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Pamela J. McLean

Researcher at Mayo Clinic

Publications -  124
Citations -  20521

Pamela J. McLean is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Alpha-synuclein & Synucleinopathies. The author has an hindex of 52, co-authored 114 publications receiving 17158 citations. Previous affiliations of Pamela J. McLean include University of Washington & University of Alabama at Birmingham.

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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy 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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Diagnosis and management of dementia with Lewy bodies Fourth consensus report of the DLB Consortium

Ian G. McKeith, +95 more
- 04 Jul 2017 - 
TL;DR: The Dementia with Lewy Bodies (DLB) Consortium has refined its recommendations about the clinical and pathologic diagnosis of DLB, updating the previous report, which has been in widespread use for the last decade.
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Gaucher Disease Glucocerebrosidase and α-Synuclein Form a Bidirectional Pathogenic Loop in Synucleinopathies

TL;DR: It is shown that functional loss of GD-linked glucocerebrosidase in primary cultures or human iPS neurons compromises lysosomal protein degradation, causes accumulation of α-synuclein (α-syn), and results in neurotoxicity through aggregation-dependent mechanisms, suggesting that GCase depletion contributes to the pathogenesis of sporadic synucleinopathies.
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Sirtuin 2 Inhibitors Rescue α-Synuclein-Mediated Toxicity in Models of Parkinson's Disease

TL;DR: A potent inhibitor of sIRT2 was identified and inhibition of SIRT2 rescued α-synuclein toxicity and modified inclusion morphology in a cellular model of Parkinson's disease, suggesting a link between neurodegeneration and aging.
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Exosomal cell-to-cell transmission of alpha synuclein oligomers

TL;DR: The data suggest that αsyn may be secreted via different secretory pathways, and hypothesize that exosome-mediated release of αsyn oligomers is a mechanism whereby cells clear toxic α synuclein oligomers when autophagic mechanisms fail to be sufficient.