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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]