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Dissertations / Theses on the topic 'Levy bodies'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

Sánchez, Castañeda Cristina. "Structural brain changes, cognitive deficits and visual hallucinations in dementia with lewy bodies and parkinson's disease with dementia." Doctoral thesis, Universitat de Barcelona, 2009. http://hdl.handle.net/10803/2281.

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La enfermedad de Parkinson (EP), la enfermedad de Parkinson con Demencia (EPD) y la Demencia con Cuerpos de Lewy (DCL) presentan una alteración del metabolismo de la alfa-sinucleína que provoca la formación de agregados proteicos llamados Cuerpos de Lewy. <br/><br/>Las sinucleinopatías son la segunda causa de demencia degenerativa después de la enfermedad de Alzheimer. Se caracterizan neuropatológicamente por inclusiones de alfa-sinucleína en el tronco cerebral, núcleos subcorticales, áreas neocorticales y límbicas, y clínicamente por demencia, alteraciones atencionales, parkinsonismo y comúnm

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2

Donaghy, Paul Christopher. "Biomarkers in dementia with Lewy bodies." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3439.

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Dementia with Lewy bodies (DLB) is the second commonest type of neurodegenerative dementia, but accurate antemortem diagnosis remains challenging, especially at the earliest (prodromal) disease stages and in the presence of mixed (Alzheimer) pathology. To investigate this we undertook two studies, an investigation of 123I-FP-CIT imaging as a possible biomarker of prodromal DLB (at the mild cognitive impairment (MCI) stage), and a study of the effect of amyloid deposition measured by 18F-Florbetapir PET on clinical phenotype in established DLB. Methods Prodromal DLB Study: 53 subjects with MCI

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3

Grace, Janet. "Fluctuations of consciousness in dementia with Lewy bodies." Thesis, University of Newcastle upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407650.

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4

Garcia, Esparcia Paula. "Identification of a risk transcriptome and proteome in Parkinson’s disease, Dementia with Lewy bodies and rapidly progressive Dementia with Lewy bodies." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/664642.

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Parkinson's disease (PD) is a neurodegenerative disorder characterized by movement impairment, or parkinsonism, for which there is still no cure. The manifest clinical signs result from neuronal loss of more than 60% in the substantia nigra pars compacta. Cognitive disorders and dementia in PD usually occur, thus leading to Parkinson disease with dementia (PDD). Moreover, Dementia with Lewy bodies (DLB) is also considered a neurodegenerative disease and one of the most common causes of dementia, with cognitive impairment symptoms similar to Alzheimer-type dementia, and wit

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Bussè, Cinzia. "Cognitive and clinical phenotype in dementia with Lewy bodies." Doctoral thesis, Università degli studi di Padova, 2017. http://hdl.handle.net/11577/3425726.

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This dissertation describes the research studies I have most occupied during my Ph. D course. Due to the limited number of studies addressing which clinical and cognitive features are most useful in diagnosing early dementia with Lewy bodies (DLB) (Jicha et al. 2010; Boeve et al. 2012) I initially focused on the visuo-constructional impairments in prodromal DLB (study 1); afterwards on visual-spatial and visual-perceptual deficits (study 2) in a different sample of prodromal DLB. Later I investigated which cognitive impairments could be predictive of DLB in regards to the memory domain (Study

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Cormack, Francesca K. "Visual perception and constructional apraxia in dementia with lewy bodies." Thesis, University of Newcastle Upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399012.

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7

Morenas, Rodríguez Estrella. "Multimodal biomarkers studies in the continuum dementia with lewy bodies – alzheimer´s disease." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/669555.

