Relevant bibliographies by topics / Neuropathology / Dissertations / Theses
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Dissertations / Theses on the topic 'Neuropathology'

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Published: 4 June 2021
Last updated: 27 July 2024

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1

Spillantini, Maria Grazia. "Molecular neuropathology of Alzheimer's disease." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282037.

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2

Huseby, Carol. "Molecular Neuropathology in Alzheimer's Disease." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1543314678552794.

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3

Betts, Joanne. "The molecular neuropathology of mitochondrial disease." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421187.

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4

Tofaris, George Kynacov. "Molecular neuropathology of Lewy body disorders." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619824.

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5

Davis, Brittany. "Modelling the neuropathology of Ehmt1 haploinsufficiency." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/73068/.

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EHMT1 is a gene that encodes an epigenetic regulator important for normal brain development. Disruption in EHMT1 is associated with a number of neurodevelopment and psychiatric conditions, like schizophrenia, Autism Spectrum Disorders, developmental delays and intellectual disabilities. In order to help elucidate the role of Ehmt1 in cortical development two models are examined: the differentiation of mouse pyramidal neurons lacking one copy of the gene and a forebrain-specific Ehmt1-haploinsufficient mouse model. Ehmt1+/- cells demonstrated changes in cell cycle, with significant differences in proliferation rates at embryonic stem cell and neural progenitor stages. Ehmt1+/- cells demonstrated significantly different transcriptional profiles in early and late stages of progenitor development, which suggested these cells, underwent precocious differentiation. In addition, the dysregulation of mRNA expression in a number of the Nrsf/Rest repressor complex members and Rest target genes was found; and Ehmt1+/- cells did not survive as post-mitotic neurons. The forebrain-specific Ehmt1-haploinsufficient mouse model, Ehmt1D6Cre/+, importantly showed normal Mendelian birth ratios, survival, motor coordination and function and no gross morphological changes in brain structure. However, these mice demonstrated differences in activity levels and anxiety-related measurements; deficits in sensorimotor gating and object recognition; and significant differences in a number of electrophysiological measurements, including abnormal event-related neural responses in the cortex and high frequency oscillatory patterns. Taken together, these data suggest that Ehmt1 expression is important for normal pyramidal development and Ehmt1 haploinsufficiency throughout development manifests cortical dysfunction, which leads to marked behavioural and electrophysiological abnormalities.
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6

Tabata, Rena Christina. "Neuropathology induced by sterol glucosides in mice." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/24178.

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Sterol glucosides are a family of compounds characterized by a carbohydrate unit bound to a tetracyclic carbon chain. They are found in high concentrations in cycad seeds which have been linked to the etiology of amyotrophic lateral scierosis-parkinsonism dementia complex (ALS-PDC). The neurotoxicities of the three main cycad sterol glucosides, campesterol β-D-glucoside, stigmasterol β-Dglucoside (SG), and β-sitosterol β-D-glucoside (BSSG) have been demonstrated previously in vitro. In the present study, we demonstrate that SC and BSSG exert neurotoxic effects in vivo. An outbred strain of mice was fed BSSG or SG (1000 μg daily) for a period of 15 wk and sacrificed immediately after or at 17 wk later. A battery of behavioural tests, including rotarod, wirehang, modified leg extension reflex test, treadmill, and open field were used to monitor behavioural disturbances. An array of histological measures was also conducted to assess the cellular impact of BSSG and SG. Behavioural test performance scores revealed that BSSG and SG impaired spinal reflexes and decreased overall movement. In addition to this, SC was found to impair motor coordination and strength. Also, ventral plane videography of performance on a treadmill and open field tests indicated that SG-exposed animals were more anxious and tended to drag and shuffle their limbs during forward movement. The cellular impact of dietary BSSG and SG exposures were also different. Animals exposed to each of the sterol glucosides showed an upregulation of activating transcription factor-3 and an increase in the incidence of phosphorylation of junser⁷³ in response to stress. However, BSSG-exposure induced neurodegeneration that primarily targeted large motor neurons whereas SC impacted a more diverse motor neuron population, including large and small motor neurons. Exposure to each of the sterol glucoside caused intense proliferation of astrocytes and microglia as well as a depletion of dopamine levels in the substantia nigra and striatum. Lastly, SG-exposure induced the pathological aggregation of either tau or transactivating DNA binding protein-43 in some animals. The insights gained from this study will be useful for elucidating the pathogenesis of ALS-PDC and related disorders.
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7

Nagy, Zsuzsanna. "Aspects of the neuropathology of Alzheimer's disease." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240537.

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8

Bleshoy, Hans. "Neuropathology and sensitivity in the keratoconic cornea." Thesis, City University London, 1990. http://openaccess.city.ac.uk/7670/.

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Corneal touch threshold (CTT) was investigated by aesthesiometry in patients with keratoconusq with and without contact lens wear. Using a matching control group it was established that CTT was significantly higher for the central corneal position in keratoconus. No difference inCTT was found in four peripheral corneal positions in keratoconic and normal corneas. Central CTT correlated inversely with central corneal curvature and central corneal thickness. Central corneal curvature was the most significant single factor to correlate with central CTT and indicates that CTT increases (sensitivity reduces) as the cornea steepens. Corneal surface irregularityq as measured by mire image distortion, correlated positively with central CTT as did corneal scarring. Central CTT did not show a relationship with duration of the disease nor the visibility of the corneal nerve fibres. Lid margin touch thresholds (LTT) were investigated for the central position on the lower and upper eyelid margins. No statistical differences were found between keratoconic and normal eyes nor between upper and lower eyelid margins. The magnitude of LTT was in the order of that established for the peripheral corneal CTT. Innervation of the human corneal stroma and epithelium was investigated by light and electron microscopy in the central and mid-peripheral positions. All nerve bundles were located in the anterior two thirds of the. corneas. In keratoconic corneas mid-peripheral stromal nerve bundles were disorganised and irregular taking up the shape of the adjacent collagen lamellae. Nerve bundles had a regular oval appearance in the control corneas. In both groups Schwann cell cytoplasm was sparse and of varying degree of electron density; axon varicosities were not uncommon and axon content with respect to organelles were similar. The axon density showed large variation in keratoconic: specimens and averaged more than threefold that of control specimens for stromal and epithelial nerves. The control corneas showed a greater proportion of large diameter stromal axons than in keratoconic corneas. This result was reversed for epithelial axons. The results are discussed with respect to the disease process and influence on tactile sensitivity.
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9

Pitts, Georgia Eloise Rollo. "Neuropathology and cognitive dysfunction after early hypoglycaemia." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10025822/.

