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Anthony R. White

Researcher at QIMR Berghofer Medical Research Institute

Publications -  192
Citations -  15338

Anthony R. White is an academic researcher from QIMR Berghofer Medical Research Institute. The author has contributed to research in topics: Neurodegeneration & Amyloid precursor protein. The author has an hindex of 49, co-authored 174 publications receiving 13879 citations. Previous affiliations of Anthony R. White include German Cancer Research Center & Murdoch University.

Papers
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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Metalloenzyme-like Activity of Alzheimer's Disease β-Amyloid Cu-DEPENDENT CATALYTIC CONVERSION OF DOPAMINE, CHOLESTEROL, AND BIOLOGICAL REDUCING AGENTS TO NEUROTOXIC H2O2

TL;DR: It is reported that microregional catalytic H( 2)O(2) production, combined with the exhaustion of reducing agents, may mediate the neurotoxicity of Abeta in Alzheimer's disease, and inhibitors of this novel activity may be of therapeutic value.
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Monoclonal antibodies inhibit prion replication and delay the development of prion disease

TL;DR: Investigating in a murine scrapie model whether anti-PrP monoclonal antibodies show similar inhibitory effects on prion replication in vivo found that peripheral PrPSc levels and prion infectivity were markedly reduced, even when the antibodies were first administered at the point of near maximal accumulation of PrP Sc in the spleen.
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Overexpression of Alzheimer's Disease Amyloid-β Opposes the Age-dependent Elevations of Brain Copper and Iron

TL;DR: It is demonstrated that overexpression of the carboxyl-terminal fragment of APP, containing Aβ, results in significantly reduced copper and iron levels in transgenic mouse brain, while overexposure of the APP in Tg2576 transgenic mice results inificantly reduced copper, but not iron, levels prior to the appearance of amyloid neuropathology and throughout the lifespan of the mouse.