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La demència amb cossos de Lewy (DCLw) es caracteritza per la seva heterogeneïtat. En aquesta tesi, el meu objectiu és investigar aquesta heterogeneïtat a través de l'anàlisi dels diferents subtipus clínics basats tant en les característiques de presentació predominants en la fase prodròmica de la malaltia com en la diversitat dels trastorns de la son presents, centrant-me en el trastorn del comportament de la son REM (TCSR). En aquesta tesi, també investigo el paper de l'activitat glial en DLB mesurant els nivells en el líquid cefaloraquidi (LCR) de les proteïnes glials YKL-40, TREM2 soluble (

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8

Molloy, Sophie. "The treatment of dementia with Lewy bodies : the role of levodopa." Thesis, University of Newcastle upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424081.

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9

Gray, Alastair Lewis. "The comparative neuropsychology of Alzeheimer's disease and dementia with Lewy bodies." Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251345.

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10

Piggott, Margaret Ann. "Dopamine systems in dementia with Lewy bodies and other neurodegenerative diseases." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366588.

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11

Fernandes, Emanuel Ferreira. "The role of Synphilin-1A/PPP1 complex in Lewy bodies formation." Master's thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/12488.

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Mestrado em Biomedicina Molecular<br>One of the major Parkinson’s disease hallmarks is the development of cytoplasmic inclusions, termed Lewy bodies, mainly within surviving neurons in the brainstem of affected patients. Many proteins have been identified in the Lewy bodies, but their formation mechanism remains unclear. Among the proteins already identified in the Lewy bodies are synphilin-1, a α-synucleininteracting protein, and synphilin-1A, a synphilin-1 splice variant. Synphilin-1 and synphilin-1A have been considered key elements in Parkinson’s disease as their overexpression in human em

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12

Anusha, Koneti. "Energy metabolism and Protein synthesis in Parkinson's disease and Dementia with Lewy Bodies." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/396207.

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Mitochondria dysfunction is documented in the substantia nigra in Parkinson's disease (PD), a region which plays a central role in the characteristic motor manifestations of the disease. Mitochondria! dysfunction is a cause of neuron energy exhaustion, oxidative stress and dopaminergic cell death. However, little is known about mitochondria! dysfunction in other brain regions in PD, the impairment of which is causative of other symptoms such as cognitive impairment and, in some cases, dementia. The present study was undertaken to analyse mitochondria! function in the frontal cortex area 8 and

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13

Erskine, Daniel. "Assessment of the visual thalamic circuitry in hallucinations in dementia with Lewy bodies." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3930.

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Background Visual hallucinations occur in 70-90% of patients with dementia with Lewy bodies (DLB) and are related to decreased quality of life for patients. However, the underlying neuropathological changes that promote the manifestation of visual hallucinations in DLB are not known. Several hypotheses of visual hallucinations in DLB have either directly implicated the lateral geniculate nucleus (LGN), pulvinar and superior colliculus or suggested impairments in their putative functions. Methods Post-mortem LGN, pulvinar and superior colliculus tissue was obtained from DLB cases with a clinica

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14

Näsström, Thomas. "Characterization of α-synuclein oligomers : Implications for Lewy Body Disorders". Doctoral thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-160102.

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Parkinson’s disease, dementia with Lewy bodies and multiple system atrophy are disorders featuring accumulation of Lewy bodies in brain. The main component of these large insoluble intracellular inclusions is the presynaptic protein alpha-synuclein (α-synuclein). It is generally believed that α-synuclein monomers adopt an abnormal conformation that favors the formation of soluble oligomers or protofibrils and, eventually, insoluble fibrils depositing as Lewy bodies. Notably, the intermediately sized oligomers/protofibrils seem to have particular neurotoxic effects. Several factors may influenc

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Kirkland, Joanne. "Dementia with lewy bodies : a descriptive functional analysis of hallucination, challenging behaviour and emotional lability." Thesis, University of Birmingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397204.

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16

Yamin, Stephanie. "Driving Performance of Older Adults with Early Dementia with Lewy Bodies or Early Alzheimer’s Disease." Thèse, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/30457.