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Hypoglycaemia is the most common metabolic problem in neonatal medicine, occurring during the first days of life and usually resolving within the same time frame. However, some neonates and infants experience severe and recurrent episodes of hypoglycaemia, the most common aetiologies being congenital hyperinsulinism (CHI) and ketotic hypoglycaemia (KH). Children with CHI are at risk of lasting brain injury, while children with KH are considered to be protected from adverse sequelae owing to the presence of ketone bodies during hypoglycaemia. This thesis investigated the neuropsychological and neuroimaging profiles of these two patient groups in neurologically normal school-aged children. Thirty-one patients with CHI and twenty-one patients with KH participated in the study alongside a cohort of healthy controls. A comprehensive battery of neuropsychological tests revealed specific impairments in attention and motor skills in both patient groups, with additional impairments observed in children with CHI. Automated and manual measurements of subcortical volumes, as well as whole brain analyses (voxel based morphometry and tract based spatial statistics) were conducted. Compared to controls, patients with CHI have reduced volume of subcortical structures, as well as extensive white matter volume loss (accompanied by decreased intracranial volume) and reduced white matter integrity across the entire brain. Patients with KH did not significantly differ from controls on any brain measures, but the only significant difference between patient groups was in thalamic and intracranial volumes. Integrity of subcortical structures and white matter was found to be predictive of scores in memory, motor skills and attention. This study is the first to show the extent of brain abnormality as a result of CHI in neurologically normal children. Furthermore, the finding that both patient groups share a similar cognitive profile refutes the notion that children with KH are protected from adverse sequelae. The implications of these findings are discussed.
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10

Henkes, Greta. "Neuropathologie primärer und sekundärer Mitochondriopathien im Rahmen entzündlicher Muskelerkrankungen." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-71313.

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Idiopathische Myositiden stellen die größte Gruppe der erworbenen Myopathien im Erwachsenenalter dar. Die Pathogenese dieser Erkrankungen ist sehr heterogen und nicht in allen Einzelheiten geklärt. Das Auftreten von mitochondrialen Veränderungen und mtDNADeletionen in idiopathischen Myositiden und deren pathophysiologische Bedeutung ist in der Literatur ein kontrovers diskutiertes Thema. Nach der Präsentation des bekannten Wissens über diese Erkrankungen wird in vorliegender Arbeit dieses Thema anhand lichtmikroskopischer Methoden unter Anwendung histologischer Spezialmethoden an Muskelbiopsien von 98 Patienten untersucht. Ziel der Arbeit ist es, mit verschiedenen histologischen Färbemethoden Hinweise für Mitochondrien-Alterationen und feinstrukturelle Charakteristika von primären Mitochondrialen Myopathien in idiopathischen Myositiden zu detektieren. Ein besonderer Schwerpunkt liegt auf der Anwendung einer neuen immunhistochemischen Methode unter Anwendung eines monoklonalen antimitochondrialen Antikörpers. Es wird der Fall eines Mädchens mit muskeldystrophischer Symptomatik dargestellt, dessen Muskelbiopsie im Alter von 7 Jahren die myohistologische Diagnose einer juvenilen Dermatomyositis und Hinweise auf eine mitochondriale Dysfunktion ergab. Die Ergebnisse der immunhistochemischen Methode korrelieren gut mit anderen bekannten mitochondrialen Färbungen, sind sensitiver und stellen möglicherweise eine gute Ergänzung zu den bekannten mitochondrialen Markern und Färbungen dar. Die beobachteten mitochondrialen Dysfunktionen sprechen für die gestörte Mitochondrienfunktion und eine früh im Krankheitsverlauf, am ehesten sekundäre, Beteiligung der Mitochondrien im Krankheitsprozess dieser primär nicht mitochondrialen Erkrankungen
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11

Querol, Vilaseca Marta. "Novel digital neuropathology methods applied to neurodegenerative diseases." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/671999.

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Cada tres segons alguna persona al món desenvolupa demència. Les malalties neurodegeneratives, amb la malaltia d’Alzheimer (MA), la malaltia de Parkinson i la demència frontotemporal com les formes més predominants, són un grup de desordres que afecten a milions de persones arreu del món. La neuropatologia de mostres post-mortem humanes encara és necessària per esclarir els mecanismes subjacents alterats en les malalties neurodegeneratives. En aquesta tesis hem combinat immunoassaigs clàssics, tècniques de microscopia òptica i eines computacionals automatitzades per investigar la neuroinflamació i l’acumulació anormal de proteïnes en les malalties neurodegeneratives. En particular, hem investigat alteracions dels astròcits i cèl·lules glials en la MA i altres taupaties. Hem aprofitat les tècniques de super-resolució emergents i hem aplicat i optimitzat l’array tomography (AT) combinant-lo amb stimulated emission depletion microscopy (STED) per estudiar les plaques d’amiloide humanes a nivell nanomètric. Finalment, hem aplicat mètodes digitals i l’AT per analitzar quantitativament els canvis cerebrals en un pacient tractat amb un inhibidor de BACE-1. Aquests tres treballs il·lustren com les eines digitals poden integrar-se amb els mètodes neuropatològics clàssics per la investigació de la MA i altres malalties neurodegeneratives.
Cada tres segundos alguien en el mundo desarrolla demencia. Las enfermedades neurodegenerativas, con la enfermedad de Alzheimer (EA), enfermedad de Parkinson y la demencia frontotemporal como las formas más prevalentes, son un grupo de desórdenes que afectan a millones de personas alrededor del mundo. La neuropatología de muestras post-mortem humanas aún es necesaria para esclarecer los mecanismos subyacentes alterados en las enfermedades neurodegenerativas. En esta tesis hemos combinado immunoensayos clásicos, técnicas de microscopía óptica y herramientas computacionales automatizadas para investigar la neuroinflamación y la acumulación anormal de proteínas en las enfermedades neurodegenerativas. En particular, hemos investigado alteraciones de los astrocitos y células gliales en la EA y otras taupatías. Hemos aprovechado las técnicas de super-resolución emergentes y hemos aplicado y optimizado el array tomography (AT) combinándolo con stimulated emission depletion microscopy (STED) para estudiar las placas de amiloide humanas a nivel nanométrico. Finalmente, hemos aplicado métodos digitales y AT para analizar cuantitativamente los cambios cerebrales en un paciente tratado con un inhibidor de BACE-1. Estos tres trabajos ilustran cómo las herramientas digitales pueden integrarse con los métodos neuropatológicos clásicos para la investigación de la EA y otras enfermedades neurodegenerativas.
Every 3 seconds someone in the world develops dementia. Neurodegenerative diseases (NDDs) with Alzheimer's disease (AD), Parkinson's disease (PD) and frontotemporal dementia (FTD) as the most prevalent forms are a group of disorders affecting millions of people worldwide. Neuropathology of post-mortem human samples is still needed to elucidate the underlying altered mechanisms of NDDs. In this thesis we combined classical immunoassays, light microscopy techniques and automated computational tools in order to investigate neuroinflammation and abnormal protein accumulation in NDDs. In particular, we investigated astrocytic and glial abnormalities in AD and other tauopathies. We took advantage of emerging super-resolution techniques and applied and optimized array tomography (AT) combined with stimulated emission depletion microscopy (STED) to study human amyloid plaques at a nanoscale level. Finally, we applied digital methods and AT to quantitative analyse the brain changes in a patient treated with a BACE-1 inhibitor. These three works illustrate how digital tools can be integrated with classical neuropathological methods in the investigation of AD and other NDDs.
Universitat Autònoma de Barcelona. Programa de Doctorat en Neurociències
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12

