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Dissertations / Theses on the topic 'Amyloid-beta peptide (A-beta)'

Author: Grafiati

Published: 9 March 2023

Last updated: 19 July 2025

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1

Han, Wei. "Development of a coarse-grained protein model and molecular dynamics studies of amyloid-[beta] peptide aggregation /." View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?CHEM%202007%20HAN.

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2

Han, Fang. "AMYLOID A-BETA PEPTIDE: IN-CELL STUDIES AND MECHANISM OF POLYPHENOL-BASED INHIBITION TO AGGREGATION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1404771350.

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3

Shirwany, Najeeb A. "Neurotoxicity induced by A[beta] 40 and A[beta] 42 in transgenic mouse models of Alzheimer's disease." Oklahoma City : [s.n.], 2009.

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4

Gulisano, Walter. "A renewed vision for Amyloid beta and tau in Alzheimer s disease pathophysiology." Doctoral thesis, Università di Catania, 2018. http://hdl.handle.net/10761/4152.

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The aim of this thesis was to study the pathogenetic mechanisms underlying Alzheimer s disease (AD), a neurodegenerative disorder affecting the elderly and characterized by memory loss, personality changes and cognitive dysfunction leading to dementia. I will discuss the main projects in which I participated aimed at understanding the role of the main molecular interactors involved in AD pathogenesis, i.e. Amyloid-beta peptide and tau protein, on hippocampal synaptic plasticity and memory in animal models. After reviewing the pathophysiological models that have been developed so far, our gener

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5

Beckett, Christina. "VARIANCE OF THE AMYLOID BETA PEPTIDE AS A METRIC FOR THE DIAGNOSIS OF ALZHEIMER'S DISEASE." UKnowledge, 2016. http://uknowledge.uky.edu/medsci_etds/6.

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Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder associated with aging. AD is by far the best understood and most studied neurodegenerative disease. Substantial advances have been made over the last decade, however it is debatable how much closer we are to a clinically useful therapy. A long standing goal in the AD field has been to improve the accuracy of early detection, with the assumption that the ability to intervene earlier in the disease process will lead to a better clinical outcome. Major facets of this effort have been the continued development and improvemen

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6

Luheshi, Leila Mohamed. "Mutational analysis of the aggregation and toxicity of the amyloid beta peptide in a Drosophila model of Alzheimer's Disease." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612965.

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7

Hilt, Silvia. "Spin Labeled Fluorene Compounds are a Versatile Sword in the Fight Against Amyloid Beta Peptide of Alzheimer's Disease." Thesis, University of California, Davis, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10182862.

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<p> Amyloid-β (Aβ) peptide is generated after sequential cleavage of the constitutively expressed amyloid precursor protein (APP) by γ and β secretases, and is recognized as the primary causative agent underlying the neuropathogenesis of Alzheimer’sDisease (AD). Once generated, monomeric Aβ demonstrates a high propensity to aggregate into toxic Aβ oligomers (AβO) of various sizes, which eventually accumulate in the brain in the form of amyloid plaques. Mutations in either the gene for APP or one or both of its processing genes, presenilin-1 (PS1) and p

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8

Jana, A. K. "Modulation of the intrinsic properties of alzheimer’s amyloid beta peptide with nanosurfaces and chemical modifications: a computational approach." Thesis(Ph.D.), CSIR-National Chemical Laboratory, Pune, 2016. http://dspace.ncl.res.in:8080/xmlui/handle/20.500.12252/2083.

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9

Ameen, Muhammad T., and Patrick C. Bradshaw. "VITAMIN B2 REDUCES AMYLOID-BETA PROTEOTOXICITY AND IMPROVES HEALTH IN A CAENORHABDITIS ELEGANS ALZHEIMER’S DISEASE MODEL." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/24.

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Alzheimer’s disease (AD) is a neurodegenerative disease and the most common form of dementia associated with amyloid-beta peptide deposition and loss of mitochondrial function and regulation. Currently, there is no cure for AD, thus, there is a need to continuously develop therapeutic strategies that could address the complex multifactorial causes of AD development. Due to this necessity, this study has investigated the role of vitamin B2 as a disease modifying drug for AD by employingamyloid-beta and mitochondrial based AD therapeutic strategies. Using a transgenic C. elegans AD worm model ex

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10

Ameen, Muhammad Tukur. "A Role of Vitamin B2 in Reducing Amyloid-beta Toxicity in a Caenorhabditis elegans Alzheimer’s Disease Model." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etd/3398.

