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Dissertations / Theses on the topic 'DOPA'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Khan, Ghulam Ahmed. "Enzymatic synthesis of L-DOPA esters." Thesis, University of Reading, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333598.

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2

Branden, Stansley. "L-dopa and the Serotonergic System." University of Toledo Health Science Campus / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=mco1429543879.

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3

Wiese, Claudia Anette Elisabeth. "Metabolismus fluorierter DOPA-Isomere in aggregierenden Hirnzellkulturen /." [S.l.] : [s.n.], 1991. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=9542.

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4

Nelson, Michelle Amy. "Protein bound 3,4 dihydroxyphenyalanine as a signal for enhanced antioxidant defences /." full text via ADT, 2008. http://erl.canberra.edu.au/public/adt-AUC20081209.125208/index.html.

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5

Moheimen, Jamil. "Striatal neuropeptides associated with L- DOPA-induced dyskinesia." Thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-209915.

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Abstract Striatal neuropeptides associated with L-DOPA-induced dyskinesia 2012-02-14 <img src="file:///page2image2248" /> Parkinson's disease (PD) is the most common neurodegenerative disease, with approximately 6 million sufferers in the world. The patients are usually diagnosed between the ages 50-70 years and as the disease progress more symptoms may occur. The cause of the disease is unknown, but the characteristic of PD is that it is a selective degeneration of dopaminergic neurons in the substantia nigra, which leads to an absence of dopamine release in striatum. This affects the motor s

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6

DIMOV, MICHEL. "Melanomes malins et 5-s-cysteinyl- dopa urinaire." Strasbourg 1, 1991. http://www.theses.fr/1991STR15033.

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7

Tison, François. "La L-Dopa endogène : aspects neurochimiques, physiologiques et étude anatomofonctionnelle par immunohistochimie dans le cerveau de rat." Bordeaux 2, 1990. http://www.theses.fr/1990BOR23037.

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8

Nelson, Michelle Amy, and n/a. "Protein Bound 3,4-Dihydroxyphenylalanine as a Signal for Enhanced Antioxidant Defences." University of Canberra. n/a, 2008. http://erl.canberra.edu.au./public/adt-AUC20081209.125208.

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Protein-bound 3,4-dihydroxyphenylalanine (PB-DOPA), a long-lived, redox-active product of protein oxidation, is capable of functioning as both a pro- and anti-oxidant. A number of in vitro and in vivo studies have demonstrated a toxic, non-toxic or even beneficial effect of free DOPA, however little investigation has examined the physiological activity of PB-DOPA. Furthermore, as free DOPA is currently the major treatment available for Parkinson?s disease, most studies have focused on the effect of DOPA within neurological cells or tissues, although the presence of PB-DOPA in other locations,

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9

Nevalainen, Nina, Martin Lundblad, Greg A. Gerhardt, and Ingrid Strömberg. "Striatal Glutamate Release in L-DOPA-Induced Dyskinetic Animals." Umeå universitet, Institutionen för strålningsvetenskaper, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-67595.

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L-DOPA-induced dyskinesia is a common side effect developed after chronic treatment with 3,4-dihydroxyphenyl-L-alanine (L-DOPA) in Parkinson's disease. The biological mechanisms behind this side effect are not fully comprehended although involvement of dopaminergic, serotonergic, and glutamatergic systems has been suggested. The present study utilizes in vivo amperometry to investigate the impact from unilateral 6-hydroxydopamine lesions and L-DOPA (4 mg/kg, including benserazide 15 mg/kg) -induced dyskinetic behavior on striatal basal extracellular glutamate concentration and potassium-evoked

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10

Cabral, Kibedi. "Towards optimisation of L-DOPA synthesis in Mucuna pruriens." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/70680/.

