パラジウム水素化物ナノ粒子による持続的水素放出がアルツハイマー病モデルマウスの認知機能障害を改善する
Oxidative stress-driven mitochondrial dysfunction is a central feature of Alzheimer's disease (AD) pathology. This study introduces small-sized palladium hydride (PdH) nanoparticles designed to carry a high hydrogen payload and release it continuously within the AD brain, overcoming the limitation of hydrogen's low aqueous solubility. The catalytic hydrogenation property of palladium endows the released hydrogen with strong bio-reductive capacity, enabling self-catalytic scavenging of cytotoxic hydroxyl radicals (·OH). In AD model mice, bio-reductive hydrogen restored mitochondrial function, suppressed amyloid-beta (Aβ) production and aggregation, prevented synaptic and neuronal apoptosis, and enhanced neuronal energy metabolism through oxidative stress elimination and activation of antioxidant signaling pathways. These combined effects led to measurable improvement in cognitive performance, suggesting that nanoparticle-mediated sustained hydrogen delivery represents a promising strategy for addressing AD-related neurodegeneration.
PdH nanoparticles release hydrogen in situ within the AD brain; palladium's catalytic hydrogenation selectively neutralizes hydroxyl radicals, restoring mitochondrial function, inhibiting Aβ aggregation, blocking neuronal apoptosis, and activating antioxidant pathways to improve cognition.
Intravenous hydrogen-saline infusion is a clinic-only route and is not viable for everyday self-administration. For routine hydrogen intake, inhalation is the most practical route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration 66% / 100% devices are not recommended).
See also:
https://h2-papers.org/en/papers/30703744