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Alzheimer’s disease (AD) is associated with amyloid-beta peptide deposition and loss of mitochondrial function. Using a transgenic C. elegans AD worm model expressing amyloid-beta in body wall muscle, we determined that supplementation with either of the forms of vitamin B2, flavin mononucleotide (FMN) or flavin adenine dinucleotide (FAD) protected against amyloid-beta mediated paralysis. FMN and FAD were then assayed to determine effects on ATP, oxygen consumption, and reactive oxygen species (ROS) with these compounds not significantly improving any of these mitochondrial bioenergetic functi

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11

Casley, Christopher Stuart. "Amyloid beta peptide-induced oxidative stress and mitochondrial respiratory chain damage : a mechanism for cell death in Alzheimer's disease?" Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252296.

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12

Padayachee, Eden Rebecca. "Neuronal nitric oxide synthase : a biomarker for Alzheimers disease : interaction of neuronal nitric oxide synthase with beta-amyloid peptides in the brain." Thesis, Rhodes University, 2011. http://hdl.handle.net/10962/d1007677.

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High levels of the amino acid arginine and low levels of the product citrulline in the cerebrospinal fluid of Alzheimer's patients could mean that there is a decrease in the enzymes that metabolize this amino acid. One such enzyme is neuronal nitric oxide synthase (nNOS). In this study, neuronal nitric oxide synthase (nNOS), sourced from bovine brain was extracted and concentrated using two methods of precipitation: poly (ethylene glycol) 20 000 (PEG) and ammonium sulphate [(NH₄)₂S0₄). These two techniques gave no increase in yield nor fold purification and hence were abandoned in favour of io

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13

Garrett, Hannah Mary. "A study into the influence of amyloid-beta peptide oxidation on the rate of fibril formation, with a synthesis of 2-oxo-histidine." Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8485.

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The Amyloid Cascade Hypothesis states that fibrillation of the amyloid beta (Aβ) peptide is the primary cause of Alzheimer’s pathology. The trigger for the fibrillation is a subject of much debate, although it is clear, oxidative stress is a key feature of Alzheimer’s aetiology. This thesis explores a possible role of oxidation of Aβ, in particular the effect of histidine and methionine side-chain oxidation, on Aβ fibril growth rates. Within chapters 2 and 3 of this thesis is a discussion of various approaches to chemical synthesis of 2-oxo-histidine with a view to the incorporation of the oxi

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14

ZONA, CRISTIANO. "Design and systhesis of nanoparticles for therapy and imaging of Alzheimer's disease." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/19222.

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Various types of nanoparticles (NPs), such as Liposomes, Solid Lipid NPs and Polymeric NPs, are being extensively explored for their potentialities in the medical field. NPs are attractive tools in biomedical applications thanks to their biocompatibility, non-immunogenicity, non-toxicity, biodegradability, high physical stability, possibility of drug loading and releasing, and higher probability for surface functionalization. The project is devoted to the synthesis of NPs functionalized with amyloid-beta ligands (Aβ-ligands), imaging tools and/or blood brain barrier-transporters (BBB-transpor

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15

Pavoni, Serena. "Mise au point d’un nouveau modèle d’organoïde cérébral humain pour l’étude des mécanismes d’interaction de la protéine prion et de l’amyloïde β". Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS427.

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Les mécanismes de type prion sont désormais reconnus comme sous-tendant la plupart des maladies neurodégénératives humaines, avec en premier lieu la maladie d’Alzheimer (MA) au niveau de ses 2 marqueurs spécifiques, l’amyloïde β (Aβ à l’origine de l’hypothèse étiopathogénique de la cascade amyloïde) et la protéine Tau phosphorylée. Par ailleurs la protéine du prion (PrPC) est décrite comme interagissant à de multiples niveaux avec le métabolisme de l’Aβ sans que les mécanismes physiopathologiques sous-jacents n’aient pu être expliqués. Pour sortir de l’impasse actuelle concernant le développem

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16

Fioravanzo, Lara. "Study of role of A-Beta peptides on angiogenesis related to Alzheimer's disease." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3426012.