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Little is known about the specific cognitive impairments that may be the cause of the reported increased crash rate in individuals with early dementia. Though, it is widely accepted that attention, visuospatial and perceptual abilities are central in being able to operate a vehicle safely. This study had three objectives. The first was to clarify the neuropsychological profile, with an emphasis on attention, visuospatial and perceptual abilities, of individuals with early dementia with Lewy bodies (DLB), the next was to examine the driving performances of two groups of individuals with early d

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17

Walker, Zuzana. "Dementia with Lewy bodies : the investigation of pre- and post-synaptic dopaminergic receptors with SPET." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289894.

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18

Matar, Elie. "The Phenomenology, Pathophysiology and Progression of the Core Features of Lewy Body Dementia." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/29365.

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Lewy body dementias – Dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD) - are disabling neurodegenerative conditions defined pathologically by the presence of intraneuronal α-synuclein rich aggregates (‘Lewy bodies’ and ‘Lewy neurites’). These disorders are characterized by a set of ‘core’ clinical features, namely cognitive fluctuations, visual hallucinations, motor parkinsonism, and most recently added, REM sleep behaviour disorder. These features are central to the diagnosis of Lewy bodies dementias (especially DLB) and discriminate them from other neurodegenerative dis

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19

Singh, Priyanka. "The Role of Neutral Sphingolipids in the Pathogenesis of Parkinson Disease and Dementia with Lewy Bodies." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24029.

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The molecular mechanisms underlying the association between mutations in GBA1 and risk of developing the ‘synucleinopathy’ disorders Parkinson’s disease (PD) and dementia with Lewy bodies (DLB) remain elusive. To better understand the precise molecular cascade that connects GBA1 mutations with α-synuclein dysregulation, a modified lipid extraction and HPTLC protocol was optimized to detect changes in levels of neutral sphingolipids (SLs) from neural cells and tissue expressing wild-type (WT) GBA1, mutant GBA1, or both. We demonstrate that mutant GBA1 does not confer a dominant-negative effect

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20

Barber, Robert. "MRI volumetric study of dementia with Lewy bodies : a comparison with Alzheimer's disease and normal ageing." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310175.

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21

Rcom-H'cheo-Gauthier, Alexandre Nay. "The Protective Effect of Calbindin-D28K on a-Synuclein Aggregation in α- Synucleinopathies". Thesis, Griffith University, 2016. http://hdl.handle.net/10072/368168.

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Neurodegeneration in Dementia with Lewy Bodies (DLB) and Parkinson’s disease (PD) is associated with the formation of neuronal inclusion bodies composed mainly of aggregated α-synuclein (α-syn) protein. Aggregation may be associated with disturbed Ca2+ homeostasis and oxidative stress. Post-mortem studies have shown relative sparing of neurons in PD that are positive for the Ca2+ buffering protein, Calbindin-D28k (CB). CB has been shown to be induced by the hormonal form of vitamin D, Calcitriol, and could be induced by other vitamin D analogue such as Calcipotriol (Cp). Furthermore, recent ce

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22

Watson, Rosemary. "Structural and diffusion MRI in dementia with Lewy bodies : a comparison with Alzheimer's disease and normal ageing." Thesis, University of Newcastle Upon Tyne, 2012. http://hdl.handle.net/10443/1485.

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Purpose: Dementia with Lewy bodies (DLB) is a common form of dementia, yet its clinical features remain poorly understood. We investigated in vivo structural and micro-structural changes in DLB compared to Alzheimer’s disease (AD) and normal ageing using magnetic resonance imaging (MRI) techniques and their relationship to clinical features. Methods: Study subjects (35 DLB, 36 AD, 35 Controls) completed clinical and cognitive assessments and structural and diffusion tensor MRI scans. Voxel based morphometry (VBM) techniques were used to investigate patterns of regional grey matter atrophy. To

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23

Spurden, Dean Paul. "Cholinergic system and the thalamus in dementia with Lewy bodies, Alzheimer's disease and schizophrenia : a neurochemical study." Thesis, University of Sunderland, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242135.

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24

Pérez, Pi Irene. "Design and development of a novel bead-based assay for early stage alpha-synuclein aggregation." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28761.

