Abounding evidence has shown that MHBOT promotes neurogenesis to improve life quality of patients from multiple conditions

Injury to the central nervous system (CNS) including trauma, cerebral ischemia and epileptic seizures have been reported to induce neurogenesis, and surviving cells may be functionally integrated into existing neural circuits. Consequently, further endogenous promotion of neurogenesis may hold promise for restoration of cerebral functions after CNS injury.

HBOT appears to be a potent method of oxygen delivery. It increases the oxygen partial pressure within the blood and enhances restoration of oxygen supply after ischemic stroke. Previous studies provide evidence that HBOT promotes neurogenesis, reduces infarct size as well as hemorrhagic transformation and improves neurological function, in animal models of ischemic stroke.

The first multicenter, randomized, double-blind, controlled trial in 2009 found that 40-hour HBOT of 24% oxygen at 1.3 ATM produced significant improvement in children’s overall functioning, receptive language, social interaction, eye contact, and sensory/cognitive awareness

The safety of HBOT was also evaluated and it was pointed out that, if given at proper paradigms, like 1.5 ATA for 60 minutes, HBOT will not cause oxygen toxicity. Studies show that (1.5 ATA for 90 minutes each time) caused an increase in contused hippocampus vascular density and an associated improvement in cognitive function (Harch et al., 2007). Activation of several signaling pathways and transcription factors have been suggested to play an important role in HBOT-induced neurogenesis, including Wnt, hypoxia-inducible factors and cAMP response element-binding

Studies also suggest that this process might be beneficial in the treatment of oxidative stress associated neurodegenerative diseases like AD and PD