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This study examines the potential for increasing natural L-DOPA drug biosynthesis in Mucuna pruriens by silencing or “knocking down” expression of putative DOPA/tyrosine decarboxylase (Mp-ty/ddc) in situ. Mp-ty/ddc codes for DOPA/tyrosine decarboxylase (Mp-TY/DDC) which converts L-DOPA to dopamine in plants. The hypothesis of the work was that silencing the Mp-ty/ddc gene would result in accumulation of L-DOPA in the plant tissues. This work involved isolation and characterisation of 1.73 kb putative full-length ORF of Mp-ty/ddc. The gene showed 74% homology with TY/DDC protein alignments of o

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11

Edwards, Richard. "Synthesis of [18F]F-DOPA using hypervalent iodine compounds." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/84846/.

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[18F]F-DOPA is a widely used radiotracer most commonly employed in the diagnosis of Parkinson’s disease[1] and neuroendocrine tumours (NETs).[2] In this thesis, the syntheses of suitable diaryliodonium salt precursors for [18F]F-DOPA production via fluorination with nucleophilic, no carrier added (n.c.a.) [18F]fluoride are described. The complex iodonium salt precursors are prepared by a simple and robust procedure in good yields and are bench stable compounds. Incorporation of both ‘cold’ [19F]fluoride and ‘hot’ [18F]fluoride using the prepared precursors has been investigated.[3] Fluorinatio

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12

Barnum, Christopher John. "The role of neuroinflammation in L-dopa-induced dyskinesia." Diss., Online access via UMI:, 2008.

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13

Marette, Caroline. "Approche de synthèses énantiosélectives automatisables de la 6-[18F] fluoro-L-Dopa et de la 3-O-méthyl-6-[18 Fluoro-L-Dopa." Toulouse 3, 2006. http://www.theses.fr/2006TOU30299.

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14

Aymard, Jean-Christophe. "Maladie de Parkinson : intérêt des formes retards de L Dopa." Paris 5, 1990. http://www.theses.fr/1990PA05P021.

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15

af, Bjerkén Sara. "On dopamine neurons : nerve fiber outgrowth and L-DOPA effects." Doctoral thesis, Umeå universitet, Integrativ medicinsk biologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1634.

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Parkinson’s disease is a disorder mainly characterized by progressive degeneration of dopamine producing neurons in the substantia nigra of the midbrain. The most commonly used treatment strategy is to pharmacologically restore the lost function by the administration of the dopaminergic precursor L-DOPA. Another treatment strategy is to replace the degenerated neurons with immature fetal ventral mesencephalic tissue, or ultimately stem cell-derived tissue. Grafting trials have, however, revealed poor reinnervation capacity of the grafts, leaving much of the striata dopamine-denervated. An addi

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16

Lai, Chien-Tsai. "Oxidative stress and cytotoxicity induced by catecholamines and L-DOPA." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23899.pdf.

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17

af, Bjerkén Sara. "On dopamine neurons : nerve fiber outgrowth and L-DOPA effects /." Umeå : Univ, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1634.

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18

Olofsson, Kristina. "Thiol-Ene CHemistry and Dopa-Functional Materials towards Biomedical Applications." Doctoral thesis, KTH, Ytbehandlingsteknik, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-180716.

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Thiol-ene chemistry is versatile and efficient and can be used as a powerful tool in polymer synthesis. In this thesis, the concept of thiol-ene chemistry has been central, where it has been explored as a tool for the synthesis of well-defined hydrogels and dopa-functional materials towards biomedical applications; such as hydrogels, primers for adhesive fixation of bone fractures, self-healing gels, and micelles for drug-delivery. Using thiol-ene chemistry, well-defined hydrogels were realized in order to study how the structure influences properties such as swelling, stiffness and hydrolytic

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19

Prickett, Adam. "The epigenetics and role of Dopa Decarboxylase in heart development." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/the-epigenetics-and-role-of-dopa-decarboxylase-in-heart-development(fc53be8d-af43-4fac-9160-626ee8bf4f04).html.

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Genomic imprinting in mammals subjects a handful of genes to silencing on one allele depending on the parent-of-origin of that allele. The Ddc_exonla gene transcript is under the control of genomic imprinting in the developing and neonatal mouse heart with transcription occurring solely on the paternally inherited allele, with the maternally inherited allele epigenetically silenced. In all other tissues where Ddc_exonla is expressed transcription occurs from both parentally inherited alleles. CTCF plays a central role in controlling gene expression by regulating chromatin organisation, and has

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20

Ko, Daniel. "RGS proteins in experimental Parkinsonism and L-DOPA-induced dyskinesia." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/rgs-proteins-in-experimental-parkinsonism-and-ldopainduced-dyskinesia(97c4a365-d9d5-48fb-8ccd-9c653b801427).html.

