PhD Thesis focuses on the general problem of the protein folding and misfolding in line with the research conducted in the laboratory of Protein Chemistry at CRIBI, where the work was mainly conducted. My research activity can be divided in two parts. In the first year of the PhD course I studied the effect of pH in protein fibrillogenesis using a peptide model. During the second and the third years, my research was focused into the molecular interaction between alpha-synuclein and fatty acids and its implications in alpha-synuclein aggregation. Thus, this PhD Thesis is com

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11

Čarija, Anita. "A multidisciplinary insight into the determinants of protein aggregation." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/459119.

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Els trastorns neurodegeneratius crònics, condicions mèdiques que afecten a la població principalment a la seva darrera etapa de vida, representen un problema molt important a la societat moderna. Per això, trobar nous mètodes de diagnòstic i teràpies per tractar aquestes patologies representa un objectiu que cada vegada es presenta com més urgent. Les malalties neurodegeneratives estan caracteritzats pel malplegament proteic intra i extracel•lular, que deriva en la formació d’agregats ordenats responsables de l’inici d’aquestes patologies. Per altra banda, l’agregació representa la major limit

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12

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.

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Les signatures histopathologiques de principales maladies neurodégénératives - maladie d'Alzheimer et la maladie de Parkinson - sont les enchevêtrements neurofibrillaires formés par la protéine tau et les corps de Lewy, formés par l'α-synucleine agrégée. Les mécanismes précis du repliement et de l'agrégation de ces protéines, pour la protéine tau comme pour l'α-synucleine, ne sont pas totalement compris à ce jour. Ici, nous nous sommes intéressés à cette question en utilisant des modèles in vitro et in vivo. En étudiant l'agrégation tau in vitro, nous avons mis en évidence un nouvel auto- asse

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13

Pounot, Kevin. "Dynamique des agrégats et fibres pathologiques Water restructuring upon α-synuclein fibril formation induces an increase of dynamics and entropy Tracking internal and global diffusive dynamics during protein aggregation by high-resolution neutron spectroscopy". Thesis, Université Grenoble Alpes, 2020. http://www.theses.fr/2020GRALY014.

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Les maladies neurodégénératives, comme Parkinson ou Alzheimer, sont une menace croissante,avec une prévalence augmentant sans cesse. Ces maladies sont caractérisées par la présence de dépôts protéiques, appellés amyloïdes, dans le cerveau. Plusieurs protéines ont été identifiées dans ces dépôts comme étant des marqueurs de la maladie, dont l'alpha-synucléine pour Parkinson et tau pour Alzheimer. L'agrégation amyloïde est centrale dans les maladies neurodégénératives et constitue ainsi un cible privilégiée pour le diagnostic ou les essais cliniques.L'agrégation amyloïde est caractérisée par la

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14

Lopez, Cuina Miguel. "Physiopathologie et traitement de l'atrophie multisystématisée." Thesis, Bordeaux, 2019. http://www.theses.fr/2019BORD0217.

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L'atrophie multisystematisée (AMS) est une maladie neurodégénérative rare et à évolution rapide qui affecte de nombreuses régions du système nerveux central, y compris les systèmes olivopontocérébelleux et striatonigral ainsi que divers noyaux autonomes du tronc cérébral. La caractéristique pathologique de l'AMS est la présence d'agrégats oligodendrogliaux appelés inclusions cytoplasmiques gliales dont le composant principal est la protéine a-synuclein. Le processus neurodégénératif conduit à une dysautonomie, ainsi qu'à un degré variable de syndromes parkinsoniens et cérébelleux. Il n'existe

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15

Fonseca, Ornelas Luis Eduardo. "Modulating the aggregation of alpha-synuclein and prion protein with small molecules." Thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-002B-7C8F-3.

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16

Thom, Tobias. "Role of prion protein in synucleinopathies." Doctoral thesis, 2020. http://hdl.handle.net/21.11130/00-1735-0000-0005-13D5-5.

