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1

PEIRA, ENRICO. "Advances and perspectives in amyloid PET quantitative interpretation." Doctoral thesis, Università degli studi di Genova, 2022. http://hdl.handle.net/11567/1081904.

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Amyloid imaging refers to a diagnostic examination that allows for the in-vivo detection of amyloid aggregation, considered a pathological hallmark of Alzheimer's disease (AD). The technique of choice for amyloid imaging is PET with appropriate radioligands, which has become a key tool in the diagnosis and research framework of AD. Due to the non-straightforward relationship between the presentation of the disease and the underlying molecular pathology, the diagnosis based purely on the clinical manifestation is a non-trivial task. Therefore, a great interest has developed around the methodolo
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2

Heurling, Kerstin. "Characterization of [18F]flutemetamol binding properties : A β-amyloid PET imaging ligand". Doctoral thesis, Uppsala universitet, Radiologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-262019.

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The criteria for diagnosing Alzheimer’s disease (AD) have recently been revised to include the use of biomarkers for the in vivo presence of β-amyloid, one of the neuropathological hallmarks of AD. Examples of such biomarkers are positron emission tomography (PET) β-amyloid specific ligands, including [18F]flutemetamol. The aim of this thesis was to characterize the binding properties of [18F]flutemetamol from a tracer kinetic perspective as well as by validating binding measures through comparison with tissue pathology assessments. The applicability of previously developed kinetic models of t
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3

CHINCARINI, ANDREA. "From clinics to methods and back: a tale of amyloid-PET quantification." Doctoral thesis, Università degli studi di Genova, 2018. http://hdl.handle.net/11567/929831.

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The in-vivo assessment of cerebral amyloid load is taking a leading role in the early differential diagnosis of neurodegenerative diseases. With the hopefully near introduction of disease-modifying drugs, we expect a paradigm shift in the current diagnostic pathway with an unprecedented surge in the request of exams and detailed analysis.
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4

Blaske, Susann. "Weiterentwicklung und Testung einer Auswerte-Software zur Analyse von Beta-Amyloid Hirn-PET-Daten." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-214479.

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Alzheimer-Demenz ist eine Erkrankung, die durch den demografischen Wandel immer mehr an Bedeutung gewinnt. Eine effektive und frühzeitige Diagnostik ist daher entschei-dend. Da die neuropsychiatrische Testung mit einer diagnostischen Unsicherheit von 10% bis 30% zu ungenau ist und auch erst bei Ausbruch der Symptomatik eine Alzheimer-Demenz diagnostiziert werden kann, wurde auf Parameter wie Beta-Amyloid zurückgegrif-fen. Beta-Amyloid stellt einen Hauptbestandteil der Alzheimer-Demenz Pathologie dar und ist bereits vor Ausbruch der Symptome nachweisbar. Da die visuelle Analyse, welche die Beta
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5

Nordeman, Patrik. "Development of Palladium-Promoted 11C/12C-Carbonylations and Radiosynthesis of Amyloid PET Ligands." Doctoral thesis, Uppsala universitet, Plattformen för preklinisk PET, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-213863.

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In the first part of this thesis, palladium(0)-catalyzed and -mediated carbonylations are discussed. Paper I describes a new method for the safe, efficient use of a solid carbon monoxide source in the synthesis of primary and secondary benzamides. In total, 35 benzamides were synthesized from aryl iodides (20 examples, 69-97% yield) and aryl bromides (15 examples, 32-93% yield). Reduction-prone groups were used successfully in the reactions. In paper II, the same protocol was adopted for the palladium(0)-catalyzed synthesis of N-cyanobenzamides from aryl iodides/bromides, carbon monoxide and c
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6

Salvadó, Blasco Gemma. "Detection of early cerebral amyloid-β deposition by PET imaging and its downstream effect". Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/672375.

