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Bradley J. Turner

Researcher at Florey Institute of Neuroscience and Mental Health

Publications -  91
Citations -  7557

Bradley J. Turner is an academic researcher from Florey Institute of Neuroscience and Mental Health. The author has contributed to research in topics: Amyotrophic lateral sclerosis & SOD1. The author has an hindex of 36, co-authored 83 publications receiving 5755 citations. Previous affiliations of Bradley J. Turner include John Radcliffe Hospital & La Trobe University.

Papers
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of amyotrophic lateral sclerosis

John D. Lee, +7 more
TL;DR: This Seminar summarises current concepts about the origin of the disease, what predisposes patients to develop the disorder, and why all cases of ALS are not the same.
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Transgenics, toxicity and therapeutics in rodent models of mutant SOD1-mediated familial ALS.

Bradley J. Turner, +2 more
- 01 May 2008 - 
TL;DR: mounting evidence from mice with cell restrictive, repressible or chimeric expression of mutant SOD1 transgenes and bone marrow transplants supports non-neuronal origins of neuroprotection in ALS.
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Intercellular propagated misfolding of wild-type Cu/Zn superoxide dismutase occurs via exosome-dependent and -independent mechanisms.

Leslie I. Grad, +17 more
- 04 Mar 2014 - 
TL;DR: HuWtSOD1 can traverse between cells via two nonexclusive mechanisms: protein aggregates released from dying cells and taken up by macropinocytosis, and exosomes secreted from living cells as mentioned in this paper.
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TDP-43 Triggers Mitochondrial DNA Release via mPTP to Activate cGAS/STING in ALS

Chien-Hsiung Yu, +51 more
- 29 Oct 2020 - 
TL;DR: The results identify mtDNA release and cGAS/STING activation as critical determinants of TDP-43-associated pathology and demonstrate the potential for targeting this pathway in ALS.