NIR応答型アップコンバージョン/CN/CoP光触媒による水素産生促進とアルツハイマー病への効果
Alzheimer's disease (AD) involves two central pathological features: oxidative stress from excess reactive oxygen species (ROS) and abnormal amyloid-beta (Aβ) accumulation. A composite photocatalyst, UCNP@CoP@g-C3N4, was engineered to address both factors simultaneously. The material responds to near-infrared (NIR) light, enabling photocatalytic decomposition of H2O2 within biological tissue to generate H2 continuously, circumventing the poor tissue penetration of visible light and the low solubility limitation of conventional H2 delivery. Incorporation of a CoP cocatalyst suppresses recombination of photogenerated electron-hole pairs in g-C3N4, thereby enhancing hydrogen evolution efficiency. Additionally, the metal-ion chelating capacity of g-C3N4 and the photothermal properties of CoP cooperatively inhibit Aβ aggregation. In AD mouse models, the composite reduced cerebral Aβ deposition, alleviated memory deficits, and decreased neuroinflammation, demonstrating a multi-target synergistic approach.
NIR excitation drives photocatalytic H2O2 decomposition by UCNP@CoP@g-C3N4, yielding continuous H2 that scavenges hydroxyl radicals. CoP suppresses electron-hole recombination in g-C3N4 to boost hydrogen evolution, while g-C3N4 metal-ion chelation and CoP photothermal activity jointly inhibit Aβ aggregation.
This is basic research at the cellular or molecular level. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/36688477