Moore, David Joseph. "Regional neuropathology and cognitive abilities in HIV infection /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3083453.

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13

Rahim, Rani Sadia. "Neuropathology in a Mouse Model of Zellweger Syndrome." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/367161.

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Zellweger syndrome (ZS) is a congenital peroxisome biogenesis disorder which has both features of neurodegeneration and defective neurodevelopment. ZS patients exhibit significant changes to brain morphology, prominent cell migration defects, and neurodegeneration; defects leading to severe motor and cognitive dysfunction. ZS is caused by mutation in PEX genes which encode proteins necessary for peroxisomes biogenesis. Loss of peroxisome biogenesis results in the deficiency of various peroxisomal metabolic functions, such as β-oxidation of very-long-chain-fatty acids, and biosynthesis of essential compounds that include bile acids, plasmalogens and docosahexaenoic acid. Despite these important findings, the molecular basis of ZS neuropathology is still unknown. For this study, which comprised a focus on the mechanisms/pathways involved in ZS neuropathology, mice with brain restricted deletion of the PEX13 gene were used as an animal model of ZS neuropathogenesis. PEX13 is required for the import of newly synthesized proteins into the peroxisome matrix. PEX13 brain mutant mice display characteristics typical of a milder ZS phenotype, including extended survival rate, and are therefore an appropriate model to stud neurodevelopmental changes at both early and postnatal developmental stages.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Natural Sciences
Science, Environment, Engineering and Technology
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14

Highley, J. Robin. "The asymmetry, interhemispheric connectivity, and gyral structure of the brain in schizophrenia : a post mortem study." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244561.

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15

Cotter, David Richard. "Abnormal brain development in schizophrenia : an investigation of potental mechanisms." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299927.

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16

Arotcarena, Marie-Laure. "Approches multifactorielles et translationnelles dans la modélisation des synucléinopathies : implications mécanistiques et thérapeutiques." Thesis, Bordeaux, 2019. http://www.theses.fr/2019BORD0164/document.

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Mon projet de thèse a été dédié à l’étude des synucléinopathies. Ces maladies neurodégénératives sont caractérisées par la présence d’inclusions intracytoplasmiques positives pour l’alpha-synucléine et contenues dans les neurones pour la maladie de Parkinson (i.e. les corps de Lewy) ou dans les oligodendrocytes pour l’atrophie multisystématisée (i.e. les inclusions cytoplasmiques oligodendrogliales). L’objectif de mon travail de thèse fut de proposer une approche multifactorielle et translationnelle en développant les aspects de modélisation, de mécanistiques et de thérapeutiques associées aux synucléinopathies. Nous nous sommes tout d’abord intéressés à disséquer les mécanismes sous-jacents à la neurodégénérescence induits par la protéine alpha-synucléine dans un modèle primate non-humain de la maladie de Parkinson. Nous avons ainsi souligné le rôle toxique de la protéine alpha-synucléine et mis en lumière de nouveaux processus cellulaires impliqués dans le phénomène de neurodégénérescence. Dans ce même modèle animal, nous avons étudié l’hypothèse d’une propagation de la pathologie induite par l’alpha-synucléine entre les systèmes nerveux centraux et périphériques. Nous avons ainsi pu démontrer l’existence d’une route bidirectionnelle de propagation et de neurodégénérescence de la protéine entre les deux systèmes nerveux, pouvant corroborer la présence de symptômes non moteurs précoces au cours de la pathologie. Enfin, nous nous sommes concentrés sur le rétablissement de la fonction autophagique comme cible thérapeutique commune aux synucléinopathies. Nous avons ainsi pu démontrer qu’une restauration de la machinerie de dégradation de la voie autophagie était suffisante pour rétablir les taux physiologiques de la protéine alpha-synucléine et induire une neuroprotection dans un modèle rongeur de la maladie de Parkinson et d’atrophie multi-systématisée. Ces travaux corroborent le rôle clé de la protéine alpha-synucléine dans l’étiologie des synucléinopathies et proposent de nouvelles stratégies thérapeutiques communes à toutes les synucléinopathies afin de rétablir les niveaux physiologiques cellulaires de la protéine et une neuroprotection au sein du système nerveux central
My thesis project was dedicated to the study of synucleinopathies. Synucleinopathies are neurodegenerative diseases characterized by the presence of alpha-synuclein positive intracytoplasmic inclusions which are present either in neurons for Parkinson’s disease (i.e. Lewy Bodies) or in oligodendrocytes for Multiple system atrophy (i.e. Glial Cytoplasmic Inclusions). The aim of my work was to establish a multifactorial and translational approach through modeling, mechanistic and therapeutic aspects associated with synucleinopathies. First, we focused on dissecting the underlying alpha-synuclein-mediated mechanisms of neurodegeneration using a non-human primate model of Parkinson’s disease. We confirmed the toxic role of alpha-synuclein in the pathology and highlighted unpredictable cellular processes involved in neurodegeneration. Using the same Parkinson’s disease model, we studied the hypothesis of a pathological propagation between the central and peripheric nervous systems in an attempt to decipher the initiation point and the direction of propagation of the associated pathology. We thus demonstrated a bidirectional route of propagation of alpha-synuclein between the CNS and the ENS and within the ENS. Finally, we focused on the restoration of the autophagic function as a potential common therapeutic target for all synucleinopathies. We demonstrated through a gene-based restoration of the autophagy, we efficiently reestablish alpha-synuclein physiological protein levels, while inducing neuroprotection in a Parkinson’s disease and Multiple system atrophy rodent models. Thus, this work corroborates the key role of alpha-synuclein in the etiology of synucleinopathy and offers new common therapeutic strategies for all synucleinopathies to decrease alpha-synuclein-induced toxicity into the central nervous system
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Schumann, Cynthia Mills. "Neuropathology of the amygdaloid complex in autism spectrum disorders /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2005. http://uclibs.org/PID/11984.

