Table 1.

Summary of effects of MB on neurodegenerative disorders and brain injury and related mechanisms

Condition of Interest	Observed Actions of MB	Known Mechanisms of Action
Global Cerebral Ischemia	Neuroprotection [43–45] Neurological [43] Promotes mitochondrial function [43] Improves neuroprotection in combination with hypothermia [46,47]	Oxidizes/inactivates caspase 3/6 [48] Inhibits GC and nitric oxide synthase [49] Stabilizes Hif-1α and phosphorylates Akt [44] Promotes complex IV activity [43]
Stroke	Neuroprotection and decreased infarct size and [50–53] Neurological Improvement [54,50,51,53] Preserves mitochondrial structure and function [54,51] Preserves BBB integrity [55] Improves neuroprotection in combination with normobaric hyperoxia [56] Promotes neurogenesis [54]	Upregulates mitophagy and autophagy related proteins [51] Upregulates Akt and GSK-3β [55] Upregulates complex IV expression and activity [54] Decreases pro-inflammatory factor release [55,54]
Alzheimer’s Disease	Improved cognitive function [57–62] Neuroprotection [57] Preserved mitochondrial function [57,30,63] Decreased Aβ levels [60,64] Decreased tau burden [58,62,65,66] Increased cerebral blood flow [59]	Inhibits oligimeric Aβ formation [67] Increases proteolytic clearance of Aβ [64] Decreases β-secretase activity [60] Upregulates complex IV activity [30,63] Upregulated heme synthesis [63] Decreased oxidative stress [57] Prevented tau-tau binding [66] Inhibited tau filament formation on microtubule binding domain [68] Oxidized tau cysteine residues [69]
Parkinson’s Disease	Neurological improvement [5] Improves mitochondrial function [5]	Alternative mitochondrial electron transfer [5]
Traumatic Brain Injury	Neuroprotection [70–72] Decreases infarct size [70–72] Decreases edema [73] Improves neurological function [71,73,72]	Reduces glial activation [70] Decreases pro-inflammatory factor release [73] Promotes induction of autophagy [70]