Research Topics
Genomes and GenesSpecies | Claire E ShepherdSummaryAffiliation: University of New South Wales Country: Australia Publications
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Detail Information
Publications
Histocompatibility antigens, aspirin use and cognitive performance in non-demented elderly subjectsC E Shepherd
Centre for Education and Research on Ageing, The University of Sydney, Sydney, Australia
J Neuroimmunol 148:178-82. 2004..018), respectively. HLA-DRB1*05 had a negative impact on the Boston naming test (p=0.002). Our results suggest that aspirin use and inflammatory genotype may influence cognition in non-demented subjects...- Relationship between neuronal loss and 'inflammatory plaques' in early onset Alzheimer's diseaseC E Shepherd
Prince of Wales Medical Research Institute, Sydney, NSW, Australia
Neuropathol Appl Neurobiol 33:328-33. 2007..7 +/- 0.8). These data demonstrate that EOAD cases exhibit greater neuronal cell loss in the superior frontal cortex than sporadic AD and that this effect is independent of the presence or absence of inflammatory plaque pathology... - Inflammatory S100A9 and S100A12 proteins in Alzheimer's diseaseC E Shepherd
Prince of Wales Medical Research Institute, Barker Street, Randwick, Sydney 2031, Australia
Neurobiol Aging 27:1554-63. 2006..This study indicates a potential role for pro-inflammatory S100A9 and S100A12 in pathogenesis caused by inflammation and protein complex formation in AD... - Novel 'inflammatory plaque' pathology in presenilin-1 Alzheimer's diseaseC E Shepherd
Prince of Wales Medical Research Institute, Barker Street, Randwick, Sydney 2031, Australia
Neuropathol Appl Neurobiol 31:503-11. 2005..Identification of this substance may be important for the development of future therapeutic strategies... - Positional effects of presenilin-1 mutations on tau phosphorylation in cortical plaquesClaire E Shepherd
Prince of Wales Medical Research Institute, Randwick, 2031 Sydney, Australia
Neurobiol Dis 15:115-9. 2004..These findings suggest that PS-1 mutations increase tau deposition while mutation-specific cellular responses determine phosphorylation events and may influence cell death mechanisms... - Pick bodies in a family with presenilin-1 Alzheimer's diseaseGlenda M Halliday
Prince of Wales Medical Research Institute and the University of New South Wales, Barker Street, Randwick, Sydney, 2031 NSW, Australia
Ann Neurol 57:139-43. 2005..M146L mutant PS-1 may predispose to both Pick's disease and AD by affecting multiple intracellular pathways involving tau phosphorylation and amyloid metabolism... 
Monocyte chemoattractant protein-1 plays a dominant role in the chronic inflammation observed in Alzheimer's diseaseAnna Sokolova
Prince of Wales Medical Research Institute, Barker Street, Randwick, Sydney, Australia
Brain Pathol 19:392-8. 2009..Our data support previous work on significant increases in IL-6 and IL-8 in AD but indicate that MCP-1 may play a more dominant role in chronic inflammation in AD...- Alpha-synuclein redistributes to neuromelanin lipid in the substantia nigra early in Parkinson's diseaseGlenda M Halliday
Prince of Wales Medical Research Institute and the University of New South Wales, Sydney, Australia
Brain 128:2654-64. 2005..Overall, these changes may trigger a cascade of events leading to larger intracellular aggregates of alpha-synuclein and the dispersement of protective pigment to precipitate cell death in Parkinson's disease... - Mutations in the tau gene that cause an increase in three repeat tau and frontotemporal dementiaPrudence M Stanford
Garvan Institute of Medical Research, Sydney, NSW, Australia
Brain 126:814-26. 2003..The increase in tau proteolysis was associated with increased evidence of apoptosis. This mechanism of neurodegeneration may be more applicable to the majority of FTD cases, which do not accumulate insoluble tau deposits... - Severity of gliosis in Pick's disease and frontotemporal lobar degeneration: tau-positive glia differentiate these disordersEmma Schofield
Prince of Wales Medical Research Institute and University of New South Wales, Sydney, Australia
Brain 126:827-40. 2003..In frontotemporal lobar degeneration, a significant proportion of the activated white matter microglia were tau-2-immunoreactive, suggesting direct involvement in axonal degeneration, possibly via immune processes... - Insoluble alpha-synuclein in Alzheimer's disease without Lewy body formationMelissa Broe
Prince of Wales Medical Research Institute, Sydney, 2031 Australia
Neurotox Res 7:69-76. 2005..This lipid-association of alpha-synuclein in mature AD plaques links this protein with other lipid changes thought to be important in disease pathogenesis... - Effect of anti-inflammatory medications on neuropathological findings in Alzheimer diseaseG M Halliday
Prince of Wales Medical Research Institute, High Street, Randwick, NSW 2031, Australia
Arch Neurol 57:831-6. 2000..There has been no analysis of brain tissue from longitudinally observed, cognitively tested patients to validate whether anti-inflammatory medications protect against the pathological changes of Alzheimer disease... 
C9ORF72 repeat expansion in clinical and neuropathologic frontotemporal dementia cohortsCarol Dobson-Stone
Neuroscience Research Australia, Sydney, Australia
Neurology 79:995-1001. 2012....- Neurofilament-immunoreactive neurons in Alzheimer's disease and dementia with Lewy bodiesClaire E Shepherd
Prince of Wales Medical Research Institute, University of New South Wales, Barker Street, Randwick, Sydney 2031, Australia
Neurobiol Dis 9:249-57. 2002..This increased number of cortical NF-containing neurons reveal novel widespread cortical changes, beyond those explained by Lewy body formation, that are specific for DLB... - Relationship between DNA fragmentation, morphological changes and neuronal loss in Alzheimer's disease and dementia with Lewy bodiesM Broe
Prince of Wales Medical Research Institute, Randwick, NSW, Australia
Acta Neuropathol 101:616-24. 2001..02). Abnormal nuclei were not associated with plaque or tangle pathology. Our results suggest that nuclear abnormalities appear restricted to AD cases with substantial tau deposition and are related to the degree of neuronal degeneration... - Neurofilament-immunoreactive neurons are not selectively vulnerable in Alzheimer's diseaseC E Shepherd
Prince of Wales Medical Research Institute, High Street, Randwick, 2031, Australia
Neurobiol Dis 8:136-46. 2001..Our results challenge the theory that neurons containing 200 kDa neurofilament are selectively vulnerable in Alzheimer's disease... - Intraneuronal advanced glycation endproducts in presenilin-1 Alzheimer's diseaseGerald Munch
Neuroimmunological Cell Biology IZKF, Leipzig, Germany
Neuroreport 13:601-4. 2002..These conditions of carbonyl stress may contribute to increased neuronal dysfunction and vulnerability leading to the early disease onset...