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18

Golder, Mark Stephen. "An investigation into the neuropathology of uncomplicated diverticular disease." Thesis, Queen Mary, University of London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497886.

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19

Liu, Jia [Verfasser], and Adrian [Akademischer Betreuer] Danek. "Neuropathology of Chorea-acanthocytosis / Jia Liu. Betreuer: Adrian Danek." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1098130839/34.

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Dickson, Jonathan Mark. "The neuropathology of Parkinson's disease : cognitive and motor consequences." Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340171.

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21

Van, Paesschen Wim. "Quantitative MRI and hippocampal neuropathology of temporal lobe epilepsy." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265249.

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22

McKavanagh, Rebecca. "The neuropathology of the social cognitive network in autism." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:e189c42c-7c87-470d-ab8f-c6b66a430f5e.

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Potential differences in developmental trajectory were investigated in autism at both the macro- and micro-scopic scale, using regional volumetric measurements from in-vivo scans and measurements of minicolumnar organisation of the cortex in post-mortem tissue. In addition, a study was carried out to investigate the sensitivity of measures of cortical diffusion to cortical architecture. Three key regions of interest were studied throughout this thesis, orbital frontal cortex (BA11), primary auditory cortex (BA41) and part of the inferior parietal lobe (BA40). Subjects with ASD showed increases in grey matter in left parietal cortex and decreases in left BA11 compared to controls. In addition, subjects with ASD showed increased grey matter volume with age in both BA41 and the inferior parietal lobe, whereas controls only showed a negative correlation between grey matter volume in BA41 and age. Wider minicolumns were found in ASD in all regions, suggesting pathology is not restricted to higher order association areas. Differences seemed more pronounced at younger ages suggesting an altered developmental trajectory in ASD. Such an increase in minicolumnar width arguably underlies the feature-based processing style seen in ASD. A pilot study using post-mortem DTI scans of MS brains revealed a relationship between measures of the directionality of diffusion and the width of axonal bundles in the cortex, an aspect of the minicolumnar arrangement. When extending this investigation to a set of ASD and control brains, evidence was found for different relationships between axon bundle width and measures of the directionality of diffusion in the cortex, suggesting that although differences in axon bundle width were not seen between groups, there may be differences in the composition of the axon bundles between ASD and control groups.
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Hahn, Caroline Nora. "Central neuropathology and clinicopathological correlates in equine grass sickness." Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/30244.

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Equine Grass Sickness has traditionally been known as a dysautonomia, principally affecting parasympathetic neurons in the enteric nervous system. Studies of central neuropathology have been cursory and conflicting, examining different and occasionally poorly defined central structures in variable numbers of cases and control animals. There was no agreement on the association or severity of clinical signs with the severity of central pathological changes. This study accurately describes the distribution of pathology in the brain of EGS cases. Chromatolytic neurons have a highly specific distribution which is unlike that reported in any other equine or human disease, but is apparently the same as in cats, dogs and hares with primary dysautonomias. The involvement of somatic efferent lower motor neurones suggests that EGS may be more correctly classified as a multisystem disease. This is a further incentive to search for a common aetiologic agent and may decrease the number of candidates under consideration. The nature of the pathological insult to the central neurons remains undetermined but, unlike peripheral neurons, central neurons do not appear to be dying; this study was unable to demonstrate evidence of apoptosis, axonal pathology or muscle fibre type grouping in muscles innervated by chromatolytic neurons. Phosphorylated neurofilament epitopes were labelled in the soma of somatic and visceral lower motor neurons indicating an axonal transport problem, but no consistent expression of the cell stress protein ubiquitin was evident. Smaller, CGRP-expressing dorsal root ganglia neurons are more likely to be chromatolytic than large neurons and may contribute to the observed rhinitis sicca. Electron microscopy revealed classical chromatolytic changes and no inclusion bodies. Electrodiagnostic examination of the blink reflex did not reveal a functional deficit of the facial nerve, and the characteristic ptosis of EGS cases was determined to be an expression of Horner's syndrome secondary to pathology to postganglionic sympathetic neurons. The response to the equine eyelid to alpha agonist eyedrops was defined and a significant difference found between control animals and EGS cases. The technique has been developed further as a useful non-invasive adjunct diagnostic test in Grass Sickness.
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Mudariki, Temba. "Diagnostic neuropathology of brain tumours using biophotonics and spectrometry." Thesis, University of Central Lancashire, 2016. http://clok.uclan.ac.uk/16665/.

