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Moisoi 2017 Abstract MITOEAGLE Barcelona

From Bioblast

Mitochondrial quality control signaling in Parkinson’s disease models.

Link: MitoEAGLE

Moisoi N (2017)

Event: MitoEAGLE Barcelona 2017


Parkinson’s Disease (PD) has a multifactorial ethiopathology with aging, genetic susceptibility and environmental factors being the principal contributors to its occurrence. Two main signaling pathways are involved in PD pathogenesis, namely, mitochondrial quality control and protein aggregation. Components of these signaling cascades have been found mutated in PD and by studying them we aim to understand disease mechanisms and to uncover novel pharmacological approaches to tackle disease progression.

Mitochondria are under stress from external factors as well as from their own respiratory activity. Maintenance of mitochondrial homeostasy is thus essential, particularly in disease conditions like Parkinson's.

Mitochondria quality control is fulfilled at molecular level by upregulation of chaperones and proteases to deal with the load of unfolded and misfolded proteins. At organellar level dysfunctional mitochondria is removed in the process of mitophagy. Proteins implicated in mitochondrial quality control, both at molecular level (HtrA2) or at organellar level (PINK1/Parkin) are mutated in PD.

Here I will discuss how we employ models of PD (mouse, Drosophila and cells) harbouring mutations in MQC pathways to address the role of mitochondrial stress signaling and mitochondria homeostasis in PD.

Bioblast editor: Kandolf G O2k-Network Lab: UK Leicester Moisoi N

Labels: Pathology: Parkinson's 

Event: A4 


De Montfort Univ Leicester, United Kingdom