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α-synuclein is a small presynaptic protein whose misfolding and aggregation are considered drivers of the neurological disorders Parkinson’s disease, multiple system atrophy, dementia with Lewy bodies and related synucleopathies. α-synuclein exists in a dynamic state that changes from an α-helical conformation when bound to liposomes to natively unfolded in solution, the majority being in the latter state. The disease process by which native healthy α-synuclein undergoes a change in conformation to form β-sheet oligomers and fibrils is still unresolved. The fibrillation process has been widely

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25

Grgurina, Iris. "Influence of the APOE4 risk factor on hippocampal epigenomic and transcriptomic signatures in a physiological and pathological environment indicative of Dementia with Lewy bodies (DLB)." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ013.

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La Maladie à corps de Lewy (MCL) est la deuxième pathologie neurocognitive la plus fréquente, caractérisée par le dépôt pathogène de corps de Lewy constitués d'α-synucléine dans des neurones vulnérables – notamment ceux de l'hippocampe (HC). Le facteur de risque le plus important pour la maladie d'Alzheimer (MA), et récemment démontré pour la MCL, est l'allèle ε4 de l'apolipoprotéine (APOE4) qui est une lipoprotéine principale dans le système nerveux central jouant un rôle crucial dans le maintien de l'homéostasie lipidique. Dans la première partie de ma thèse, nous avons démontré que l'APOE4

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Gray, Madison T. "On α-synuclein in the Human Enteric Nervous System". Thèse, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/30664.

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Parkinson’s disease is a neurodegenerative disease resulting primarily from loss of dopaminergic innervation in the striatum subsequent to cell loss in the substantia nigra pars compacta. The abnormal accumulation of the normal pre-synaptic protein α-synuclein (αsyn) forms intraneuronal inclusions known as Lewy neurites and Lewy bodies. The origins of central Lewy pathology have been suggested to lie in the enteric nervous system, ascending through the vagus nerve to the dorsal motor nucleus of the vagus. To ascertain gastrointestinal regions most likely to be the source of central Lewy pathol

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Recasens, Ibabe Ariadna. "Initiation, progression and extension of parkinson’s disease: role of α-synuclein". Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/284438.

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La malaltia de Parkinson és un trastorn neurodegeneratiu freqüent d’origen desconegut que es caracteritza principalment per la pèrdua de neurones dopaminèrgiques de la substància nigra pars compacta (SNpc) i la presencia d’inclusions proteiques intacitoplasmàtiques anomenades cossos de Lewy (CL), en diverses regions cerebrals afectades. Tot i que els CL es van descriure per primera vegada fa una dècada, encara es desconeix la seva rellevància en el procés patològic de la MP. Recentment s’ha suggerit que l’ α-synucleina, el principal component dels CL, pot iniciar i extendre el procés patològi

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Szeto, Yan Yee Jennifer. "Mild Cognitive Impairment in Parkinson’s Disease." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/16944.

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The concept of Mild Cognitive Impairment is a newly defined entity within the context of Parkinson’s Disease (PD-MCI) with recent development of diagnostic criteria, biomarker research programs and therapeutic strategies. However, it is well-established that MCI represents a heterogeneous entity with different clinical phenotypes, rates of progression, and perhaps underlying pathological processes. As such, while the application of the MCI construct has provided a framework for understanding cognitive decline in PD, additional research is required to validate and/or refine the proposed PD-MCI

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Lyras, Leonidas. "Oxidative stress and neurodegenerative diseases : measurement of lipid, protein and DNA damage in brain tissue from Alzheimer's disease, amyotrophic lateral sclerosis and dementia with Lewy bodies." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298464.

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30

Chabran, Eléna. "Étude des bases cérébrales de la maladie à corps de Lewy par IRM multimodale." Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ088.

