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Robert E. Burke

Researcher at Columbia University

Publications -  186
Citations -  20599

Robert E. Burke is an academic researcher from Columbia University. The author has contributed to research in topics: Substantia nigra & Dopaminergic. The author has an hindex of 63, co-authored 186 publications receiving 19121 citations. Previous affiliations of Robert E. Burke include NewYork–Presbyterian Hospital & Oregon Health & Science University.

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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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Validity and reliability of a rating scale for the primary torsion dystonias

TL;DR: The Movement Scale was a valid and reliable indicator of the severity of primary torsion dystonia and was found to be compatible with scores on the Disability Scale.
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Clinical progression in Parkinson disease and the neurobiology of axons.

TL;DR: It is proposed that ongoing degeneration of axons, not cell bodies, is the primary determinant of clinically apparent progression of disease, and that future experimental therapeutics intended to forestall disease progression will benefit from a new focus on the distinct mechanisms of axon degeneration.
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Time course and morphology of dopaminergic neuronal death caused by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine

TL;DR: This study demonstrates that the MPTP mouse model replicates several key features of neurodegeneration of DA neurons in PD and provides no in vivo evidence that, using this specific paradigm of injection, MPTP kills DA neurons by apoptosis.
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Resistance of alpha -synuclein null mice to the parkinsonian neurotoxin MPTP.

TL;DR: It is shown that α-synuclein null mice display striking resistance to MPTP-induced degeneration of DA neurons and DA release, and this resistance appears to result from an inability of the toxin to inhibit complex I.