アルツハイマー病における抗酸化物質の新たな役割：生理学的・病理学的メカニズムと管理への洞察
Alzheimer's disease (AD) is a progressive neurodegenerative condition marked by memory impairment, cognitive deterioration, and hippocampal atrophy. Key pathological features include tau protein accumulation, amyloid plaque deposition, neuronal loss, and chronic neuroinflammation. Because oxidative stress is implicated in AD pathogenesis through multiple mechanisms, various antioxidants—including glutathione, astaxanthin, ascorbyl palmitate, catalase, and molecular hydrogen—have been investigated for their potential to neutralize free radicals and mitigate neurodegeneration. While animal model studies have demonstrated encouraging outcomes, results from human clinical trials remain inconsistent, raising questions about translational efficacy. This review highlights the need for more targeted antioxidant strategies that also account for the well-established link between neuroinflammation and AD progression, with the aim of supporting the development of more effective intervention approaches.
Antioxidants including molecular hydrogen are proposed to neutralize free radicals, thereby reducing oxidative damage, suppressing neuroinflammation, and attenuating tau accumulation and amyloid plaque formation that drive neurodegeneration in AD.
The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/41550171