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Parkinson’s disease (PD) is a progressive neurodegenerative disorder producing a clinical syndrome of bradykinesia, rigidity and resting tremor. These motor symptoms appear due to the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc) and loss of dopamine in the striatum, which subsequently leads to an imbalance of the basal ganglia motor circuit. The most effective pharmacological treatment for PD is L-3,4-dihydroxyphenylalanine (L-DOPA), the immediate metabolic precursor of dopamine, which effectively restores motor function. L-DOPA is catabolised into dopamine

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21

Wynne, Martin F. "Peptidyl DOPA biochemistry and immunobiology in the protochordate Pyura stolonifera /." St. Lucia, Qld, 2000. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16370.pdf.

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22

Nevalainen, Nina. "Dysfunction in the nigrostriatal system : effects of L-DOPA and GDNF." Doctoral thesis, Umeå universitet, Histologi med cellbiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-64149.

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Parkinson’s disease is a common neurodegenerative disorder caused by nigrostriatal dopamine loss, with motor deficiencies as the primary outcome. To increase the striatal dopamine content, patients are treated with 3,4-dihydroxyphenyl-l-alanine (l-DOPA). Beneficial relief of the motor symptoms is achieved initially, although the efficacy is lost with time and severe side effects, referred to as l-DOPA-induced dyskinesia, manifest in the majority of patients. Biological mechanisms responsible for the dopaminergic degeneration and the upcoming of dyskinesia are still unclear, and thus knowledge

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23

Lefebvre, Marie Julie Christine. "The quantification of L-dopa induced dyskinesia in Parkinson's disease patients." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27701.

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Parkinson's disease (PD) patients experience postural instability as a primary motor symptom (Parkinson, 1817). The majority of PD patients use L-dopa to treat motor symptoms associated with the disease; however, extended use of L-dopa can cause involuntary movement production termed L-dopa induced dyskinesia (LID) (Bezard et al., 2001). Recently, researchers have speculated that postural sway variability (CoP variability) is associated with clinically unapparent LID (Rocchi et al., 2004). This experiment sought to determine the relationship between CoP variability and LID in PD patients. Eigh

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24

Stevenson, James. "Manual tracking in Parkinson's disease : implications for L-dopa-induced dyskinesias." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/34934.

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Though Parkinson’s disease (PD) is considered to be a prototypical basal ganglia disorder, it has become increasingly clear that this traditional view does not capture the complexity of the disease pathophysiology. For instance, imaging studies demonstrate altered cerebellar activity in PD that may compensate for and/or contribute to the symptoms of the disease. L-dopa-induced dyskinesias (LID) are involuntary writhing movements that commonly occur as a side effect of L-dopa therapy, and despite the prevalence of LID their underlying mechanisms are poorly understood. Altered cerebellar activit

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25

Perera, Aruna B. Kane Robert R. "Modification of fresh tissue surfaces ; synthesis of labeled L-dopa analogs; and synthesis of metoclopramide analogs /." Waco, Tex. : Baylor University, 2005. http://hdl.handle.net/2104/2998.

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26

GOZLAN, DIDIER. "Evolution des parkinsoniens traites par dopatherapie : a propos de 25 cas." Limoges, 1988. http://www.theses.fr/1988LIMO0203.

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27

Fischer, Diana Gabriela. "Dopa-responsive Dystonie molekulargenetische Untersuchungen am Guanosintriphosphat-Cyclohydrolase-I- und TorsinA-Gen /." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=965417115.

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28

Balci, Meral. "Periodische Beinbewegungen beim Obstruktiven Schlafapnoesyndrom: Einfluss der CPAP-Therapie + L-Dopa-Medikation." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=974509620.

