Alzheimer's is a debilitating neurodegenerative disease that affects every aspect of patients life, from
speech to memory and everyday life.

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AD is characterized by accumulation of extracellular amyloid-beta (Aβ) plaques, intracellular hyperphosphorylated tau deposits, loss of synapses and dendritic spines.

 

In addition to those disease hallmarks, AD patients also suffer from mitochondrial dysfunction and elevated oxidative stress. Hyperbaric oxygen therapy (HBOT) is the administration of 100% oxygen at an atmospheric pressure greater than one.

 

Several studies showed HBOT improves both quality of life and alleviate
dementia symptoms. HBOT led to a reduction in amyloid beta levels in both male and female 5xFAD mice. Notably, the treatment ameliorated oxidative stress in male 5xFAD mice, which initially exhibited higher levels of oxidative stress compared to WT mice. This effect was attributed to the elevation of antioxidant enzymatic activity, specifically superoxide dismutase (SOD) and catalase.

 

Mitochondrial dysfunction, a hallmark of AD, was assessed by examining mitochondrial respiration and complex levels. While no significant differences were observed in mitochondrial respiration among the groups, an increase in complex V levels was observed, suggesting potential improvements in mitochondrial function following HBOT.

 

Furthermore, in female mice, mitochondrial respiration mediated by complex I, complex II, and
complex IV was impaired in the 5xFAD group, but HBOT resulted in a significant improvement in their activities.

 

Since AD is diagnosed at a late stage of the disease, there are currently no effective drugs or
treatment to inhibit the cognitive decline. There is a need for interventions that will alleviate patient
symptoms even at those stages, we are hopeful that this study will provide an understanding of the
molecular mechanism of AD and potential mitigation of disease progression for patients.