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Deuxième pathologie neurodégénérative cognitive la plus fréquente après la maladie d’Alzheimer (MA), lamaladie à corps de Lewy (MCL) demeure pourtant mal connue et constitue encore aujourd’hui un réelchallenge, à la fois sur les plans clinique et scientifique et en matière de santé publique. L’imagerie parrésonance magnétique (IRM), technique non invasive et multimodale, constitue une approche particulièrementprometteuse pour enrichir la compréhension des mécanismes cérébraux sous-jacents à cette maladie. Dans lecadre de ce travail de thèse, nous nous sommes intéressés aux modifications cérébr

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Fenyi, Alexis. "Typage moléculaire des maladies neurodégénératives dues à l’agrégation de la protéine alpha synucléine." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS053.

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Les synucléinopathies regroupent les maladies neurodégénératives de Parkinson, les démences à corps de Lewy et l'atrophie multi-systématisée. Des études suggèrent que les synucléinopathies seraient des maladies à prion. Aujourd'hui, certains aspects manquent pour que l'α-synucléine soit reconnue comme un prion. Par exemple, il est à démontrer que chaque synucléinopathie est causée par une souche précise d'α-synucléine. Durant ma thèse j’ai mis au point une méthode d'amplification fiable des dépôts présents dans le cerveau des patients atteints de synucléinopathies. J’ai aussi documenté les pro

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Psol, Maryna [Verfasser], Sebastian [Akademischer Betreuer] Kügler, Tiago Fleming [Gutachter] Outeiro та Markus [Gutachter] Zweckstetter. "Neurotoxicity and aggregation of β-synuclein and its P123H and V70M mutants associated with dementia with Lewy bodies / Maryna Psol ; Gutachter: Tiago Fleming Outeiro, Markus Zweckstetter ; Betreuer: Sebastian Kügler". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2019. http://d-nb.info/1188886878/34.

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Mondon, Karl. "Etude phénotypique des démences extrapyramidales : apport de la neuropsychologie dans le diagnostic différentiel." Thesis, Tours, 2011. http://www.theses.fr/2011TOUR3146.

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Les situations cliniques associant des troubles moteurs et une détérioration cognitive sont fréquentes et déroutantes pour le clinicien, qui est confronté à la difficile question du diagnostic différentiel entre plusieurs cadres nosographiques dont la maladie de Parkinson avec démence (MPD) et la démence à corps de Lewy Diffus (DCLD). Dans ce travail, nous avons étudié les caractéristiques neuropsychologiques pouvant différencier les deux affections. Nous avons, dans une première étude, montré que la mémoire de reconnaissance visuelle était altérée de façon différente. Dans un second travail,

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Hirsch, Étienne. "Approche physiopathologique de la maladie de parkinson : analyse immunocytochimique du systeme mesostriatal et caracterisation de deux antigenes du corps de lewy." Paris 6, 1988. http://www.theses.fr/1988PA066627.

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Description des lesions de la voie mesostriatale par utilisation d'une methode immunocytochimique, permettant de mettre en evidence la degenerescence selective des neurones dynaminergiques et la presence des corps de lewy

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Casini, Elisa. "Le sommeil : une enjeu pour les couples confrontés aux maladies neuro dégénératives." Thesis, Lille 3, 2017. http://www.theses.fr/2017LIL30016/document.

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Cette thèse de sociologie porte sur les pratiques de sommeil des couples vieillissants confrontés à une maladie neurodégénérative. Elle se fixe comme objectif de saisir les dynamiques temporelles et spatiales de ces pratiques de sommeil, centrales dans la vie du couple, au fil de l'évolution de la maladie en accordant une attention particulière aux relations de genre. Nous avons interviewé 30 couples à domicile, dont 12 concernés par la maladie à corps de Lewy et 18 par la maladie d'Alzheimer et nous avons intégré des dispositifs d'enquête tels que la rédaction de journaux de sommeil, de journ

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Mazère, Joachim. "Interactions acétylcholine-dopamine dans les maladies neurodégénératives : approche d’imagerie moléculaire." Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21873/document.