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One of the main difficulties for the success of tissue and organ transplantation is the deficiency of techniques that ensure regular and stable vascularisation. The knowledge of mechanisms involved in the formation of new vessels could allow application of clinic strategies to facilitate tissue and organ transplantation on the one hand and the reduction of excessive vascular growth in many pathologies on the other. Angiogenesis is a complex process, where several cell types and mediators interact to establish a specific microenvironment suitable for the formation of new vessels (Bouïs et al,

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17

THERIN, SEBASTIEN. "USE OF A CELL PERMEABLE PEPTIDE TO MODULATE ADAM10 SYNAPTIC LOCALIZATION AND ACTIVITY IN A MOUSE MODEL OF ALZHEIMER'S DISEASE." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/649095.

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Alzheimer’s disease (AD) is characterized by the aggregation of amyloid beta peptide (Aβ). Aβ derives from the amyloid precursor protein (APP), which can undergo two mutually exclusive pathways. The amyloidogenic pathway involves BACE and γ-secretase activities and leads to Aβ formation. While, the non-amyloidogenic pathway involves ADAM10, a disintegrin and metalloproteinase 10, which cleaves APP within the domain corresponding to Aβ, thus precluding Aβ production. Recently, we identified a new ADAM10 binding partner, named AP2, which is responsible for ADAM10 internalization, therefore affec

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18

Nicklagård, Erik. "Quantification of Alzheimer DiseaseAmyloid β Peptide 43 in Human BrainWith a Newly Developed Enzyme-LinkedImmunosorbent Assay (ELISA)". Thesis, Linköpings universitet, Biokemi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-70490.

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A 20 weeks project at Karolinska Institutet (KI), Huddinge, Sweden is in this master thesis summarized. Alzheimer’s disease is the most common form of dementia in the world. One of the pathological hallmarks seen in AD patients consists of amyloid plaques assembled of beta amyloid (Aβ) peptide aggregates. A lot of research has been done on Aβ40 and Aβ42 but not on the longer variant with 43 residues. An earlier study by Welander et al, quantified the Aβ43 peptide from amyloid plaque cores with high-performance liquid chromatography coupled to mass-spectrometry (HPLC-MS/MS)1. Here, I present th

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19

Ninot, Pedrosa Martí. "Towards the validation of a druggable amyloid-beta oligomer as a target for Alzheimer´s disease = Cap a la validació d’un oligomer de beta-amiloide com a diana en la malaltia d’Alzheimer." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/565537.

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Amyloid-beta peptide (Aβ) is strongly linked to the aetiology of Alzheimer’s disease (AD). Aβ is the main component of the amyloid plaques found in the brain of AD patients, however, Aβ is also present in the brain of healthy humans. It has been described that for this peptide to be neurotoxic, aggregation is needed. The accumulation of Aβ causes aggregation from low order oligomers through different intermediate species up to the formation of amyloid fibrils. However, is not the presence of the fibrils what correlates the harmfulness of the disease, but the concentration of soluble oligomeric

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20

Wu, Haifan. "Gamma-AApeptides as a New Class of Peptidomimetics: Synthesis, Structures, and Functions." Scholar Commons, 2015. https://scholarcommons.usf.edu/etd/5601.

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Peptidomimetics are synthetic oligomers that resemble the activities of peptides. Their advantages over peptides include high stability towards proteolysis and enormous chemical diversity. Over the past two decades, there have been extensive efforts to develop peptide mimics, such as beta-peptides, peptoids, D-peptides, etc. The research on peptidomimetics have led to many important applications in both medicinal and material science. In order to explore new functions, the discovery of peptidomimetics with novel frameworks is essential. We reported the synthesis and evaluation of a new class o

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21

Xu, Yaochun. "Fluorinated Peptidomimetics : Synthesis, Conformational Studies and Evaluation as Amyloid Proteins Aggregation Modulators." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS585/document.