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29

Aljabri, Hareb Mohammed. "Comparative analysis of Anopheles gambiae L-tyrosine decarboxylase and L-DOPA decarboxylase." Thesis, Virginia Tech, 2010. http://hdl.handle.net/10919/34788.

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A major pathway of tyramine and dopamine synthesis in insects is through the decarboxylation of tyrosine and DOPA, respectively. Although tyrosine decarboxylase (TDC) has been mentioned in some reports, it has never been critically analyzed. The high sequence identity shared by tyrosine decarboxylase and DOPA decarboxylase in insects, and the similar structures of the substrates, tyrosine and DOPA, raise the possibility that both tyrosine decarboxylase and DOPA decarboxylase (DDC) have activities to tyrosine and DOPA. In this study, after tyrosine decarboxylase and DOPA decarboxylase enzymes o

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30

BRIQUE, SERGE. "Dystonie dopa-sensible : donnees cliniques et biochimiques a propos d'une nouvelle famille." Lille 2, 1994. http://www.theses.fr/1994LIL2M274.

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31

Bruneau, Gilles. "Études structurales et localisations chromosomiques des gènes de la L-DOPA décarboxylase de rat et de l'histidine décarboxylase humaine." Paris 12, 1993. http://www.theses.fr/1993PA120022.

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La dopa decarboxylase et l'histidine decarboxylase appartiennent a une famille d'enzymes de decarboxylation phylogenetiquement reliees et utilisant le phosphate de pyridoxal comme cofacteur. Le gene de la ddc de rat possede deux promoteurs dont l'expression tissu-specifique conduit a la formation de deux arnm differant par leurs extremites 5 non codantes. Les deux regions promotrices possedent une boite tata et un seul site d'initiation de la transcription. Aucune ne presente les caracteristiques des promoteurs de genes housekeeping. Les organisations structurales des genes ddc de l'homme et d

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32

Göldner, Alexander. "Therapeutische Wirksamkeit von L-Dopa bei Amyotropher Lateralsklerose - eine Analyse von 50 therapeutischen Heilversuchen." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-65195.

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33

Lira, Sonja. "Therapeutische Wirksamkeit von L-Dopa bei Amyotropher Lateralsklerose - eine Beobachtung von 39 Patienten im Langzeitverlauf." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-65969.

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34

Holiga, Štefan. "Personalizing functional Magnetic Resonance Protocols for Studying Neural Substrates of Motor Deficits in Parkinson’s Disease." Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-124904.

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Parkinson’s disease (PD) is a progressive neurodegenerative movement disorder characterized by a large number of motor and non-motor deficits, which significantly contribute to reduced quality of life. Despite the definition of the broad spectrum of clinical characteristics, mechanisms triggering illness, the nature of its progression and a character of therapeutic effects still remain unknown. The enormous advances in magnetic resonance imaging (MRI) in the last decades have significantly affected the research attempts to uncover the functional and structural abnormalities in PD and have help

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35

Simmons, Donald Karl. "L-DOPA production in a liquid membrane enzyme reactor: process development and modeling." Diss., Georgia Institute of Technology, 1990. http://hdl.handle.net/1853/10120.

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36

Riahi, Golnasim. "Implication of the serotoninergic systems in Parkinson's disease and L-Dopa-induced dyskinesia." Thesis, Université Laval, 2012. http://www.theses.ulaval.ca/2012/28974/28974.pdf.

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37

Malerbi, Marion. "Rôle de Narp dans le développement des dyskinésies induites par la L-DOPA." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066025/document.

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Le traitement substitutif par la L-DOPA, indiqué dans la maladie de Parkinson, induit à terme des complications motrices appelées les dyskinésies induites par la L-DOPA. L'apparition des dyskinésies est due, au moins en partie, à la mise en place d'une plasticité aberrante dans le striatum, qui fait suite à des modifications transcriptionnelles induites par la L-DOPA. Une analyse du transcriptome nous a permis d'identifier le gène Nptx2, codant pour la neuropentraxine Narp, comme étant un candidat potentiellement impliqué dans l'apparition des dyskinésies. L'objectif de ce travail était d'étud

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38

Fuhrer, Hannah [Verfasser]. "Die Auswirkungen von L-Dopa auf nicht-deklarative und deklarative Gedächtnisprozesse / Hannah Fuhrer." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1068209194/34.

