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Table 1 Summary of mitochondria-related changes in brain disease

From: Mitochondria as a target for neuroprotection: role of methylene blue and photobiomodulation

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, 28,29,30,31]
• Aberrant mitochondrial enzymes [32,33,34,35]
• 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) [42,43,44]
• Impaired mitochondrial trafficking [45,46,47]
• 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 [53,54,55,56,57]
• Impaired mitopahgy [58]
Stroke • Failure of membrane ion pump, cellular potassium efflux, sodium influx, and the depolarization of the membrane [59,60,61]
• The dysregulation of mitochondrial Ca2+ homeostasis [62,63,64]
• Cytochrome c release induced apoptosis [65, 66]
• Excessive mitochondrial superoxide production [67,68,69]
• Mitochondrial dynamics defects [70,71,72,73,74]
• Abnormal mitophagy [75,76,77]
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 [81,82,83,84,85]
• 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 [92,93,94,95]
• Excessive ROS production [90, 96, 97]
• Mitochondrial dynamics defects [98,99,100]
• Mitochondrial Ca2+ overload in DA neurons [101, 102]
• Inappropriate trafficking of damaged mitochondria [103]
• Compromised mitophagy [104]