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. Author manuscript; available in PMC: 2020 Oct 1.
Published in final edited form as: Neurochem Int. 2019 Jun 21;129:104495. doi: 10.1016/j.neuint.2019.104495

Table 1.

Features of mitochondrial dysfunction observed in sporadic Parkinson’s disease cybrids

Phenotype References
Altered mitochondrial ultrastructure: e.g. rounded, swollen mitochondria; mitochondrial matrix with few or disrupted cristae; presence of intramitochondrial inclusions. [43, 161–163]
Decreased complex I activity [42, 43, 163–165]
Mitochondrial depolarisation [43]
Reduced mitochondrial ability to buffer cytosolic calcium/altered calcium homeostasis [166, 167]
Reduced ATP levels [43, 163, 168]
Apoptosis: altered levels of apoptosis-related proteins [43, 169, 170]
Reduced mtDNA content [50, 171]
Microtubule depolymerisation [163, 168]
Increased alpha-synuclein oligomerization [163, 166, 168]
Existence of fibrillar and vesicular inclusions (cybrid Lewy bodies) [163, 172]
Reduced respiratory reserve capacity [165]
Increased toxin susceptibility [42, 43]
Significantly reduced mitochondrial axonal transport [171]
Increased ROS production [42, 163]

ATP = Adenosine triphosphate; mtDNA = Mitochondrial DNA; ROS = reactive oxygen species