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Classification of tumours such as gliomas, which are on a continuous spectrum of histology and malignancy into distinct categories is still a challenge using histopathology. There has been significant advances in the techniques used to fight cancer in the past two decades. A number of studies have looked at different approaches to improve the accuracy in diagnosis using histopathology. This study evaluated a number of techniques to compliment histopathology. One study looked at vibrational spectroscopy, Raman and attenuated total reflection-fourier transform infrared (ATR-FTIR) looking at brain tumour cell lines. This study investigated the potential application of vibrational spectroscopy in the segregation of different types of brain tumours using two tumour cell lines, U87MG, 1321N1 and a control, SVGP12. Another study looked at two approaches, elemental profiling of both tissue and serum using inductively coupled plasma-mass spectrometry. Trace elements increase or deficiency has been linked to cancer development and progression. The final study looked at the diagnostic application of Raman spectroscopy to distinguish between gliomas, meningiomas, medulloblastoma and several other brain tumours from histological normal brain tissue from brain tumour patients used as controls. The three cell lines U87MG, SVGP12 and 1321N1 were cultured and grown on calcium fluoride slides in triplicates. Spectra from each cell line was taken using both Raman and ATR-FTIR. The spectra was then analysed using multivariate statistics. In the elemental profiling study serum and tissue samples from 55 patients with brain tumours were collected and analysed using ICP-MS. The elemental data was then evaluated using multivariate statistics to investigate significant differences. In the analysis of human brain tumours tissue blocks of both tumour and histological normal brain that were formalin fixed and paraffin embedded (FFPE) were processed and mounted on low-E slides, dewaxed using Xylene, washed with alcohol and water before storage at room temperature until analysis. Raman and ATR-FTIR were able to separate U87MG, SVGP12 and 1321N1 with very high classification accuracy. All the brain tumour groups investigated showed a deficiency of Mg, Fe, Cu, and Zn concentrations against reported levels from healthy individuals in the literature. Raman spectroscopy coupled with multivariate statistics was able to distinguish between normal brain tissue and normal brain tumour tissue used as controls. Classification of gliomas based on the degree of malignancy was also apparent with very high classification accuracy. Spectral panels were developed that can be used as biomarkers in the diagnosis of brain tumours. Raman and Infrared spectroscopy are types of vibrational spectroscopy which have the potential to be used as diagnostic tools in neuropathology. They provide an intrinsic molecular fingerprint of the sample based on the interaction of light. The panels can accurately identify and classify specific brain tumours alleviating the need to use complex statistical models. Raman and ATR-FTIR were able to elucidate chemical information from the samples which was used to differentiate the three cell lines with very high classification accuracy. Diagnosis of a brain tumour is not always a straight forward process and the current techniques used lack the desired level of precision in diagnosis and cytoreductive surgery.
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Ordway, Gregory A. "Neuropathology of Central Norepinephrine in Psychiatric Disorders: Postmortem Research." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/8613.

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The postmortem human brain as a tool to study central nervous system disease Abnormalities in noradrenergic transmission are likely to play a role in behavioral expressions of a number of psychiatric and neurological disorders. The extent to which these abnormalities are pathognomonic, or even principal pathological features contributing to the illness, remains debatable. Interest in the potential for pathological abnormalities in central norepinephrine in central nervous system (CNS) disorders derives from the three general observations: (1) disruption of behaviors known to be heavily influenced by noradrenergic transmission that are associated with the illness; (2) demonstration that pharmacological manipulation of noradrenergic transmission can precipitate, modify, or alleviate symptoms of these disorders; and (3) certain CNS disorders are characterized pathologically by a loss of noradrenergic neurons in the brain. Research on the pathology of central noradrenergic systems in CNS diseases and their relationship to behavioral alterations utilizes a variety of techniques, most of which are technically indirect, given that we currently are unable to directly measure noradrenergic neuron activity, noradrenergic receptor signaling, or norepinephrine release in vivo in living humans. In vivo imaging methods now permit investigators to measure occupancy of certain receptors, but application of these methods specifically to noradrenergic proteins, such as receptors, enzymes or transporters, has been limited. One method to study the role of norepinephrine in the CNS disorders is to utilize postmortem brain tissue from subjects with a given psychiatric or neurological condition.
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Lanoue, Amelie Cecile. "Neuropathology in the dorsolateral prefrontal cortex in Parkinson's disease." Thesis, Boston University, 2013. https://hdl.handle.net/2144/11112.

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Thesis (Ph.D.)--Boston University
Degeneration of dopaminergic neurons in the substantia nigra pars compacta is the hallmark neuropathological feature of Parkinson's disease (PD). Multiple lines of evidence from anatomical and imaging studies indicate that cell loss or cell dysfunction also occur in other brain regions. The dorsolateral prefrontal cortex (DLPFC) is a region of interest because it could be implicated in both cognitive and motor symptoms of PD. However, studies in this brain region are limited and the extent of pathology is unclear. Work in this thesis was aimed at identifying possible neuropathology in post-mortem PD tissue from Brodmann area 9 (BA9), a region of the DLPFC. In the first study, using design-based stereology and radioisotopic in situ hybridization histochemistry (ISHH), we found that expression of two mitochondrial genes, NDUFS1 and COX1, was not altered and that no global loss of neurons occurs in BA9 in PD. In a second study, using ISHH and gene expression microarray analysis (One-Color Agilent 60-mer Whole Human Genome Microarray), we found decreased gene expression of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD67) in BA9 in PD, an effect that was not paralleled by a decrease in the numbers of GAD67 mRNA-expressing neurons. In a third study, using ISHH, we found that gene expression of the calcium-binding protein parvalbumin, which is selectively expressed in a subset of cortical GABAergic interneurons, is decreased in BA9 in PD. However, we found no loss of immunolabeled parvalbumin-positive neurons in BA9 in PD. In summary, the results indicate that expression of two key markers of GABAergic activity, GAD67 and parvalbumin, is depressed in BA9 in PD and that these effects are not due to a loss of neurons. This suggests that GABAergic neurotransmission is deficient in the DLPFC in PD and we propose that treatments aimed at restoring GABAergic inhibition in BA9 would have therapeutic efficacy in the symptomatic treatment of PD.
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Bristow, Greg. "Investigations of the potential schizophrenia susceptibility gene Kinase Interacting with Stathmin (KIS)." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:432fc195-815c-4bc6-945f-c2b59aa3538c.

