Hydrogen Water Protects Brain Cells from Alzheimer's Protein Damage

Authors
Journal
Chemico-Biological Interactions
Year
DOI
10.1016/j.cbi.2015.07.013
Study Type
Cell Culture
Outcome
Positive
Peer Reviewed
Yes
Country
Taiwan
Health Condition
Alzheimer's Disease
Body System
Nervous System

TL;DR

Drinking hydrogen-rich water could potentially help protect the brain from the damage that leads to Alzheimer's disease by fighting off harmful oxidative stress.

Key Finding

Hydrogen-rich water protected brain cells from amyloid beta damage by both directly neutralizing harmful free radicals and activating the cells' own antioxidant defense pathways.

Summary

Researchers studied how hydrogen-rich water might protect brain cells from damage caused by amyloid beta, a protein linked to Alzheimer's disease. Using lab-grown brain cells, they found that hydrogen-rich water reduced cell death in two ways: it directly neutralized harmful molecules called free radicals, and it activated protective pathways inside cells that boost the body's natural antioxidant defenses.

Practical Takeaway

This is early laboratory research in isolated cells, not human studies, so it's too preliminary to draw conclusions about hydrogen water's effects on Alzheimer's disease or brain health in people. The findings suggest a potential mechanism worth investigating further, but much more research—including animal and human studies—would be needed before any health claims could be supported.

Abstract

Amyloid β (Aβ) peptides are identified in cause of neurodegenerative diseases such as Alzheimer's disease (AD). Previous evidence suggests Aβ-induced neurotoxicity is linked to the stimulation of reactive oxygen species (ROS) production. The accumulation of Aβ-induced ROS leads to increased mitochondrial dysfunction and triggers apoptotic cell death. This suggests antioxidant therapies may be beneficial for preventing ROS-related diseases such as AD. Recently, hydrogen-rich water (HRW) has been proven effective in treating oxidative stress-induced disorders because of its ROS-scavenging abilities. However, the precise molecular mechanisms whereby HRW prevents neuronal death are still unclear. In the present study, we evaluated the putative pathways by which HRW protects against Aβ-induced cytotoxicity. Our results indicated that HRW directly counteracts oxidative damage by neutralizing excessive ROS, leading to the alleviation of Aβ-induced cell death. In addition, HRW also stimulated AMP-activated protein kinase (AMPK) in a sirtuin 1 (Sirt1)-dependent pathway, which upregulates forkhead box protein O3a (FoxO3a) downstream antioxidant response and diminishes Aβ-induced mitochondrial potential loss and oxidative stress. Taken together, our findings suggest that HRW may have potential therapeutic value to inhibit Aβ-induced neurotoxicity.