Hydrogen Therapy Delays ALS Progression in Mice

Authors
Journal
Neurochemical Research
Year
DOI
10.1007/s11064-015-1750-7
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Amyotrophic Lateral Sclerosis (ALS)
Body System
Nervous System

TL;DR

Treating mice with a form of ALS with hydrogen-rich saline improved their symptoms and extended their lives by reducing harmful oxidative stress and preserving nerve cell health.

Key Finding

Hydrogen-rich saline treatment significantly delayed disease onset and extended survival in mice with ALS while reducing nerve cell death and protecting mitochondrial function.

Summary

Researchers tested whether hydrogen-rich saline (a solution containing dissolved hydrogen gas) could help slow down ALS, a disease that damages nerve cells controlling muscles. In mice genetically engineered to develop ALS, the treatment delayed when symptoms started, extended survival time, and reduced nerve cell death. The hydrogen appeared to work by reducing harmful molecules called free radicals (unstable atoms that damage cells) and protecting the energy-producing structures inside cells called mitochondria.

Practical Takeaway

This is an early-stage animal study showing hydrogen may have protective effects against ALS-related nerve damage through antioxidant mechanisms. However, results in mice do not automatically translate to humans, and no human trials have been conducted. Much more research, including human clinical trials, would be needed before any conclusions could be drawn about hydrogen's usefulness for ALS patients.

Abstract

Amyotrophic lateral sclerosis (ALS) is the most frequent adult-onset motor neuron disease, and accumulating evidence indicates that oxidative mechanisms contribute to ALS pathology, but classical antioxidants have not performed well in clinical trials. The aim of this work was to investigate the effect of treatment with hydrogen molecule on the development of disease in mutant SOD1 G93A transgenic mouse model of ALS. Treatment of mutant SOD1 G93A mice with hydrogen-rich saline (HRS, i.p.) significantly delayed disease onset and prolonged survival, and attenuated loss of motor neurons and suppressed microglial and glial activation. Treatment of mutant SOD1 G93A mice with HRS inhibited the release of mitochondrial apoptogenic factors and the subsequent activation of downstream caspase-3. Furthermore, treatment of mutant SOD1 G93A mice with HRS reduced levels of protein carbonyl and 3-nitrotyrosine, and suppressed formation of reactive oxygen species (ROS), peroxynitrite, and malondialdehyde. Treatment of mutant SOD1 G93A mice with HRS preserved mitochondrial function, marked by restored activities of Complex I and IV, reduced mitochondrial ROS formation and enhanced mitochondrial adenosine triphosphate synthesis. In conclusion, hydrogen molecule may be neuroprotective against ALS, possibly through abating oxidative and nitrosative stress and preserving mitochondrial function.