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Alzheimer's disease (AD) is the leading cause of dementia worldwide. This disease, however, starts decades before any clinical symptom appears with the accumulation in the brain of aggregates of two main proteins: amyloid-β (Aβ) and tau. In recent years, the appearance of in vivo biomarkers capable to track biological changes has boosted the research interest to earlier phases of the disease. With these concepts in mind, the general objective of this thesis was to investigate Aβ deposition and its downstream effects in the earliest stages of the Alzheimer's continuum. To this aim, the four stu
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7

Bensaïdane, Mohamed Réda. "Clinical utility of amyloid PET imaging in the differential diagnosis of atypical dementias and its impact on caregivers." Master's thesis, Université Laval, 2016. http://hdl.handle.net/20.500.11794/27113.

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La maladie d'Alzheimer (MA) se caractérise pathologiquement par l'accumulation de plaques amyloïde dans le cerveau. La tomographie par émission de positrons (TEP) permet d'imager les plaques amyloïde in vivo. Le but de ce projet est d’évaluer le rôle de la TEP amyloïde dans le processus diagnostique de la MA dans des cas de démences atypiques. Le deuxième but de ce projet est de déterminer l'impact de la révélation d’un diagnostic plus certain chez les proches aidants. 28 patients sans diagnostic malgré une investigation exhaustive ont été sélectionnées et imagées avec le traceur amyloïde 18F-
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8

Lilamand, Matthieu. "Apports des biomarquers amyloïdes dans la caractérisation de la plainte mnésique du sujet âgé." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS342.

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Les biomarqueurs de la maladie d’Alzheimer (MA) permettraient d’identifier les processus pathologiques de la maladie plusieurs années avant l’apparition des premiers signes cliniques. Ainsi, la tomographie par émission de positons (TEP) reposant sur les radio-traceurs liant les plaques amyloïdes, a ouvert de nouvelles perspectives en matière d’identification précoce de la maladie, in vivo, très en amont des premiers symptômes. Cependant, l’utilisation de ces biomarqueurs est restée limitée à de faibles effectifs de sujets, rarement suivis au-delà de quelques mois et le coût important de ces ou
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9

Engler, Henry. "PET and the Multitracer Concept: An Approach to Neuroimaging Pathology." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8687.

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<p>Patients suffering from different forms of neurodegenerative diseases, such as: Creutzfeldt Jacob Disease (CJD), Alzheimer disease (AD), mild cognitive impairment (MCI), frontotemporal dementia and Parkinson’s disease (PD) were examined with Positron Emission Tomography (PET) and the combination of different radiotracers: <sup>15</sup>O-water, N-[<sup>11</sup>C-methyl]-L-deuterodeprenyl (DED), [<sup>18</sup>F] 2-fluorodeoxyglucose: (FDG), N-methyl-[<sup>11</sup>C]2-(4-methylaminophenyl)-6-hydroxybenzothiazole (PIB) and L-[<sup>11</sup>C]-3,4-dihydroxiphenyl-alanine (DOPA). The radiotracers
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10

Niu, Zheng [Verfasser], Bernd [Akademischer Betreuer] Reif, Bernd [Gutachter] Reif та Aphrodite [Gutachter] Kapurniotu. "NMR Studies to Characterize Amyloid Inhibitors and Aβ-PET Tracer Complexes / Zheng Niu ; Gutachter: Bernd Reif, Aphrodite Kapurniotu ; Betreuer: Bernd Reif". München : Universitätsbibliothek der TU München, 2019. http://d-nb.info/119244180X/34.

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11

Rötzer, Christina [Verfasser], та Axel [Akademischer Betreuer] Rominger. "Monitoring einer chronischen Behandlung mit einem γ- Sekretase-Modulator mittels Amyloid-PET im transgenen Alzheimer-Mausmodell / Christina Rötzer ; Betreuer: Axel Rominger". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1121507832/34.

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12

Blaske, Susann [Verfasser], Henryk [Akademischer Betreuer] Barthel, Swen [Gutachter] Hesse, and Winfried [Gutachter] Brenner. "Weiterentwicklung und Testung einer Auswerte-Software zur Analyse von Beta-Amyloid Hirn-PET-Daten / Susann Blaske ; Gutachter: Swen Hesse, Winfried Brenner ; Betreuer: Henryk Barthel." Leipzig : Universitätsbibliothek Leipzig, 2016. http://d-nb.info/1240695489/34.

