University of Groningen
Pathogenicity of alpha-synuclein in various cell models for Parkinson’s disease
Quevedo Melo, Thaiany
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Publication date: 2018
Link to publication in University of Groningen/UMCG research database
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Quevedo Melo, T. (2018). Pathogenicity of alpha-synuclein in various cell models for Parkinson’s disease. University of Groningen.
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1
Propositions
accompanying this PhD thesis
Pathogenicity of alpha-synuclein in various cell models
for Parkinson’s disease
Thaiany Quevedo Melo
1. Impairment of mitochondrial trafficking is a common feature in sporadic and familial in vitro models for Parkinson´s disease (PD) (this thesis)
2. A53T Alpha-synuclein disrupts retrograde trafficking earlier than anterograde trafficking in vitro (this thesis)
3. Absence of Miro prevents mitochondrial damage and cellular stress caused by A53T alpha-synuclein (this thesis)
4. Endoplasmic reticulum stress is caused by mitochondrial dysfunction in yeasts that express A53T alpha-synuclein (this thesis)
5. Alpha-synuclein oligomers-associate mitochondria are the primary cause of dopaminergic degeneration in familial PD (this thesis)
6. A53T Alpha-synuclein damages all events involved in mitochondrial dynamics through direct association with Miro
7. Dopaminergic neurons are more and firstly damaged by alterations in the mitochondrial dynamics than any other neuron
8. Different models are required to explore and unveil the cellular and molecular mechanisms behind neuronal death in PD and then to create effective therapies for the disease
9. A government which is interested in people well-being invests in science. It is impossible to improve the quality of life without scientific investment
