Thesis (Ph.D.)--Memorial University of Newfoundland, 2005. / Bibliography: leaves 370-404.

Thesis (Ph. D.)--University of California, San Diego and San Diego State University, 2003. / Vita. Includes bibliographical references.

No description available.

Thesis (Ph. D.)--University of California, San Diego, 1998. / Vita. Includes bibliographical references (leaves 165-174).

Thesis (M.A.)--Carleton University, 1993. / Also available in electronic format on the Internet.

München, Techn. Univ., Diss., 2005.

Compared with saline injected controls, rats with bilateral injections of kainic acid (KA) in the dorsal striatum showed temporary aphagia and adipsia, long-lasting body weight decreases, increased locomotor response to d-amphetamine, increased spontaneous nocturnal locomotor activity, increased resistance to extinction, impaired acquisition and retention of avoidance behavior and increased latencies to leave start boxes in various mazes. The KA injections resulted in loss of local neurons in the dorsal striatum, with no appreciable damage either to dopaminergic terminals or to extrinisic myelinated axons, thus supporting both the selective neurotoxic action of KA on neuronal perikarya and the proposed similarity of KA-induced striatal lesions with those found in the caudate-putamen of patients with Huntington's disease (HD). The present results demonstrate that KA striatal lesioned rats also show behavioral and pharmacological similarities with HD patients. In addition, they support the view that HD is characterized by a "subcortical dementia syndrome". A review of HD is also presented. / Medicine, Faculty of / Graduate

Bakgrund: Huntingtons sjukdom innebär ofta såväl motoriska, kognitiva som psykiatriska symtom. Chorea är ett tidigt motoriskt symtom och innebär överrörelser som kan förekomma i hela kroppen. Få studier beskriver den subjektiva upplevelsen av chorea.   Syfte: Att undersöka upplevelser av chorea hos fem personer med Huntingtons sjukdom samt att undersöka hur chorean påverkade deras förmåga till fysisk aktivitet.    Design och metod: Explorativ kvalitativ design. Semistrukturerade intervjuer med fem personer med Huntingtons sjukdom. En kvalitativ innehållsanalys användes för databearbetning.   Resultat: Utifrån studiens två frågeställningar identifierades tre teman: Att finna sin plats i tillvaron; Att finna sig i förändring; Att omvärdera rörelse. Dessa teman består av nio kategorier: Oro; Vardagliga hinder; En kropp som inte lyder; Förståelse från andra; Ett accepterande förhållningssätt; Omgivning; Att möta motgångar; Hitta rätt tillvägagångssätt; Att inse sina begränsningar.   Konklusion: För vissa av informanterna rådde en omedvetenhet kring chorea, medan den för andra låg till grund för stort lidande. De påtalade även hur chorea på olika sätt utgjorde en fysisk begränsning. Detta bör fungera som ett incitament för personcentrering i mötet med personer med Huntingtons sjukdom. / Background: Huntington's disease results in a combination of motor, cognitive and psychiatric symptoms. Chorea is an early symptom which entails involuntary movements that can affect various body parts. There are few studies addressing the subjective experiences of having chorea.   Purpose: To investigate experiences of having chorea in five people with Huntington's disease and to investigate how the chorea affected their ability to be physically active.   Design and method: Explorative qualitative design. Semi-structured interviews of five people with Huntington's disease. A qualitative content analysis was conducted. Results: Based on the two questions of the study, three themes were identified: Finding your place; Finding yourself in change; Revaluating movement. These themes consist of nine categories: Concern; Everyday obstacles; A disobedient body; Comprehension from others; An accepting approach; Surroundings; Facing setbacks; Finding the right strategies; Realizing your limitations.   Conclusion: Some of the informants were unaware of their chorea while in others it caused a great suffering. They also underlined how chorea in different ways could imply a physical limitation. This could function as an incentive for person-centered care when meeting people with Huntington's disease.

This essay is a study about how Carl Ulrik Sondén, a Swedish doctor during the 19th century, described and with his descriptions medicalized religious ecstasy in his thesis from 1842. The essay uses Vera Syrakvash theoretical model of medicalization to analyse how Sondén medicalized religious ecstasy, Chorea s:t Viti, to show how his thesis plays a part in the medicalization of Chorea s:t Viti. Sondéns medicalization, and how it is a part of the secularization that took place in Sweden during the 19th century is also discussed. To analyse this, Thorleif Pettersson’s work about secularization is used, and Sondéns thesis is applied to Petterssons theory of the three levels of secularization. The essay shows how Sondéns thesis fills all three of Syrakvash’s levels of medicalization and therefore fully medicalizes Chorea s:t Viti. This medicalization is then applied in to Pettersson’s theoretic model, and it fulfils the first level of secularization.

Huntington's disease (HD) is a devastating autosomal dominantly inherited neurological disorder caused by an abnormal expansion of CAG trinucleotide repeats in the gene coding for the Nterminal region of the huntingtin (Htt) protein, which leads to the formation of a polyglutamine stretch. The greater the CAG repeats, the earlier the onset of the disease. The polyglutamine stretch destabilizes the Htt protein leading to misfolding, abnormal processing, aggregation, and inclusion formation. Mutant Htt protein is believed to damage and kill neurons in the striatum by a mechanism involving increased oxidative and metabolic stress, and impaired adaptive cellular stress responses. A large number of abnormalities have been reported in HD, including transcription deficits, energy impairment, excitotoxicity, and lack of trophic support. Reduced trophic support contributes importantly to striatal degeneration in human HD. Specifically, brainderived neurotrophic factor (BDNF) expression is reduced in patients with HD. BDNF is also decreased in brain tissue from mice transgenic for mutant Htt. BDNF levels influences the onset and the severity of motor dysfunction in HD mice. In addition to BDNF, levels of the molecular chaperones heat shock proteins (Hsp40 and 70) decrease progressively in HD brain. Hsp70 is a highly stress-inducible member of a chaperone family of proteins that functions to prevent misfolding and aggregation of newly synthesized mutant proteins and stress-denatured proteins. Hsps appear to play a critical role in HD since expression of active heat shock factor HSF1, a transcription factor responsible for the induction of Hsps, markedly reduces polyglutamine aggregate formation in both cell and mouse models. Many efforts have been made to develop preventive treatments for HD because of the strong genetic link and a freely available genetic test to identify individuals at risk. At present, only symptomatic therapy is available and effective therapeutic approaches to slow the disease iv process have yet to be developed. Previous studies have shown that electroconvulsive shock (ECS) induces the production of growth factors including BDNF and the molecular chaperones HSP40 and HSP70. Because ECS can stimulate the production of neuroprotective proteins, we determined whether ECS treatment could slow the progressive nature of the disease process and provide a therapeutic benefit in a mouse model of HD. ECS or sham treatment was administered to male N171-82Q Htt mutant mice. End points measured included motor function, striatal and cortical pathology, and levels of neurotrophic factors, protein chaperones, and proteins involved in synaptic plasticity. ECS treatment delayed the onset of motor symptoms, reduced body weight loss and extended the survival of HD mice. Striatal neurodegeneration was attenuated and levels of neurotrophic factors, protein chaperones and mitochondria-stabilizing protein were elevated in striatal cells of ECS-treated compared to sham-treated HD mice. Our findings suggest that ECS can increase the resistance of neurons to mutant huntingtin resulting in improved functional outcome and extended survival. The potential of ECS as a treatment for HD patients merits further consideration.