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Le rôle que pourrait jouer l’interaction des systèmes cholinergiques (ACh) et dopaminergiques (DA) semble crucial dans la physiopathologie de certaines maladies neurodégénératives, en particulier dans la démence à corps de Lewy (DCL). Ce travail de thèse se propose de valider un protocole d’imagerie moléculaire en tomographie d’émission monophotonique, consistant en un marquage de l’ACh et de la DA chez un même individu, afin de pouvoir étudier in vivo les interactions ACh/DA.Après avoir mis au point chez des sujets âgés et des patients atteints de maladie d’Alzheimer une méthode d’imagerie cé

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Chang, Yen-Ting, та 張雁婷. "Investigating amyloid β mediated α-Synuclein-induced neurotoxicity in Dementia with Lewy Bodies". Thesis, 2016. http://ndltd.ncl.edu.tw/handle/p28y39.

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碩士<br>中山醫學大學<br>醫學研究所<br>104<br>Dementia with Lewy bodies (DLB) is the second most common cause of dementia, trailing Alzheimer’s disease (AD), which possessing a large proportion of demented population. In these two diseases, α-Synucleinand beta-Amyloid (Aβ) are the main pathologies in DLB and ADpatients brain respectively, and both proteins involved the mechanism of misfolded proteins in neurodegeneration. In the past, patients with DLB revealed similar pathology with AD in their brains; thus, the name LB variant of AD was used in previous documents. Comparing to AD patients,DLB patientsdeve

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Musgrove, REJ. "Alpha-synuclein in the neurodegenerative mechanisms of Parkinson's disease and dementia with Lewy bodies." Thesis, 2012. https://eprints.utas.edu.au/15311/3/whole-musgrove-thesis-2012.pdf.

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Parkinson’s disease (PD) and Dementia with Lewy bodies (DLB) are characterised by Lewy body pathology and the degeneration of midbrain-dopaminergic and cortical neurons, respectively. The mechanisms underlying the selective degeneration of these neuronal populations are not known. Gene mutations associated with PD and DLB have highlighted the role of oxidative stress and mitochondrial dysfunction in the pathogenesis of these conditions. Substitution mutations in the SNCA gene encoding alpha-synuclein are the most common cause of familial disease and alpha-synuclein also comprises the pr

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Shen, Mei-Shiuan, and 沈枚萱. "Ceftriaxone Prevents Cognitive and Neuronal Deficits in a Rat Model of Dementia with Lewy Bodies." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/8y4yvn.

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Chiu, Pai-Yi, and 邱百誼. "Comparison studies of the neuropsychiatric symptoms of Parkinson’s diseae dementia, dementia with Lewy bodies, and Alzheimer’s disease." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/65166450957842234535.

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博士<br>中山醫學大學<br>醫學研究所<br>104<br>Objective：Previous studies on the clinical and pathological manifestations of Parkinson’s disease dementia (PDD) have reported findings more similar to dementia with Lewy bodies (DLB) than to Alzheimer’s disease (AD). The first aim of this study was to investigate the neuropsychiatric symptoms of PDD compared to DLB and AD. The second was to provide the evidence of whether PDD and DLB belong to the same disease entity. Methods and Materials： First, we conducted a case-control study on 125 newly diagnosed consecutive PDD patients and age- and dementia stage-match

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Dieks, Jana-Katharina. "Liquorproteomveränderungen bei Patienten mit Lewy-Körperchen Demenz." Doctoral thesis, 2013. http://hdl.handle.net/11858/00-1735-0000-0001-BB2D-0.