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13

Fang, Xiaotian T. "Preclinical PET imaging of Alzheimer's disease progression." Doctoral thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-333220.

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Amyloid PET imaging with [11C]PIB enabled detection of Aβ for the first time in vivo. However, [11C]PIB is a small molecule that binds only the insoluble Aβ plaque. Rather, the soluble Aβ aggregates are considered the cause of Alzheimer’s disease (AD). As such, a more sensitive and specific PET tracer is needed for tracking longitudinal AD pathology. Soluble Aβ aggregates likely interact with the metabotropic glutamate receptor 5 (mGluR5) to cause neurotoxic effects. However, with [11C]ABP688 PET we were unable to detect aberrant mGluR5 binding in AD mouse models, although we find elevated mGl
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14

Silvestri, Erica. "Simultaneous PET/MRI for Connectivity Mapping: Quantitative Methods in Clinical Setting." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3426715.

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In recent years, the study of brain connectivity has received growing interest from neuroscience field, from a point of view both of analysis of pathological condition and of a healthy brain. Hybrid PET/MRI scanners are promising tools to study this complex phenomenon. This thesis presents a general framework for the acquisition and analysis of simultaneous multi-modal PET/MRI imaging data to study brain connectivity in a clinical setting. Several aspects are faced ranging from the planning of an acquisition protocol consistent with clinical constraint to the off-line PET image reconstruction,
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15

Manook, André [Verfasser], Markus [Akademischer Betreuer] Schwaiger, and Johann [Akademischer Betreuer] Förstl. "Preclinical PET as Translational Tool for Imaging Alzheimer's Disease : Small-Animal PET Imaging of Beta-Amyloid Plaques with [11C]PiB, its Multi-Modal Validation and Application to the Evaluation and Ranking of New AD Tracers / André Manook. Gutachter: Markus Schwaiger ; Johann Förstl. Betreuer: Markus Schwaiger." München : Universitätsbibliothek der TU München, 2012. http://d-nb.info/1047883465/34.

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16

Degerman, Gunnarsson Malin. "Biomarkers as Monitors of Drug Effect, Diagnostic Tools and Predictors of Deterioration Rate in Alzheimer’s Disease." Doctoral thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-196965.

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Decreased amyloid-ß42 (Aß42), increased total tau (t-tau) and phosphorylated tau (p-tau) in cerebrospinal fluid (CSF) reflect histopathological core changes in the most common dementia disorder, Alzheimer’s disease (AD). They discriminate AD from healthy controls and predict conversion to AD with a relatively high accuracy. Memantine, an uncompetitive NMDA-receptor antagonist, is indicated for symptomatic treatment of AD. The first aim of this thesis was to investigate effects of memantine on CSF concentrations of Aβ42, tau and p-tau. Secondly, the aim was to explore the relation between these
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17

Jensen, Jordan Royce. "Development of Tau-Selective Imaging Agents for Improved Diagnosis of Alzheimer’s Disease and Other Tauopathies." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1306441097.

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18

Angermann, Susanne [Verfasser], Timo [Akademischer Betreuer] Grimmer, Alexander [Akademischer Betreuer] Drzezga, and Alexander [Akademischer Betreuer] Kurz. "Der Zusammenhang zwischen klinischer Progression und PIB-PET als Marker der zerebralen Amyloid-Pathologie bei Patienten mit Alzheimer-Krankheit im zeitlichen Verlauf / Susanne Vera Tholen. Gutachter: Alexander Drzezga ; Alexander Kurz. Betreuer: Timo Grimmer." München : Universitätsbibliothek der TU München, 2011. http://d-nb.info/1019590084/34.

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19

Reutern, Boris Gerhard Jaroslav von [Verfasser], Alexander [Akademischer Betreuer] Drzezga, Sibylle [Akademischer Betreuer] Ziegler та Ambros [Akademischer Betreuer] Beer. "Relationship between in-vivo [11C]PiB PET Signal and Amyloid-β Plaque Pathology in different transgenic Mouse Models of Alzheimer's Disease / Boris Gerhard Jaroslav von Reutern. Gutachter: Alexander Drzezga ; Sibylle Ziegler ; Ambros Beer. Betreuer: Alexander Drzezga". München : Universitätsbibliothek der TU München, 2012. http://d-nb.info/103107516X/34.

