An NIR-Driven Upconversion/C3N4/CoP Photocatalyst for Efficient Hydrogen Production by Inhibiting Electron–Hole Pair Recombination for Alzheimer’s Disease Therapy

Redox imbalance and abnormal amyloid protein (Aβ) buildup are key factors in the etiology of Alzheimer's disease (AD). As an antioxidant, the hydrogen molecule (H₂) has the potential to cure AD by specifically scavenging highly harmful reactive oxygen species (ROS) such as ^•OH. However, due to the low solubility of H₂ (1.6 ppm), the traditional H₂ administration pathway cannot easily achieve long-term and effective accumulation of H₂ in the foci. Therefore, how to achieve the continuous release of H₂ in situ is the key to improve the therapeutic effect on AD. As a corollary, we designed a rare earth ion doped g-C₃N₄ upconversion photocatalyst, which can respond to NIR and realize the continuous production of H₂ by photocatalytic decomposition of H₂O in biological tissue, which avoids the problem of the poor penetration of visible light. The introduction of CoP cocatalyst accelerates the separation and transfer of photogenerated electrons in g-C₃N₄, thus improving the photocatalytic activity of hydrogen evolution reaction. The morphology of the composite photocatalyst was shown by transmission electron microscopy, and the crystal structure was studied by X-ray diffractometry and Raman analysis. In addition, the ability of g-C₃N₄ to chelate metal ions and the photothermal properties of CoP can inhibit Aβ and reduce the deposition of Aβ in the brain. Efficient in situ hydrogen production therapy combined with multitarget synergism solves the problem of a poor therapeutic effect of a single target. In vivo studies have shown that UCNP@CoP@g-C₃N₄ can reduce Aβ deposition, improve memory impairment, and reduce neuroinflammation in AD mice.