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Impaired degradation of mutant alpha-synuclein by chaperone-mediated autophagy.
It is found that wild-type alpha-synuclein was selectively translocated into lysosomes for degradation by the chaperone-mediated autophagy pathway, which may underlie the toxic gain-of-function by the pathogenic A53T and A30P mutants. Expand
Impaired Degradation of Mutant α-Synuclein by Chaperone-Mediated Autophagy
It is found that wild-type α-synuclein was selectively translocated into lysosomes for degradation by the chaperone-mediated autophagy pathway, which may underlie the toxic gain-of-function by the A53T and A30P mutants. Expand
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
There continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes, so it is important to update guidelines for monitoring autophagic activity in different organisms. Expand
Wild Type α-Synuclein Is Degraded by Chaperone-mediated Autophagy and Macroautophagy in Neuronal Cells*
It is shown that CMA and macroautophagy are important pathways for WT ASYN degradation in neurons and underline the importance of CMA as degradation machinery in the nervous system. Expand
Cell-Produced α-Synuclein Is Secreted in a Calcium-Dependent Manner by Exosomes and Impacts Neuronal Survival
The results show for the first time that cell-produced α- Synuclein is secreted via an exosomal, calcium-dependent mechanism and suggest that α-synuclein secretion serves to amplify and propagate Parkinson's disease-related pathology. Expand
Apoptosis in neurodegenerative disorders.
There is supportive, but not definitive, evidence for apoptosis in a number of neurodegenerative disorders, and tissue culture models, animal models and human pathological studies are discussed. Expand
Expression of A53T Mutant But Not Wild-Type α-Synuclein in PC12 Cells Induces Alterations of the Ubiquitin-Dependent Degradation System, Loss of Dopamine Release, and Autophagic Cell Death
These cells may serve as a model to study the effects of aberrant α-synuclein on dopaminergic cell function and survival and raise the possibility that the primary abnormality in these cells may involve one or more deficits in the lysosomal and/or proteasomal degradation pathways, which in turn lead to loss of dopamine capacity and, ultimately, to death. Expand
α-Synuclein in Parkinson's disease.
  • L. Stefanis
  • Biology, Medicine
  • Cold Spring Harbor perspectives in medicine
  • 1 February 2012
Targeting the toxic functions conferred by α-synuclein when it is dysregulated may lead to novel therapeutic strategies not only in PD, but also in other neurodegenerative conditions, termed synucleinopathies. Expand
Abberant α-Synuclein Confers Toxicity to Neurons in Part through Inhibition of Chaperone-Mediated Autophagy
CMA dysfunction mediates aberrant ASYN toxicity, and may be a target for therapeutic intervention in PD and related disorders. Expand
α-Synuclein Overexpression in PC12 and Chromaffin Cells Impairs Catecholamine Release by Interfering with a Late Step in Exocytosis
Overexpression of wild-type or A30P mutant α-syn in PC12 cell lines inhibited evoked catecholamine release without altering calcium threshold or cooperativity of release, and inhibits a vesicle “priming” step, after secretory vesicular trafficking to “docked” sites but before calcium-dependent vesicles membrane fusion. Expand