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39

Militza, Monteverde. "det är inte hud, det är puder : dopa min kropp vs. dopamin-kropp." Thesis, Kungl. Konsthögskolan, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:kkh:diva-215.

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ska jag springa runt i 3D-labbet för att tänka på hur leder fungerar, en animerad figur som inte får röra sig som en robot, min dröm är att hitta den där parfymen som luktar plastdocka lika mycket som jag tänker ge min pojkvän parfymen som luktar nytryckt bok, det börjar med Fountain of Youth och slutar i syntetisk biologi och DNA-mutation, – allt för att hålla sig vid liv, eller åtminstone ge intryck av att göra så

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40

BOI, LAURA. "Neuroinflammation in Parkinson’s Disease: role in neuropathology and L-DOPA-induced motor complications." Doctoral thesis, Università degli Studi di Cagliari, 2020. http://hdl.handle.net/11584/284805.

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Parkinson Disease (PD) is a neurodegenerative disorder characterized by the progressive dopaminergic loss in the Substantia Nigra (SN) and the presence of intracellular Lewy Bodies (LB) containing deposits of the protein α-synuclein (α-syn). Several studies identified the neuroinflammatory processes as important factors in the neuropathology of PD, involving mainly microglia cells. Indeed, in PD microglia lose their ability to autoregulate, sustaining a chronic pro-inflammatory environment in dopaminergic areas which exacerbates the neurodegenerative process. Moreover, recent pre-clinical stud

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41

Oueslati, Abid. "Implication des systèmes à acides aminés excitateurs dans la maladie de Parkinson et ses traitements." Aix-Marseille 2, 2008. http://theses.univ-amu.fr.lama.univ-amu.fr/2008AIX22015.pdf.

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L’expression des symptômes moteurs de la maladie de Parkinson (MP) est associée à une activation anormale des systèmes glutamatergiques dans les ganglions de la base (GB), incluant le noyau subthalamique (NST). De fait, le traitement chirurgical de la MP par stimulation à haute fréquence (SHF) du NST s’est imposé au cours de ces dernières années comme une option thérapeutique de choix pour les patients à des stades avancés de la maladie chez lesquels le traitement de référence à la L-DOPA induit à long terme des effets indésirables sévères. Cependant, les bases cellulaires de ses effets thérap

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42

DUMAS, MYRIAM. "Les problemes bucco-dentaires chez le parkinsonien." Lyon 1, 1987. http://www.theses.fr/1987LYO1A021.

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43

Ma, Bonita. "Augmentation of L-DOPA-evoked dopamine efflux by Methylphenidate : role for the D2 autoreceptor?" Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/50926.

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Using a 6-OHDA model of Parkinson’s disease, we have preliminary evidence that L-DOPA-derived dopamine (DA) ceases to be released through conventional mechanisms of exocytosis under severe denervation. This may be problematic, as large, and possibly unregulated release of L-DOPA-derived DA would be expected to cause abnormal patterns of DA stimulation at the postsynaptic receptors, likely contributing to the development of dyskinesia. This issue may be overcome with the Dopamine Transporter (DAT) blocker Methylphenidate (MPD). Ahn and Phillips observed that MPD augmented the L-DOPA-derived D

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44

Challapa, Velásquez Nancy Mariela. "Fisicoquímica del neurotransmisor dopamina y su precursor L-DOPA utilizando métodos teóricos y experimentales." Bachelor's thesis, Universidad Nacional Mayor de San Marcos, 2018. https://hdl.handle.net/20.500.12672/8026.

