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J. Mark Cooper

Researcher at University College London

Publications -  42
Citations -  10314

J. Mark Cooper is an academic researcher from University College London. The author has contributed to research in topics: Mitochondrial DNA & Substantia nigra. The author has an hindex of 31, co-authored 42 publications receiving 9349 citations. Previous affiliations of J. Mark Cooper include Royal Free Hospital.

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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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Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy

TL;DR: Overexpression and RNAi studies indicated that PINK1 and parkin were required for mitophagy following CCCP-induced mitochondrial damage, and inhibition of this pathway may lead to the accumulation of defective mitochondria which may contribute to PD pathogenesis.
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Chaperone-Mediated Autophagy Markers in Parkinson Disease Brains

TL;DR: It is demonstrated that decreased LAMP2A levels in dopaminergic cell lines reduced chaperone-mediated autophagy activity and increased the half-life of α-synuclein, suggesting that this pathway may be a suitable therapeutic target in PD.
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Glucocerebrosidase deficiency in substantia nigra of parkinson disease brains

TL;DR: This work investigated the enzymatic activity of glucocerebrosidase (GCase) in PD brains carrying heterozygote GBA mutations (PD+GBA) and sporadic PD brains.
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Ambroxol improves lysosomal biochemistry in glucocerebrosidase mutation-linked Parkinson disease cells

TL;DR: Using Parkinson’s disease patient derived fibroblasts McNeill et al. show that Ambroxol treatment improved glucosylceramidase activity and reduced oxidative stress in these cells.