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Single nucleotide polymorphisms (SNPs) within the gene encoding the serine threonine kinase KIS (Kinase Interacting with Stathmin, also known as UHMK1) have recently been associated with schizophrenia. However, little is known about the neurobiology of KIS or the mechanisms through which disease-associated SNPs may increase susceptibility to schizophrenia. The studies presented in this thesis focus on the distribution of KIS and its mRNA, address the mechanisms through which KIS may confer susceptibility to schizophrenia, and investigate the physiological role(s) of KIS in the brain using two lines of knockout mice. The regional and cellular distribution of KIS was characterised in the brains of adult humans and mice, and through mouse neurodevelopment. The results of these experiments demonstrated that KIS is widely expressed in neurons in the brain regions examined in both species, its encoded protein is localised to the nucleus and cytoplasm, and KIS expression in mouse brain peaked around seven days after birth. KIS protein and mRNA was quantified in two large human post-mortem brain series to determine if KIS expression is altered in schizophrenia or bipolar disorder, or in relation to the leading schizophrenia-associated SNP (rs7513662). Using tissue from the superior temporal gyrus, dorsolateral prefrontal cortex, anterior cingulate cortex, and cerebellum, no difference in KIS expression (either mRNA or protein) was found between diagnostic or genotype groups in any brain region examined. Furthermore, KIS expression in lymphoblast cell lines also did not differ between diagnostic or genotype groups. Lastly, KIS expression (mRNA and protein) was characterised in two separate lines of KIS knockout mice. The results were complex, and left uncertainty as to whether either line was a true knockout or, conversely, whether any of the available KIS antibodies were specific. Nevertheless, the absence of KIS mRNA was robustly confirmed in one knockout mouse line, and brains from this line were subsequently used in three experiments. First, investigation of the quantity and phosphorylation state of the KIS targets stathmin and p27kip1; no differences were found compared to wildtype mice. Second, quantification of mRNA expression of several other genes of interest with regard to schizophrenia; altered expression of GAP43, VGlut1, MAP2, spinophilin, and stathmin was found. Finally, stereological measurements were performed, and while no differences in whole or regional brain volumes in KIS knockout mice were found, there was a relative reduction in hippocampal volume. The results of these studies do not support the hypothesis that altered expression is the mechanism by which genetic variation of KIS may increase susceptibility to schizophrenia, nor that KIS expression is altered in the disease. However, the knockout mice data suggest that KIS may play a role in synaptic plasticity and function, providing novel information on the potential neurobiological roles of KIS.
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Mochida, Rumi. "Survey of Neuropathology in Obese and Diabetic ZDSD Rat Brain." Available to subscribers only, 2009. http://proquest.umi.com/pqdweb?did=1966536741&sid=1&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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29

Thompson, Lachlan H. (Lachlan Heath) 1974. "Receptor and neurochemical changes in models of Alzheimer-like neuropathology." Monash University, Dept. of Pharmacology, 2002. http://arrow.monash.edu.au/hdl/1959.1/7931.

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30

Thomas, Alan J. "A study of vascular neuropathology in late-life major depression." Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394641.

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31

West, Daniel Alexander. "The development of experimental models for NMR studies of neuropathology." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406284.

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32

Genoud, Sian. "The role of biometals in the neuropathology of Parkinson’s disease." Thesis, The University of Sydney, 2020. https://hdl.handle.net/2123/22449.

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Parkinson’s disease (PD) is a neurodegenerative disorder characterised by the progressive loss of dopaminergic neurons, particularly in the ventral substantia nigra. Growing evidence implicates biometal dyshomeostasis and subsequent metal-catalysed neurotoxicity in vulnerable regions of the PD brain. Through meta-analysis, I confirm previously reported reductions in Cu, and elevations in Fe specifically in the substantia nigra of the PD brain, which are not reflected by similar changes in biofluid tissues. These changes are further restricted to the soluble fraction of nigral tissue – suggesting that soluble metalloproteins may be affected by these biometal perturbations. Superoxide dismutase 1 (SOD1) is one soluble Cu-associated protein that has recently demonstrated impaired antioxidant capacity and altered structural conformation in the PD brain and may present with an altered metalation profile in PD brain. I describe, for the first time, the cutting-edge technique of simultaneous synchrotron X-ray fluorescence microscopy and ptychography performed in situ to identify and directly image Lewy bodies, SOD1 aggregates and neuromelanin in human PD substantia nigra. The resulting nanoscale imaging demonstrate that SOD1 and Lewy body proteinopathies share similar structures. SOD1 and Lewy aggregates also exhibited similar elemental compositions, suggesting that these distinct proteinaceous aggregates may share an overlapping protein misfolding pathway. Further, I demonstrate an altered Cu:Zn ratio in SOD1 aggregates, supporting the hypothesis that altered metalation of SOD1 results in aggregate formation in this Cu-deficient region. These data suggest that Cu dyshomeostasis in the vulnerable substantia nigra of the PD brain may be attenuated by biometal modulation therapies, and that SOD1 may present as a viable therapeutic target for PD.
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33

Milosevic, Javorina, Sigrid C. Schwarz, Vera Ogunlade, Anne K. Meyer, Alexander Storch, and Johannes Schwarz. "Emerging role of LRRK2 in human neural progenitor cell cycle progression, survival and differentiation." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-184308.

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Despite a comprehensive mapping of the Parkinson's disease (PD)-related mRNA and protein leucine-rich repeat kinase 2 (LRRK2) in the mammalian brain, its physiological function in healthy individuals remains enigmatic. Based on its structural features and kinase properties, LRRK2 may interact with other proteins involved in signalling pathways. Here, we show a widespread LRRK2 mRNA and/or protein expression in expanded or differentiated human mesencephalic neural progenitor cells (hmNPCs) and in post-mortem substantia nigra PD patients. Using small interfering RNA duplexes targeting LRRK2 in hmNPCs following their differentiation into glia and neurons, we observed a reduced number of dopaminergic neurons due to apoptosis in LRRK2 knockdown samples. LRRK2-deficient hmNPCs exhibited elevated cell cycle- and cell death-related markers. In conclusion, a reduction of LRRK2 expression in hmNPCs severely impaired dopaminergic differentiation and/or survival of dopaminergic neurons most likely via preserving or reactivating the cell cycle.
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34

Cullen, Thomas. "The neuropathology of the prefrontal cortex and mediodorsal thalamus in schizophrenia." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427875.

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35

Kam, Korey. "On neuronal hyperexcitability in a mouse model of B-amyloid neuropathology." Thesis, New York University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10192483.

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At present, Alzheimer’s disease (AD) is an incurable neurodegenerative dementia. It has been suggested that neuronal hyperexcitability contributes to AD, so we asked how hyperexcitability develops in a common mouse model of β-amyloid neuropathology - Tg2576 mice. These mice overexpress the Swedish familial mutation of human-amyloid precursor protein (hAPP). Using video-EEG recordings, we found synchronized, large amplitude potentials resembling interictal spikes (IIS) in epilepsy at just 5 weeks of age, long before memory impairments or β-amyloid deposition. Seizures were uncommon, but occurred later in life, suggesting that IIS are possibly the earliest form of hyperexcitability. Interestingly, IIS primarily occurred during rapid-eye movement (REM) sleep prior to the deposition of β-amyloid. The interests are twofold. First, REM sleep is associated with increased cholinergic tone. Second, cholinergic impairments as well as degeneration are implicated in AD. Although previous studies suggest that cholinergic antagonists would worsen pathophysiology, the muscarinic antagonist atropine but not nicotinic antagonists reduced IIS frequency in animals prior to β-amyloid deposition. In addition, we found a role for brain hyperexcitability during general anesthesia. Epileptiform discharges are both hyperexcitable and hypersynchronous across age in Tg2576 mice and wildtypes. Our findings identify that epileptiform discharges elicited during anesthesia mediates cognitive dysfunction and is exacerbated in Aβ depositing brains. Taken together with results from prior studies, the data suggest that surprising and multiple mechanisms contribute to neural hyperexcitability. The data also suggest that IIS during sleep may be a biomarker for early detection of AD.

