Hydrogen Water Protects Brain Function in Vascular Dementia Study

Authors
Journal
Behavioural Brain Research
Year
DOI
10.1016/j.bbr.2018.05.023
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Vascular Dementia
Body System
Nervous System

TL;DR

Drinking hydrogen-rich water improved memory and brain health in rats with a type of dementia caused by poor blood flow to the brain.

Key Finding

Hydrogen-rich water significantly improved memory and learning in rats with vascular dementia and protected brain cells from damage, with effects comparable to the standard medication donepezil.

Summary

Researchers tested hydrogen-rich water in rats with vascular dementia (a type of cognitive decline caused by reduced blood flow to the brain). The treatment improved memory and learning, protected brain cells from damage, and worked through a cellular process called autophagy (where cells break down damaged parts). The effects were similar to a standard dementia medication called donepezil.

Practical Takeaway

This rat study suggests hydrogen-rich water may have neuroprotective effects in vascular dementia, but it is early-stage research in animals only. Human clinical trials would be needed before any conclusions about effectiveness in people can be drawn. The study does not establish that hydrogen water is a treatment for dementia in humans.

Abstract

Vascular dementia (VD) is a heterogeneous group of brain disorders in which cognitive impairment is attributed to cerebrovascular pathologies. Autophagy, a self-cannibalization mechanism, has been demonstrated to be involved in VD progression. Molecular hydrogen is known for its powerful anti-oxidative, anti-apoptotic, and anti-inflammatory activities, and it is also involved in autophagy. However, the effects of hydrogen on VD remain unclear. The current study found that hydrogen-rich water (HRW) significantly alleviated spatial learning and memory impairments. Similar to donepezil treatment, HRW also inhibited neuron loss and shrinkage in the hippocampal CA1 region. In addition, we found that HRW significantly increased the Bcl-2/Bax expression ratio and decreased cleaved caspase-3 expression levels in the hippocampus of VD rats. Moreover, electron microscopy revealed that HRW decreased the number of autophagosomes. We also observed that HRW reduced the increased ratio of LC3-II/I and Beclin 1 expression and saliently upregulated p62 expression. Furthermore, FoxO1 (a major mediator of autophagy regulation) and Atg7 levels were apparently decreased in the hippocampus of HRW-treated bilateral common carotid artery occlusion (2VO) rats. Taken together, these data show that molecular hydrogen exerts beneficial effects on cognitive impairment induced by chronic cerebral hypoperfusion. FoxO1-mediated autophagy plays an important role in the neuroprotective effects of hydrogen in a rat model of VD. Furthermore, the present findings highlight that HRW should be further investigated as a new therapeutic strategy for VD treatment in the future.