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17

Bellomo, Giovanni. "Computational Aspects of Protein Aggregation in Neurodegenerative Diseases." Doctoral thesis, 2019. http://hdl.handle.net/2158/1169391.

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The research work performed during the doctorate focused on the computational aspects of the kinetics of aggregation and interaction of amyloidogenic proteins involved in neurological disorders. Incorrectly folded proteins may lose their colloidal stability, resulting in the formation of soluble oligomers and insoluble amyloidogenic aggregates. Amyloid fibrils are protein aggregates characterized by a filamentous β-sheet-rich structure. Although specific amyloidogenic proteins, such as α-synuclein (α-syn), β-amyloid (Aβ), huntingtin, prion protein (PrP), etc., are known to be involved in neur

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18

Wu, Kuen-Phon. "NMR characterization of intrinsically disordered alpha-synuclein implication for aggregation in Parkinson's disease /." 2010. http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.000052165.

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19

Bertoncini, Carlos Walter. "Structure and dynamics of the aggregation mechanism of the Parkinson´s disease-associated protein alpha-synuclein." Doctoral thesis, 2006. http://hdl.handle.net/11858/00-1735-0000-0006-AC24-4.

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20

Bertoncini, Carlos Walter [Verfasser]. "Structure and dynamics of the aggregation mechanism of the Parkinson's disease-associated protein α-synuclein [alpha-synuclein] / vorgelegt von Carlos Walter Bertoncini". 2006. http://d-nb.info/981835260/34.

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21

Hasadsri, Linda. "Functional protein delivery using polymeric nanoparticles : a novel therapeutic approach to alpha-synuclein aggregation and Parkinson's disease /." 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3337786.

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Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2008.<br>Source: Dissertation Abstracts International, Volume: 69-11, Section: B, page: 6601. Advisers: David F. Clayton; Julia M. George. Includes bibliographical references (leaves 157-199) Available on microfilm from Pro Quest Information and Learning.

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22

Antonschmidt, Leif. "On the molecular basis of α-synuclein aggregation on phospholipid membranes in the presence and absence of anle138b". Doctoral thesis, 2019. http://hdl.handle.net/21.11130/00-1735-0000-0005-1428-8.

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23

Afitska, Kseniia. "Výzkum a inhibice agregace alfa-synukleinu." Doctoral thesis, 2019. http://www.nusl.cz/ntk/nusl-411972.

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α-Synuclein (AS) is a small intrinsically disordered protein expressed in neurons and abundantly present in synapses where it is involved in regulation of synaptic vesicle-mediated protein trafficking. Misfolding of AS into amyloid fibrils is a key process in progression of Parkinson's disease (PD), the second most common neurodegenerative disorder which has no cure to date. Inhibition of AS aggregation and blocking of cell-to-cell spreading of AS fibrils is a promising strategy for PD treatment. However, rational design of inhibitors of this type remains complicated due to the lack of thoroug

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24

Wender, Nora. "Cellular function and toxicity of the Parkinson’s disease-related genes α-synuclein and catp-6 in C. elegans". Doctoral thesis, 2012. http://hdl.handle.net/11858/00-1735-0000-0015-97E4-A.

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25

Bologna, Sara. "Expression and characterization of human proteins involved in neurological disorders." Doctoral thesis, 2019. http://hdl.handle.net/2158/1179619.

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My Ph.D. research project, entitled “Expression and characterization of human proteins involved in neurodegenerative diseases”, was focused on the application of molecular biology and proteomics methodologies to prepare samples of proteins involved in neurodegenerative diseases. The target proteins were α-synuclein (α-syn) and the amyloid-beta peptides (Aβ), involved in the pathogenesis of Parkinson’s disease (PD) and Alzheimer’s disease (AD), respectively. The aim of my research activity was the optimization of the expression and purification of the neurodegeneration-associated proteins to ca

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