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Die Demenz mit Lewy-Körperchen (DLB) ist eine progrediente neurodegenerative Erkrankung und stellt nach der Alzheimer-Erkrankung eine der häufigsten Ursachen einer Demenz dar. Betroffene leiden neben dem zentralen Merkmal Demenz an Fluktuationen der Kognition, Parkinsonismus und visuellen Halluzinationen. Charakteristische neuropatholgische Kennzeichen der DLB sind α-Synuklein-enthaltende Lewy-Körperchen und -Neuriten, die sich in kortikalen und subkortikalen Hirnregionen finden. Bei der klinischen Diagnostik dieser Erkrankung sind neben der Beurteilung klinischer Befunde laborchemische, psych

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Psol, Maryna. "Neurotoxicity and aggregation of β-synuclein and its P123H and V70M mutants associated with dementia with Lewy bodies". Doctoral thesis, 2018. http://hdl.handle.net/21.11130/00-1735-0000-0003-C133-9.

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Candelise, Niccolò. "Seeding and structural varibility in α-synucleinopathies". Doctoral thesis, 2019. http://hdl.handle.net/21.11130/00-1735-0000-0003-C12C-2.

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Hsieh, Chia-Ling, and 謝佳羚. "Glucagon-like peptide 1 (GLP-1) signaling attenuates dementia with Lewy bodies (DLB) associated neurotoxicity through restoration of insulin signaling." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/pkr9p2.

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碩士<br>中山醫學大學<br>醫學研究所<br>106<br>Dementia with Lewy bodies (DLB) is the second most common neurodegenerative dementia only to Alzheimer''s disease (AD). In fact, DLB shares common pathological features with AD and Parkinson''s disease (PD), that simultaneously accompany α-synuclein and Aβ. These misfolded proteins accumulate in the brain and result in a large number of neuronal damage and brain atrophy, eventually leading to of the damages of the corresponding neurological function. However, there is currently no clinical treatment of drugs for the improvement of DLB. It is in urgent need for d

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Baake, Daniel. "Einfluss systemischer Infektionen und ihrer Behandlungen auf den Krankheitsverlauf im Maus-Modell des Morbus Parkinson." Doctoral thesis, 2011. http://hdl.handle.net/11858/00-1735-0000-0006-B203-1.

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Strohäker, Timo. "Structural characterization of alpha-synuclein aggregates seeded by patient material." Doctoral thesis, 2018. http://hdl.handle.net/21.11130/00-1735-0000-0005-12CD-0.

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Tuineag, Maria. "Psychiatric symptoms in idiopathic rapid-eye-movement sleep behaviour disorder." Thèse, 2012. http://hdl.handle.net/1866/8466.

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Le trouble comportemental en sommeil paradoxal (TCSP) idiopathique est caractérisé par une activité motrice indésirable et souvent violente au cours du sommeil paradoxal. Le TCSP idiopathique est considéré comme un facteur de risque de certaines maladies neurodégénératives, particulièrement la maladie de Parkinson (MP) et la démence à corps de Lewy (DCL). La dépression et les troubles anxieux sont fréquents dans la MP et la DCL. L’objectif de cette étude est d’évaluer la sévérité des symptômes dépressifs et anxieux dans le TCSP idiopathique. Cinquante-cinq patients avec un TCSP idiopathique sa

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Rodrigues, Brazète Jessica. "Marqueurs électroencéphalographiques du développement d’une maladie neurodégénérative dans le trouble comportemental en sommeil paradoxal." Thèse, 2015. http://hdl.handle.net/1866/13748.

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(5930060), Paola C. Montenegro. "MOLECULAR PERTURBATIONS IN SYNUCLEINOPATHY DISORDERS: INSIGHTS FROM PRE-CLINICAL TO HUMAN NEUROPATHOLOGY." Thesis, 2019.

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<div><p>Parkinson’s disease (PD) is a devastating neurodegenerative disorder that affects 10 million people worldwide and is characterized by pronounced motor symptoms. Dementia with Lewy Bodies (DLB) involves both cognitive and motor deficits and affects ~1 million people in the United States. To date there is no cure for PD or DLB, and current treatments address only a subset of the symptoms that define these diseases. PD and DLB are ‘synucleinopathies’, defined as disorders involving the accumulation in patients’ brains of Lewy bodies. Lewy bodies are cellular inclusions that consist largel

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