In today's open access paper, researchers report a modest improvement in cerebral blood flow and cognitive performance in a small study of older individuals suffering cognitive impairment as a result of sustained hyperbaric oxygen treatment over a period of months. This seems a compensatory approach to therapy, in that improvements in cerebral blood flow should be expected to improve cognitive function at any age. This is the mechanism by which exercise rapidly improves memory function, for example. A direct comparison of hyperbaric oxygen treatment and exercise would be interesting.
This result might help to inform discussions of the degree to which loss of blood supply to the brain contributes to cognitive decline in patients diagnosed with neurodegenerative conditions. Vascular dementia is an acknowledged and well-researched condition, but to what degree is the impairment of Alzheimer's patients at various stages due to vascular aging and consequent reduced blood flow to the brain, versus the harmful protein aggregation and neuroinflammation characteristic of Alzheimer's? Absent a way to remove just one of these pathologies, it is hard to answer that question.
It is worth noting that this study was conducted and published by the same groups who put together the poor study and accompanying overhyped media materials regarding the effects of hyperbaric oxygen treatment on measures of metabolism related to aging. It is most likely a good idea to treat this and any future work conducted by these researchers with an appropriately greater level of scrutiny and skepticism.
Vascular dysfunction is entwined with aging and the pathogenesis of Alzheimer's disease (AD), and contributes to reduced cerebral blood flow (CBF) and consequently, hypoxia. Hyperbaric oxygen therapy (HBOT) is in clinical use for a wide range of medical conditions. In the current study, we exposed 5XFAD mice, a well-studied AD model that presents impaired cognitive abilities, to HBOT and then investigated the therapeutical effects. HBOT increased arteriolar luminal diameter and elevated CBF, thus contributing to reduced hypoxia. Furthermore, HBOT reduced amyloid burden by reducing the volume of pre-existing plaques and attenuating the formation of new ones. This was associated with changes in amyloid precursor protein processing, elevated degradation and clearance of amyloid-ß protein and improved behavior of 5XFAD mice. Hence, our findings are consistent with the effects of HBOT being mediated partially through a persistent structural change in blood vessels that reduces brain hypoxia.
To understand whether the ability of HBOT to change CBF and affect cognitive function also applied to elderly people, we performed a human study in which six elderly patients (age 70.00 ± 2.68 years) with significant memory loss at baseline (memory domain score < 100) were treated with HBOT (60 daily HBOT sessions within 3 months). CBF and cognitive function were evaluated before and after HBOT. CBF was measured by MRI, while cognitive functions were evaluated using computerized cognitive tests. Following HBOT, there were significant CBF increases in several brain areas.
At baseline, patients attained a mean global cognitive score (102.4±7.3) similar to the average score in the general population normalized for age and education level (100), while memory scores were significantly lower (86.6 ± 9.2). Cognitive assessment following HBOT revealed a significant increase in the global cognitive score (102.4 ± 7.3 to 109.5 ± 5.8), where memory, attention and information processing speed domain scores were the most ameliorated. Moreover, post-HBOT mean memory scores improved to the mean score (100.9 ± 7.8), normalized per age and education level (100). The improvements in these scores correlate with improved short and working memory, and reduced times of calculation and response, as well as increased capacity to choose and concentrate on a relevant stimulus.