. 2020 Jun 1;9:19. doi: 10.1186/s40035-020-00197-z

Table 1.

Summary of mitochondria-related changes in brain disease

Condition of interest	Observed mitochondria-related changes in brain disease
Alzheimer ‘s disease	• Increased ROS production [26, 27]
	• Impaired balance of mitochondrial fission and fusion [8, 28–31]
	• Aberrant mitochondrial enzymes [32–35]
	• Increased mtDNA mutation [36]
	• Abnormal function of mitochondrial import channels [37]
	• Inflammation [38, 39]
	• Accumulation of APP/Aβ in mitochondrial import channels [37]
	• Mitochondrial dysfunction-induced apoptosis [6, 40, 41]
	• Impaired Na⁺/Ca²⁺ exchanger (mitochondrial Ca²⁺ overload) [42–44]
	• Impaired mitochondrial trafficking [45–47]
	• Mitophagy defects [48, 49]
Traumatic Brain Injury	• Decreased mitochondrial membrane potential [50]
	• Mitochondrial Ca²⁺ overload [50, 51]
	• Reduced oxidase complex activity [52]
	• Imbalance of mitochondrial fusion and fission induced mitochondrial respiration dysfunction, increased ROS production, and release of apoptosis- related factors [53–57]
	• Impaired mitopahgy [58]
Stroke	• Failure of membrane ion pump, cellular potassium efflux, sodium influx, and the depolarization of the membrane [59–61]
	• The dysregulation of mitochondrial Ca²⁺ homeostasis [62–64]
	• Cytochrome c release induced apoptosis [65, 66]
	• Excessive mitochondrial superoxide production [67–69]
	• Mitochondrial dynamics defects [70–74]
	• Abnormal mitophagy [75–77]
Depression	• Inhibition of mitochondrial OXPHOS activity [78]
	• Decreased content of mitochondrial enzymes [79, 80]
	• Inhibition of complexes in the mitochondrial respiratory chain and the activity of Na+, K + -ATPase [81–85]
	• Increased mtDNA mutation [78, 86, 87]
	• Impaired mitochondrial ETC [78, 88, 89]
Parkinson’s disease	• Mitochondrial respiration defects [90, 91]
	• Genetic mutation induced mitochondrial dysfunction [92–95]
	• Excessive ROS production [90, 96, 97]
	• Mitochondrial dynamics defects [98–100]
	• Mitochondrial Ca²⁺ overload in DA neurons [101, 102]
	• Inappropriate trafficking of damaged mitochondria [103]
	• Compromised mitophagy [104]