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36

Manner, Cathyryne Kapiolani. "The consequences of CAT2 arginine transporter ablation in cancer and neuropathology /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3091320.

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37

Heath, P. D. "Cortical somatosensory evoked potentials in parkinsonism." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233645.

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38

Jamieson, Elizabeth Ann. "Distribution and regulation of proteins related to neuronal degeneration." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284705.

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39

Paine, Simon Marcus Liddell. "Conditional proteasome gene deletion : molecular neuropathology and the pathogenesis of Parkinson’s disease." Thesis, University of Nottingham, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.580175.

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Parkinson's disease is an archetypal sporadic neurodegenerative disease: it is age-related and results in region-specific neurodegeneration with intracellular inclusions in many of the remaining neurones. Despite three decades of intense study, disease modifying therapies remain beyond the horizon, reflecting our understanding of the pathological process and the intrinsic challenges that the degenerative diseases of the brain present. Dysfunction in a number of cellular systems has been implicated in the development of Parkinson's disease. Protein homeostasis in terminally differentiated neurones is of particular import; unlike most other cells, they have no progeny with which to gift troublesome proteins. The ubiquitin proteasome system is the cell's main regulated proteolytic pathway and observations from neuropathological, genetic and animal studies have consistently found evidence that it may be aetiologically important in Parkinson's disease. Using a Cre/loxP approach Psmc1, which encodes an essential component of the 26S proteasome, was spatially deleted in catecholaminergic neurones in mice. This model reproduced both the region-specific neuronal loss and intraneuronal inclusions that define the sporadic human disease. In this work, I describe the further characterization of this unique model and use it to test hypotheses regarding the nature of the process that leads to these neuropathological features. Specifically, I show that in response to Psmcl deletion genes encoding sub- units of the 26S proteasome are up-regulated; using whole-genome microarray analysis I identify differentially expressed transcripts in micro dissected brain regions and then use the model to demonstrate that α-synuclein is not essential for the neurodegeneration or inclusion formation that result from Psmc1 deletion. These data underline the relevance of this model to the study of the pathogenesis of Parkinson's disease and identify avenues for further investigation.
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40

Brown, Nolan J. "Localization of hemoglobin in MS cortex and its relevance to MS neuropathology." Kent State University Honors College / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ksuhonors1399400834.

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41

Turner, Gareth David Huw. "An immunohistochemical study of the pathology of malaria." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318458.

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42

Pearce, Janice. "The trafficking of apolipoprotein E and its effect upon tau phosphorylation." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325158.

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43

Österman, Hanna. "Olfactory performance and neuropathology in the Tg6799 strain of Alzheimer’s disease model mice." Thesis, Linköpings universitet, Institutionen för fysik, kemi och biologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-56816.

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The present study evaluated olfactory and cognitive abilities of the Tg6799 (also called 5xFAD) strain of Alzheimer’s disease (AD) model mice of two different age groups (2-3 and 8-10 months of age), and one group of healthy control mice (9-10 months). Employment of an operant conditioning paradigm using an automated olfactometer, an olfactory habituation/dishabituation test and a spatial learning test with non olfactory cues resulted in data showing that the 5xFAD mice develop olfactory impairments already at 2-3 months of age. The impairments consisted in a robust impairment in olfactory sensitivity, decreased responsiveness to novel odors and an inability to discriminate between enantiomeric odor molecules in the 5xFAD mice compared to control mice. Spatial learning deficits were also detected at this age, suggesting that cognitive functions were also affected. No differences in magnitude of the olfactory or spatial learning impairments could be detected between the age groups of model mice tested. Histological examination of development and presence of amyloid β (Aβ) plaques in the brains showed that plaques develop mainly between the ages of 3 and 8 months. This indicates that soluble Aβ rather than the formation of plaques might be responsible for the olfactory impairment and spatial learning impairments found. By 10 months of age plaque load of the 5xFAD mice was massive. The results of the present study clearly show that the 5xFAD strain might be suitable for research on human AD with regard to the early onset of olfactory impairments.
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44

Bayram-Weston, Zubeyde. "Longitudinal characterisation of neuropathology in transgenic and knock-in Huntington's disease mouse lines." Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/14609/.

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The work presented in this thesis consists of 4 manuscripts, focussed on characterising the distribution of mutant huntingtin protein in transgenic and knock-in mouse models of Huntington’s disease. The mouse lines showed a different expression level of mutant huntingtin across the different time points. In the R6/1 mice, the inclusions were present and widespread from 3.5 weeks of age. In the YAC128 mice, inclusions were not present until 15 months of age, but then developed rapidly throughout the brain. In the HdhQ92 and HdhQ150 mice, intra nuclear inclusions (NIIs) were apparent at 10 and 5 months of age, respectively, and spread anterior to posterior and ventral-dorsal directions. In this thesis, the study has shown no increase in GFAP immunoactivity in the striatum of each mice line. However we detected a small increase in GFAP immunoactivity in the cortex of transgenic mouse models. With electron microscopy, we observed ultrastructural pathology with vacuolization, uneven cell membrane and degenerated mitochondria in these mouse lines along side with the presence of inclusions. Each mouse line showed different levels of degeneration such as YAC128 and HdhQ92 mice exhibited apoptitic neurons, whereas HdhQ150 mice has shown signs of necrosis. The results demonstrate that each of the mouse lines studied has a unique pattern of development of neuropathology. Inclusion formations may not be pathogenic per se, but may be representative of the dysfunctional neuronal populations that underpin the functional disturbances found in each of these mouse lines. Electron microscopy shows different cell death morphology in these mouse lines.
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45

Purushothuman, Sivaraman. "The neuropathology of age-related degenerations: Cause and protection assessed in rodent models." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/11488.

