Neurodegeneration is a collective term for the progressive loss of structure, function or even death of neurons. This includes diseases like Alzheimer’s disease, frontotemporal dementia, Parkinson’s disease and motor neuron disease. Recent researches have shown great interest in the role of tau proteins, which have versatile functions including microtubule stabilization and signal relay in the central nervous system. Retina and optic nerve, being part of the central nervous system, can also be affected by similar processes. In neurodegenerative diseases visual disturbances including difficulties in reading and finding object, depth perception, perceiving structure from motion, color recognition and impairment in spatial contrast sensitivity have all been observed. Some of these defects may be attributed to changes at ocular level. The effect of tau mutation was investigated in this study utilizing a transgenic P301L tau mice model. Morphometric analysis has been utilized to quatify the neurodegenerative changes, including the thickness of inner nuclear layer(INL), density of retinal ganglion cells(RGCs) and size of RGCs. Retinal sections stained by hematoxylin and eosin(H&E) were analyzed. Comparisons were made between the P301L tau mice and the control mice in addition to comparisons between different age groups. The study found that there was a significant decrease of thickness of INL of P301L tau mice when compared with control mice. The effect was more pronounced in the peripheral area and the effect increased with age. Regarding density of RGCs, P301L tau mice showed a similar age-related decline as control mice. And regarding the size of RGCs, the RGCs from P301L tau mice increased in size with age and the RGCs from control mice decreased in size with age. / published_or_final_version / Anatomy / Master / Master of Medical Sciences

published_or_final_version / abstract / Pharmacology / Master / Master of Philosophy

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Includes bibliographical references (leaves 150-183). / xii, 183 leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Considers the tubule and capillary barriers from the point of view of anatomy, physiological function and possible factors which may cause the tubule barrier to be breached or influence substance exchange across the capillary wall. / Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Sciences, 1994

"August 2002" / Bibliography: leaves 141-176. / ix, 179 leaves : ill. (some col.) ; 30 cm / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Changes in maternal-foetal zinc homeostasis resulting in a foetal deficiency may be an important contributing factor in ethanol-realted teratogenicity. Ethanol induces expression of hepatic metallothionein, causing zinc transfer from the plasma to the liver. Rodent studies show that changes in plasma zinc correlate with a high incidence of abnormal fetuses in MT+/+ mice. Demonstrates a clear link between maternal hepatic MT induction, decreased foetal zinc supply, and teratogenicity, which has major implications for binge alcohol consumption in early pregnancy. The demonstration that zinc treatment is effective in preventing teratogenicity indicates potential treatment strategies. / Thesis (Ph.D.)--University of Adelaide, Dept. of Physiology, 2003

Alzheimer's Disease is one of the most fearsome diseases worldwide. The study of Alzheimer's Disease (AD) is broad and many have focused on investigating the various proteins involved in neurons. A popular hypothesis of the cellular mechanism of AD is the accumulation of beta-Amyloid. Kinesin is a large group of motor proteins, which plays an extensive role in mitosis and intracellular cargo transport, including that of the Amyloid Protein Precursor. In the present study we have performed fear conditioning behaviour tests on Kif5b conditional knockout (CKO) mouse. Kif5b CKO mouse shows an impair contextual memory compared to the wild type, but does not display an impaired auditory memory. Heterozygous Kif5b knock out mouse shows no significant difference to the wild type. The study has also generated Kif5b fragments and used them to pull-down proteins in mouse brain lysate. The study has identified Clathrin and alpha-Adaptin as binding partners of Kif5b in mouse neuronal cells. The binding domain of Kif5b for these proteins is between amino acid residue 891-935. Finally this study has made a number of recommendations for further study. / published_or_final_version / Biochemistry / Master / Master of Medical Sciences

Osteoarthritis (OA) affects nearly 27 million people alone and is the leading cause of chronic disability in the US. Current treatment methods target pain relief for OA via non-steroidal anti-inflammatory drugs (NSAIDs) since there are currently no clinically approved disease modifying osteoarthritis drugs (DMOADs) demonstrating efficacy. Despite multiple pre-clinical DMOAD experiments being conducted, the screening rate for drugs is severely limited by the lack of sensitivity of outcome measures and the time consuming process to achieve them. Our lab has previously developed and validated a technique to evaluate articular cartilage changes with micro-CT. The objective of this thesis was to examine two distinct treatment strategies for OA in a rat joint degeneration model using equilibrium partitioning of an ionic contrast agent based micro-CT (EPIC-µCT). We hypothesized that these novel therapeutics will assist in preventing degradation of cartilage after injury and will be measurable by EPIC-µCT. First, we characterized two of the commonly used rat joint degeneration models - monosodium iodoacetate injection (MIA) and transection of medial meniscus (MMT) in rats using EPIC-µCT. The MMT model was then used to test the effects of a matrix metalloproteinase inhibitor (MMPi) using EPIC-µCT to detect changes in articular cartilage. Finally, micronized dehydrated human amnion/chorion membrane (dHACM) was delivered intra-articularly in the MMT model and evaluated as a disease modifying OA drug.

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