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Publicación a texto completo no autorizada por el autor<br>Estudia las propiedades de estabilidad termodinámica y reactividad por transferencia protónica intrínsecas (en fase gas) del neurotransmisor dopamina y su precursor L-DOPA. Para ello hace uso de la Metodología DFT (B3LYP) y “ab-initio” (métodos G3 y G4) para el estudio conformacional en especies neutras, protonadas y desprotonadas, en fase gaseosa; y la determinación experimental, mediante espectrometría de masas de triple-cuadrupolo con fuente ESI (electrospray), de la afinidad protónica y basicidad de la Dopamina y acidez de la L-DOP

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45

Charbonnier-Beaupel, Fanny. "Mécanismes moléculaires des dyskinésies induites par la l-dopa dans la maladie de parkinson." Paris 6, 2013. http://www.theses.fr/2013PA066582.

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Dans la maladie de Parkinson, le traitement par la L-DOPA est associé à l’apparition des dyskinésies (LID). Une des hypothèses majeures est qu’elles résultent de l’induction d’un programme transcriptionnel aberrant dans les neurones striataux via l’hypersensibilisation des récepteurs D1 et l’activation de ERK. Pour identifier les gènes induits par la L-DOPA, dépendants de ERK et associés au développement des LID, nous avons effectué des analyses du transcriptome dans le striatum de souris lésées à la 6-hydroxydopamine. Tout d’abord, des souris ont été sacrifiées 0, 1, 3 et 6 h après la L-DOPA.

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46

BOREK, MICHAEL. "Pharmacocinetique de la l-dopa et de la 3-o methyldopa chez des parkinsoniens fluctuants et non fluctuants et determination des taux plasmatiques de dopa en phaseon et off : etude retrospective sur 55 cas." Lyon 1, 1992. http://www.theses.fr/1992LYO1M059.

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47

Elabi, Osama. "The effect of L-dopa and neuroprotective agents on cell replacement therapy for Parkinson's disease." Thesis, Cardiff University, 2017. http://orca.cf.ac.uk/103900/.

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Parkinson disease (PD) is the second most common neurodegenerative disease affecting 1.8% of population aged over 65 years. The current medications that control the symptoms of the disease are associated with limited efficacy and induction of side effects (dyskinesia) at later stages of the disease. One promising future therapy in PD is cell replacement therapy, however clinical trials declared inconsistent outcomes and developing dyskinesia related to the graft. Studies later suggested suboptimal conditions contributed on these outcomes. This thesis builds on this knowledge endeavouring to su

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48

Santos, Bruno Lopes dos. "Análise de preditores clínicos e genéticos para o surgimento de discinesias induzidas por L-DOPA na doença de Parkinson." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17140/tde-06042018-094440/.

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A doença de Parkinson (DP) é a segunda doença neurodegenerativa mais comum do mundo, e seu tratamento atual se baseia principalmente no uso de medicações que facilitam a transmissão dopaminérgica nos núcleos da base. A L-DOPA é a principal medicação usada no tratamento da DP, contudo seu uso crônico está associado ao surgimento de complicações motoras, como as discinesias induzidas por L-DOPA (DIL). As DIL ocorrem em cerca de 50% dos pacientes com DP que usaram LDOPA por cerca de 4 a 6 anos, e podem causar uma série de impactos negativos aos pacientes. Pela incapacidade adicional que esta comp

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Moutinho, Daniela Mesquita. "Human ceruloplasmin and neurotransmitters: complex stabilization and crystallization." Master's thesis, Faculdade de Ciências e Tecnologia, 2013. http://hdl.handle.net/10362/10853.

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Dissertation to obtain a Master Degree in Molecular Genetics and Biomedicine at Faculty of Sciences and Technology,Universidade Nova de Lisboa<br>Human ceruloplasmin (hCp) is the molecular linker between the copper and iron metabolism and its importance in the homeostasis of human body has been implied in some neurological diseases. This plasma cuproenzyme has ferroxidase activity, oxidizing Fe2+ to Fe3+ and incorporating it into apotransferrin. hCp also has aminoxidase activity regulating the levels of amine stress hormones in the bloodstream and brain. Thus, it is thought to have an import

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BELLONNET, CHRISTINE. "Influence de la dietetique sur les fluctuations motrices des parkinsoniens traites par la levodopa." Clermont-Ferrand 1, 1989. http://www.theses.fr/1989CLF13044.

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