Fig. 1: Mitochondrial adaptability in Parkinson’s neurons.

Mitochondrial quality control (MQC) operates through the intricate cooperation of three processes: synthesis and import of new building blocks for mitochondria; correct protein folding and degradation to maintain protein homoeostasis within the organelle; alongside mitochondrial dynamics and mitophagy to turnover dysfunctional mitochondria. This MQC system allows neuronal mitochondria to monitor and adapt themselves to a certain degree of damage, such as OxPhos defects, oxidative stress and protein aggregation, without causing interference to neuron homoeostasis. It is hypothesised that the MQC system is impaired in PD; the weakening mitochondrial adaptability is unable to compensate for the increasing burden of oxidative damage and protein degradation that advancing with age, leads to premature neuronal death (a). In this study, we investigated the expression change of key MQC signalling proteins on PD neurons using imaging mass cytometry (IMC) (b). These tested proteins were categorised into three major groups based on their most well-known function for easy interpretation.