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Parkinson's disease : behavioural effects following extracellular deposition of non-beta amyloid component and pharmacological interventionsElliott, Jennifer Jane January 2004 (has links)
No description available.
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Parkin protects against pathogenic mechanisms involved in cell deathDowman, Julia Rebecca Louise January 2005 (has links)
No description available.
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An investigation of the potential antiparkinsonian activity of combined dopamine D2 and serotonin 1A receptor agonistsJohnston, Louisa Clare January 2004 (has links)
No description available.
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In vitro and in vivo investigations of the potential neuroprotective effects of propargylamines and dopamine receptor agonistsWakselman, Shirley January 2007 (has links)
No description available.
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The role of group II and III metabotropc glutamate receptors in the basal ganglia and their potential as a treatment target for Parkinson's diseaseMessenger, Marcus John January 2003 (has links)
No description available.
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The neuronal nicotinic acetylcholine receptor as a potential symptomatic and neuroprotective target in Parkinson's diseaseVisanji, Naomi January 2004 (has links)
No description available.
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A behavioural and biochemical evaluation of the momoamine uptake inhibitor BTS 73 398 in the 6-hydroxydopamine lesioned rat model of Parkinson's diseaseLane, Emma Louise January 2004 (has links)
No description available.
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A behavioural and biochemical evaluation of α₂-adrenoceptor antagonist fipamezole in experimental models of Parkinson's diseaseCroft, Neil Ramsay January 2006 (has links)
No description available.
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Nicotinamide : neuroprotection and neurodegeneration mechanisms in Parkinson's diseaseCartwright, Lindsay Sarah January 2005 (has links)
No description available.
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An evaluation of the potentially neuroprotective properties of cannabinoids in a cell culture model of Parkinson's diseaseZeissler, Marie-Louise January 2013 (has links)
Parkinson's disease (PD) is a neurodegenerative disorder affecting the dopaminergic neurons within the substantia nigra pars compacta. There is evidence of increased cannabinoid receptor CB 1 signalling as well as exacerbated levels of its endogenous ligands anandamide (AEA) and 2- arachidonoyl glycerol (2-AG), also referred to as endocannabinoids in PD. Due to their ability to dampen synaptic transmission it is currently thought that these changes are part of an autoregulatory response aimed to counteract changes in synaptic transmission caused by the loss of dopamine. However, cannabinoids such as Δ9-tetrahydrocananbinol (Δ9-THC) also have neuroprotective properties and there is evidence for this in models of PD. The aim of this study was to identify whether changes in the endocannabinoid system may occur as a direct response to neurotoxicity and how increased endocannabinoid levels influence cell viability in a 1-methyl-4-phenylpyridium (MPP+) cell culture model of PD. Furthermore this study aimed to identify the mechanism through which Δ9THC is protective. This study discovered that cannabinoid receptor 1 (CB1) expression, as well as AEA metabolism, is increased as a direct response to neuronal injury induced by MPP+. Inhibition of AEA hydrolysis with URB597 was neuroprotective by reducing MPP+ induced oxidative stress in a CB1 receptor independent manner. In contrast, increased 2-AG levels potentiated MPP+ toxicity by elevating oxidative stress.
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