Affiliation: University of Tasmania
- Vaccination strategies for Alzheimer's disease: A new hope?Adele Woodhouse
School of Medicine, NeuroRepair Group, University of Tasmania, Hobart, Tasmania, Australia
Drugs Aging 24:107-19. 2007..The vigour of international research on immunotherapy for AD provides significant hope for a strong therapeutic lead for the escalating number of individuals who will develop this otherwise incurable condition...
- Cytoplasmic cytochrome c immunolabelling in dystrophic neurites in Alzheimer's diseaseAdele Woodhouse
NeuroRepair Group, School of Medicine, University of Tasmania, Private Bag 29, Hobart, TAS, 7001 Australia
Acta Neuropathol 112:429-37. 2006..Although cytochrome c release is indicative of the activation of the intrinsic apoptotic pathway, cytoplasmic cytochrome c may also indicate mitochondrial damage or dysfunction...
- Dystrophic neurites in TgCRND8 and Tg2576 mice mimic human pathological brain agingAdele Woodhouse
NeuroRepair Group, Menzies Research Institute, 43 Collins Street, Hobart, 7001 Tasmania, Australia
Neurobiol Aging 30:864-74. 2009..These results suggest that neuronal pathology in these mice represent an accurate and valuable model for understanding, and developing treatments for, the early brain changes of AD...
- Cytoskeletal alterations differentiate presenilin-1 and sporadic Alzheimer's diseaseAdele Woodhouse
Wicking Dementia Research and Education Centre and NeuroRepair Group, Menzies Research Institute, Private Bag 29, Hobart, TAS, 7001, Australia
Acta Neuropathol 117:19-29. 2009..These differences in cytoskeletal pathology in PS1 cases suggest an accelerated rate of neuritic pathology development, potentially due to mutant PS1 influencing multiple pathogenic pathways...
- No difference in expression of apoptosis-related proteins and apoptotic morphology in control, pathologically aged and Alzheimer's disease casesAdele Woodhouse
NeuroRepair Group, School of Medicine, Private Bag 29, University of Tasmania, Hobart, Tasmania 7001, Australia
Neurobiol Dis 22:323-33. 2006..Apoptosis may not play a major role in the pathogenesis of neuronal degeneration of AD...
- Does beta-amyloid plaque formation cause structural injury to neuronal processes?Adele Woodhouse
NeuroRepair Group, School of Medicine, University of Tasmania, Australia
Neurotox Res 7:5-15. 2005..Identification of the key neuronal alterations underlying the pathology of Alzheimer's disease may provide new avenues for therapeutic intervention...
- The native copper- and zinc-binding protein metallothionein blocks copper-mediated Abeta aggregation and toxicity in rat cortical neuronsRoger S Chung
NeuroRepair Group, Menzies Research Institute, University of Tasmania, Hobart, Australia
PLoS ONE 5:e12030. 2010..A major pathological hallmark of AD is the deposition of insoluble extracellular beta-amyloid (Abeta) plaques. There are compelling data suggesting that Abeta aggregation is catalysed by reaction with the metals zinc and copper...
- Spinal cord tissue affects ensheathing cell proliferation and apoptosisAdele Woodhouse
NeuroRepair Group, School of Medicine, University of Tasmania, Private Bag 24, Hobart, Tasmania 7001, Australia
Neuroreport 16:737-40. 2005..These results suggest that delaying transplantation after spinal cord injury may be beneficial to ensheathing cell survival...
- Axonopathy and cytoskeletal disruption in degenerative diseases of the central nervous systemJames C Vickers
NeuroRepair Group and Wicking Dementia Research and Education Centre, Menzies Research Institute, University of Tasmania, Hobart, Tasmania, Australia
Brain Res Bull 80:217-23. 2009..The identification of a degenerative process initiated in the axon may provide new therapeutic targets for early intervention to inhibit the grim outcomes related to the progression of these diseases...