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20

Göttler, Jens Franz [Verfasser], Claus [Akademischer Betreuer] Zimmer, Stefan [Akademischer Betreuer] Förster, and Markus [Akademischer Betreuer] Schwaiger. "Die Verbindung der Amyloid-Pathologie mit eingeschränkter Kognition durch gestörte intrinsische zerebrale Netzwerke bei prodromaler Alzheimer-Erkrankung – eine fMRT- und PiB PET-Studie / Jens Franz Göttler. Betreuer: Claus Zimmer. Gutachter: Claus Zimmer ; Stefan Förster ; Markus Schwaiger." München : Universitätsbibliothek der TU München, 2015. http://d-nb.info/1082034134/34.

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21

Gosselin, Thomas. "ANIMAL Antidépresseurs, neuroinflammation et maladie d'alzheimer." Thesis, Tours, 2016. http://www.theses.fr/2016TOUR3305/document.

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Aujourd’hui, malgré la description des mécanismes à l’origine du développement de la dépression et de la MA, aucun traitement curatif n’existe pour ces pathologies suggérant l’implication d’un autre phénomène. L’un des processus retrouvé communément dans ces pathologies est la neuroinflammation. Or pour le moment, les essais cliniques entrepris dans la MA afin de réduire la neuroinflammation n’ont pas permis d’aboutir à une amélioration significative des symptômes. L’une des raisons de cet échec serait une mauvaise fenêtre thérapeutique qui aurait pour conséquence d’exacerber les effets délétè
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22

Gómez, Vallejo Vanessa. "Development of new strategies for the synthesis of radiotracers labeled with short-lived isotopes: application to 11C and 13N." Doctoral thesis, Universitat Ramon Llull, 2010. http://hdl.handle.net/10803/9301.

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S'ha desenvolupat una nova estratègia per la síntesi ràpida i eficient de L-[metil-11C]metionina basada en el captive solvent method. La reacció de L-homocisteína (dissolució bàsica en aigua/etanol 1:1) amb [11C]CH3I en un loop de HPLC va permetre la formació del radiotraçador desitjat amb elevat rendiment radioquímic (38.4 ± 4.1%) en un temps curt (< 12 min). Tots el paràmetres analítics compleixen les especificacions requerides per la versió actual de la Farmacopea Espanyola, tot i que els valors d'activitat específica obtinguts van ser relativament baixos. Degut a això, es van estudiar i qu
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23

Cisek, Katryna. "Rational Optimization of Small Molecules for Alzheimer’s Disease Premortem Diagnosis." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1338325484.

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24

Fiorenzato, Eleonora. "Cognitive and Brain Imaging Changes in Parkinsonism." Doctoral thesis, Università degli studi di Padova, 2017. http://hdl.handle.net/11577/3424966.

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The present thesis comprises three main parts: one theoretical and two experimental. The first part, composed of two chapters, will introduce the clinical and neuropathological features underlying parkinsonian disorders, namely in Parkinson’s disease (PD) as well as in atypical parkinsonisms — multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) (Chapter 1). In this regard, PD and MSA are defined as synucleinopathies due to the presence of synuclein aggregates; while PSP that is characterized by tau protein accumulations, is part of tauopathies. Further, Chapter 2 will provi
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25

Lilja, Johan. "[18F]Flutemetamol PET image processing, visualization and quantification targeting clinical routine." Doctoral thesis, Uppsala universitet, Radiologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-317688.