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La maladie d'Alzheimer représente un défi mondial pour la société. Il n'y a pas à ce jour de traitement efficace pour traiter ou ralentir les symptômes de la maladie d'Alzheimer. Cette maladie est caractérisée par une perte de synapses, une augmentation du nombre de plaques extracellulaires d'Abêta et une augmentation de Tau hyperphosphorylée agrégée intracellulaire (neurodégénérescence fibrillaire). Il est communément admis que la maladie d'Alzheimer est principalement liée à l’oligomérisation et à la fibrillation de peptides amyloïdes bêta, et que les oligomères Abêta solubles et les fibres

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22

Lindström, Fredrick. "Biological membrane interfaces involved in diseases : a biophysical study." Doctoral thesis, Umeå universitet, Kemi, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-806.

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Interactions between peptides and biological lipid membranes play a crucial role in many cellular processes such as in the mechanism behind Alzheimer’s disease where amyloid-beta peptide (Abeta)is thought to be a key component. The initial step of binding between a surface active peptide and its target membrane or membrane receptor can involve a non specific electrostatic association where positively charged amino acid residues and a negatively charged membrane surface interact. Here, the use of high resolution MAS NMR provides a highly sensitive and non perturbing way of studying the electros

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23

Deleanu, Mihai. "Taylor dispersion analysis : a powerful size-based characterization technique for monitoring the aggregation of β-amyloid peptides". Thesis, Université de Montpellier (2022-….), 2022. http://www.theses.fr/2022UMONS003.

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La maladie d'Alzheimer (MA) est l'un des principaux défis de santé publique du 21ème siècle et son développement repose sur l'hypothèse amyloïde qui stipule que la formation extracellulaire de plaques amyloïdes et l'accumulation intracellulaire d'enchevêtrements neurofibrillaires Tau (NFTs) sont causées par l'agrégation de peptides β-amyloïdes (Aβ). Plusieurs techniques biophysiques ont été employées pour étudier le processus d'agrégation des peptides Aβ, comme le dosage de la thioflavine T (ThT), la diffusion dynamique de la lumière (DLS), l'électrophorèse capillaire (CE), la microscopie élec

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24

Nunes, Emilene Arusievicz. "Estudos da ação de íons metálicos e da SOD1 em danos a biomoléculas em culturas de células neuronais sob neurodegeneração e estresse oxidativo." reponame:Repositório Institucional da UFABC, 2018.

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Orientadora: Profa. Dra. Giselle Cerchiaro<br>Tese (doutorado) - Universidade Federal do ABC, Programa de Pós-Graduação em Biossistemas, Santo André, 2018.<br>Em doencas neurodegenerativas amiloidais o estresse oxidativo tem um papel importante juntamente com a proteina ¿À-amiloide (A¿À), associada a formacao de placas senis na Doenca de Alzheimer. Tais condicoes demonstraram desbalanco de metais, como cobre e zinco, tanto na concentracao celular e quanto nos processos antioxidantes. A Cu,Zn-Superoxido Dismutase (SOD1), em condicoes neurodegenerativas, pode demonstrar alteracoes estruturais e

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25

Chung, Teng-Wen, and 鍾騰文. "Characterization of rationally mutated beta-amyloid peptide in a lipid environment by NMR spectroscopy." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/67992195438071204869.

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碩士<br>國立陽明大學<br>生命科學暨基因體科學研究所<br>97<br>Alzheimer’s disease (AD) is a neurodegenerative disease which leads to progressive dementia and neuronal death. The main histopathological hallmarks of AD are the senile plaques within the cerebral cortex and the neurofibrillary tangles within the nerve cells. The primary component of senile plaques is beta-amyloid peptide (Ab).�nRecent studies have suggested that Ab has neurotoxic properties in an aggregated state. Thus, knowing the molecular mechanism of the aggregation process of Ab may facilitate the design and development of fibrillogenesis inhibitor

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26

Yan, Li-Mei [Verfasser]. "Identification and characterization of IAPP derived inhibitors of cytotoxic self-assembly and amyloidogenesis of islet amyloid polypeptide (IAPP) and ß-amyloid [beta amyloid] peptide (Aß) [A beta] / vorgelegt von Li-Mei Yan." 2010. http://d-nb.info/1009587390/34.

