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Georgia Minakaki

Researcher at University of Erlangen-Nuremberg

Publications -  20
Citations -  6148

Georgia Minakaki is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Alpha-synuclein & Gait (human). The author has an hindex of 13, co-authored 20 publications receiving 5449 citations. Previous affiliations of Georgia Minakaki include Northwestern University.

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Journal ArticleDOI

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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Autophagy inhibition promotes SNCA/alpha-synuclein release and transfer via extracellular vesicles with a hybrid autophagosome-exosome-like phenotype

Georgia Minakaki, +20 more
- 15 Jan 2018 - 
TL;DR: Competing evidence is provided that a) ALP inhibition increases SNCA in neuronal EVs, b) distinct ALP components are present in EVs, and c) CSF EVs transfer S NCA from cell to cell in vivo is provided.
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FoxO Function Is Essential for Maintenance of Autophagic Flux and Neuronal Morphogenesis in Adult Neurogenesis.

Iris Schäffner, +14 more
- 19 Sep 2018 - 
TL;DR: Findings reveal a novel link between FoxO transcription factors, autophagic flux, and maturation of developing neurons in adult mouse hippocampus.
Journal ArticleDOI

Sulfasalazine impacts on ferroptotic cell death and alleviates the tumor microenvironment and glioma-induced brain edema

Tina Sehm, +10 more
- 08 Apr 2016 - 
TL;DR: It is shown that SAS can be utilized for targeting the glutamate antiporter xCT activity as a tumor microenvironment-normalizing drug, while crucial cytotoxic effects in brain tumors are minor.
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Abrogating Native α-Synuclein Tetramers in Mice Causes a L-DOPA-Responsive Motor Syndrome Closely Resembling Parkinson's Disease

Silke Nuber, +9 more
- 10 Oct 2018 - 
TL;DR: The fully penetrant phenotype of mice expressing the fPD E46K mutation plus 2 homologous E→K mutations in adjacent KTKEGV motifs indicates that tetramers are required for normal αS homeostasis and that chronically shifting tetramer to monomers may result in Parkinson's disease, with attendant therapeutic implications.