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Alzheimer’s disease (AD) is the leading cause of dementia and is alone responsible for 60-70% of all cases of dementia. Though sharing clinical symptoms with other types of dementia, the hallmarks of AD are the abundance of extracellular depositions of β-amyloid (Aβ) plaques, intracellular neurofibrillary tangles of hyper phosphorylated tau proteins and synaptic depletion. The onset of the physiological hallmarks may precede clinical symptoms with a decade or more, and once clinical symptoms occur it may be difficult to separate AD from other types of dementia based on clinical symptoms alone.
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26

Schütz, Lisa. "Durchführbarkeit und Patientenakzeptanz der kombinierten Amyloid-PET/MRT in der Alzheimer-Diagnostik." 2018. https://ul.qucosa.de/id/qucosa%3A32599.

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Zur Verbesserung der Diagnostik der Alzheimer-Erkrankung wird die klinische Testung zunehmend durch Biomarker ergänzt. Diese können sowohl mittels Hirnbildgebung als auch mittels Liquor-Analyse erhoben werden. Aufgrund der großen Bedeutung in der Pathogenese der Alzheimer-Erkrankung wurde das ß-Amyloid als diagnostisches Kriterium implementiert, ebenso wie die mediale Temporallappenatrophie. Bis zur Einführung der kombinierten PET/MRT konnten die Informationen zu den genannten Bildgebungsparametern nur separat mit Hilfe mehrerer Aufnahmen gewonnen werden. Ziel der Studie war es deshalb, erstma
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27

Kaye, Edward David. "Correlating Neuropsychiatric Symptoms with Regional Beta-Amyloid Load in the Alzheimer’s Disease Brain Using [11C]SB-13 Positron Emission Tomography." Thesis, 2010. http://hdl.handle.net/1807/25722.

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Correlations between neuropsychiatric symptoms and beta-amyloid (Aβ) burden in specific brain regions in living Alzheimer’s disease (AD) patients remain to be elucidated. Ten mild AD patients underwent MR and [11C]SB-13 PET imaging. Neuropsychiatric symptoms were quantified with the Neuropsychiatric Inventory (NPI). NPI-depression/dysphoria, -apathy, -agitation/aggression, -anxiety, and -appetite/eating disorders scores were hypothesized to correlate with Aβ burden in particular brain regions. Pearson’s correlation coefficient revealed that depression/dysphoria scores positively correlated (p<
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28

Straßner, Bernd [Verfasser]. "Zusammenhänge zwischen dem zerebralen Glukosemetabolismus (F-18-FDG-PET), genetischer Marker (APOE) und den Biomarkern (TAU und β-Amyloid [Beta-Amyloid] im Liquor cerebrospinalis) bei Patienten mit einer Alzheimer-Krankheit (AD) und Patienten mit leichter kognitiver Beeinträchtigung (mild cognitive impairment, MCI) / Bernd Straßner". 2007. http://d-nb.info/988204223/34.

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29

Gomes, Pedro Miguel Oliveira. "New molecules for diagnosis of Alzheimer’s disease by Positron Emission Tomography (PET)." Master's thesis, 2019. http://hdl.handle.net/10773/30117.

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Alzheimer's disease is the most prevalent form of dementia currently affecting 50 million people, with a new case occurring every 3 seconds. Forecasts point to 152 million people by 2050. There are two forms of Alzheimer's disease: familial or sporadic. The main causes of familial form are genetic mutations, while for the sporadic form it is known that oxidative stress plays a key role, being a cause and consequence of the disease, activating signaling pathways that promote the aggregation of Aβ peptides promoting the formation of senile plaques and neurofibrillary aggregates (NFTs) o
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30

Nguyen, Hoan. "Characterizing the symmetry of amyloid beta protein retention in Alzheimer's disease using florbetapir positron emission tomography - a study using data from the Alzheimer's disease neuroimaging initiative." Thesis, 2014. https://hdl.handle.net/2144/14667.

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Progression of Alzheimer's disease has been associated with the deposition of aggregated amyloid beta (Aβ) protein in the brain. Though first described in post-mortal tissue, the development of Aβ specific tracers for positron emission tomography (PET) permits in-vivo mapping of its distribution in the brain. One of the well-known and early-developed tracers is the Pittsburgh Compound B (PiB) (Klunk et al., 2004). However, the challenge with PiB lies in the stability of the radioisotope 11C. 11C's short half-life of only 20 minutes hinders its transportation and usage at imaging facilities tha
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