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Neurodegenerative diseases such as age-related dementia (ARD; Alzheimer’s disease) and Parkinson’s disease are a consequence of age-related pathological changes in the central nervous system (CNS). There is a growing body of evidence that ARD is a vascular dementia, caused by micro-haemorrhages from cerebral capillaries. Oxidative stress and mitochondrial dysfunction caused by haemorrhage are then thought to cause the features of the demented brain which Alzheimer described (senile plaques, neurofibrillary tangles and inflammation) and the cell death, synaptic loss and the formation of abnormal proteins described since. In this project, I have used rodent models to test the causal relationship between cerebral haemorrhage and the formation of plaques and neurofibrillary tangles, and to test the potential of two neuroprotectants, dietary saffron and photobiomodulation (with near infrared light), to mitigate neuropathological changes in rodent models of cerebral degenerations. Further, a detailed analysis is presented of the effect of haemorrhage on tissue flanking a haemorrhage site; the analysis suggests the upregulation of protective mechanisms in this flanking tissue. It is possible that the neuroprotectants, saffron and photobiomodulation act by upregulating these endogenous protective mechanisms. Overall, the results provide support for the microvascular hypothesis of age-related dementia, and provide evidence that preconditioning brain tissue can mitigate the pathology associated with dementia, and give insight into underlying mechanisms.
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46

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 studies have suggested a role of neuroinflammation in the pathophysiology of L-DOPA-induced dyskinesia, showing that the chronic administration of L-DOPA exacerbates the pre-existing inflammatory environment which may contribute to the altered neurotransmission associated with dyskinesia. The main component of LB is α-synuclein in its fibrillar form, but recent evidence suggests that the most toxic strain of α-synuclein are small soluble α-synuclein oligomers. Moreover, structure-based features have been suggested to mediate the toxicity of highly toxic α-synuclein oligomers. While the central role of α-synuclein in PD is generally acknowledged, the mechanisms underlying the neurotoxicity of α-synuclein oligomers, and their pathological interaction with Central Nervous System (CNS) immune-cells within PD-related neuroinflammation is still largely unknown. In the first part of our project (part I), we tested the neurotoxicity in vivo of α-synuclein oligomers previously recognized to hold a structure that confers high toxicity in in vitro models, and we focused on the inflammatory response elicited by these toxic α-synuclein oligomers and on their interaction with microglial cells. Thereafter, in the second part of our project (part II) we addressed the role of neuroinflammation in L-DOPA-induced dyskinesia. L-DOPA therapy is the gold standard for PD, however long-term administration leads to the onset of L-DOPA-induced abnormal involuntary movements named dyskinesia. Recent studies have suggested that neuroinflammatory processes play a pivotal role in dyskinesia, and the proinflammatory cytokine Tumor Necrosis Factor (TNF)-α may be a key player being also involved in synaptic strength mechanisms and in angiogenesis, another important component in the neuropathology of L-DOPA-induced dyskinesia (LID). Here, we tested whether the immunomodulatory drugs thalidomide (TLD) and its more potent derivative 3,6-dithiothalidomide (DTT), which specifically inhibit the synthesis of TNF-α, were effective in alleviating the L-DOPA-induced dyskinetic outcome in a rat model of PD. Oligomer infusion caused a gradual development of PD neuropathology. Microgliosis and increased levels of inflammatory cytokines were measured one month after oligomers-infusion, without any evidence of neurodegeneration and behavioral deficits. Notably, three months after the injection, rats displayed motor impairment, associated with 40% loss of dopaminergic neurons in the oligomers-treated SN, reaching a 50% cell loss after five months. Dopamine levels were significantly reduced by 40% in the striatum homolateral to α-synuclein infusion. An intense inflammatory response with reactive microglia and high levels of TNF-α immunoreactivity were detected in SNpc. Large deposits of p-αsyn were found within microglial cells three and five months post-infusion. TLD and DTT significantly reduced the severity of AIMs while not affecting the contralateral turning. Both drugs inhibited the L-DOPA-induced microgliosis and excessive TNF-α in the Str and SNpr, while restoring control levels of the anti-inflammatory cytokine interleukine (IL)-10 at striatal level. DTT inhibited L-DOPA-induced angiogenesis in SNpr and Str. GLUR1 analysis revealed that L-DOPA-induced an overexpression of this GLUR1 subunit in the Str, that was restored to normal levels by DTT.
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47

Milosevic, Javorina, Sigrid C. Schwarz, Vera Ogunlade, Anne K. Meyer, Alexander Storch, and Johannes Schwarz. "Emerging role of LRRK2 in human neural progenitor cell cycle progression, survival and differentiation." Biomed Central, 2009. https://tud.qucosa.de/id/qucosa%3A28998.

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Despite a comprehensive mapping of the Parkinson's disease (PD)-related mRNA and protein leucine-rich repeat kinase 2 (LRRK2) in the mammalian brain, its physiological function in healthy individuals remains enigmatic. Based on its structural features and kinase properties, LRRK2 may interact with other proteins involved in signalling pathways. Here, we show a widespread LRRK2 mRNA and/or protein expression in expanded or differentiated human mesencephalic neural progenitor cells (hmNPCs) and in post-mortem substantia nigra PD patients. Using small interfering RNA duplexes targeting LRRK2 in hmNPCs following their differentiation into glia and neurons, we observed a reduced number of dopaminergic neurons due to apoptosis in LRRK2 knockdown samples. LRRK2-deficient hmNPCs exhibited elevated cell cycle- and cell death-related markers. In conclusion, a reduction of LRRK2 expression in hmNPCs severely impaired dopaminergic differentiation and/or survival of dopaminergic neurons most likely via preserving or reactivating the cell cycle.
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48

TAKAHASHI, AKIRA, YOSHIO HASHIZUME, and NOBUKO UJIHIRA. "A CLINICO-NEUROPATHOLOGICAL STUDY ON BRAIN DEATH." Nagoya University School of Medicine, 1993. http://hdl.handle.net/2237/15930.

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49

Sloan, Maximilian. "The behavioural and molecular characterisation of a novel LRRK2 BAC transgenic rat model of Parkinson's disease." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:c2058b71-df43-47cd-a794-13184bacf313.

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50

IRITANI, SHUJI. "What Happens in the Brain of Schizophrenia Patients?: An Investigation from the Viewpoint of Neuropathology." Nagoya University School of Medicine, 2013. http://hdl.handle.net/2237/17597.

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