分子状水素の神経保護および神経疾患予防効果に関するレビュー
This review examines the neuroprotective capacity of molecular hydrogen (H₂) and its potential relevance to neurodegenerative conditions such as Parkinson's and Alzheimer's diseases, for which disease-modifying pharmacological options remain limited. Multiple mechanisms are discussed, including suppression of reactive oxygen species (ROS)—encompassing both hydroxyl radicals and superoxide—anti-inflammatory signaling, and endocrine regulation through the gut-brain axis. In Parkinson's disease model mice, sustained H₂ intake was associated with increased ghrelin secretion from the stomach. In Alzheimer's disease model mice, sex-dependent neuroprotection was observed: female mice showed preservation of estrogen and estrogen receptor-β (ERβ) levels, accompanied by upregulation of brain-derived neurotrophic factor (BDNF) and its receptor TrkB. The precise molecular targets through which H₂ modulates endocrine pathways and exerts these effects remain to be identified, representing a key direction for future research.
H₂ suppresses ROS generation including hydroxyl radicals and superoxide, exerts anti-inflammatory effects, and modulates the gut-brain endocrine axis by promoting ghrelin release and preserving estrogen/ERβ levels, thereby upregulating BDNF and TrkB expression in neural tissue.
Hydrogen-rich water is a low-risk delivery route, but the achievable systemic hydrogen dose is bounded. For clinical applications, inhalation is the most efficient route; inhalation, however, carries explosion risk, and concentration matters (empirical LFL of 10% applies to inhalation environments; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/33076798