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27

Williamson, Ritchie, A. Usardi, D. P. Hanger, and B. H. Anderton. "Membrane-bound beta-amyloid oligomers are recruited into lipid rafts by a fyn-dependent mechanism." 2008. http://hdl.handle.net/10454/6237.

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Recently published research indicates that soluble oligomers of beta-amyloid (Abeta) may be the key neurotoxic species associated with the progression of Alzheimer's disease (AD) and that the process of Abeta aggregation may drive this event. Furthermore, soluble oligomers of Abeta and tau accumulate in the lipid rafts of brains from AD patients through an as yet unknown mechanism. Using cell culture models we report a novel action of Abeta on neuronal plasma membranes where exogenously applied Abeta in the form of ADDLs can be trafficked on the neuronal membrane and accumulate in lipid rafts.

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28

Lee, Jian-Bin, and 李健賓. "A Replica-Exchange Molecular Dynamics Study of the Configurations of Alzheimer Amyloid beta-Peptide within Membrane: Implications for Aggregation and Toxicity." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/7xq4ab.

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博士<br>國立中央大學<br>化學學系<br>103<br>Extracellular deposits of amyloidbeta (Abeta) aggregates in brain is the hallmark of Alzheimer’s disease (AD). Abeta peptide is produced from the amyloid precursor protein (APP) within membrane by the proteolytic action of thebeta- and γ-secretases. Therefore, it is crucial to determine the configuration of Abeta peptide within a membrane to provide insights at atomic levels for the aggregation mechanism and toxicity. In this thesis, we employed replica-exchange molecular dynamics in conjunction with an implicit membrane model to investigate the mutation and se

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29

BONAFINI, Clara. "Investigations into Alzheimer's disease pathogenetic mechanisms using normal adult human astrocytes in culture." Doctoral thesis, 2011. http://hdl.handle.net/11562/350599.

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La malattia di Alzheimer è una delle principali patologie neurodegenerative legate alla terza età: i casi infatti che si sviluppano in età precoce rappresentano meno dell’1% e sono dovuti ad alterazioni geniche specifiche. L’eziologia di questa malattia resta ancora sconosciuta, sebbene la presenza di placche senili, composte principalmente di Aβ1-40 e Aβ1-42, o aggregati fibrillari intraneuronali della proteina tau, siano caratteristiche ormai note del suo stadio avanzato. Diversi processi patologici sono stati messi in relazione con il danno neuronale e il declino cognitivo tipici della mala

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30

Kulic, Luka [Verfasser]. "Differenzielle Effekte von Presenilin-Mutationen auf die Generierung des Amyloid-β-Peptids [Amyloid-beta-Peptids] (Aβ) [A beta]) und die Endoproteolyse des Notch-Rezeptors / vorgelegt von Luka Kulic". 2003. http://d-nb.info/96886631X/34.

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31

Oliveira, Patrícia Isabel Machado. "Relatório de Estágio e Monografia intitulada “Mecanismos de Neurodegeneração na Doença de Alzheimer e a sua Modulação por Polifenóis"." Master's thesis, 2020. http://hdl.handle.net/10316/92966.

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Relatório de Estágio do Mestrado Integrado em Ciências Farmacêuticas apresentado à Faculdade de Farmácia<br>Alzheimer’s Disease (AD) is the most prevalent neurodegenerative disease and also represents the major common type of dementia, affecting mainly individuals over 65 years. It is an extremely disabling disease that is characterized, fundamentally, by a progressive decline in cognitive capabilities, which ultimately leads to dependence on others to perform the tasks of daily routine.The neurodegeneration that occurs mainly at the hippocampus and cerebral cortex, the presence of senile plaq

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32

Meier-Stephenson, Felix. "A New Theory of Alzheimer's Disease." 2014. http://hdl.handle.net/10222/48590.

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Alzheimer’s Disease (AD) is a chronic progressive neurological condition, clinically characterized by memory deficits, cognitive and physical impairment, and personality changes. Traditionally, AD was considered a type of protein folding disorder. Here, the concept of AD as an autoimmune disease of the innate immune system was developed. After exploring evolutionary connections between the AD peptide β-amyloid (Aβ) and known antimicrobial peptides (AMPs), and elucidating the structural similarities between Aβ and AMPs, a mechanism of action for Aβ’s antimicrobial activity is proposed that

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