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Reasonable design of the nanostructure of heterogeneous photocatalysts is of great significance for improving their performance and stability. We report the design and fabrication of hollow sandwich-layered octahedral Cu2–x S/CdS/Bi2S3 p–n–p type tandem heterojunctions constructed via the continuous growth deposition method on the surface of hollow octahedral Cu2–x S with well-defined structures and interfaces. The unique hollow sandwich nanostructure has a large specific surface area and abundant reaction sites and enhances the separation and transfer of photogenerated carriers. In addition, the formation of a p–n–p heterojunction coupled with the surface plasmon resonance effect of Cu2–x S could also aid in photocatalytic H2 evolution performance and photocatalytic degradation efficiency. Under vis–NIR light irradiation, the optimized Cu2–x S/CdS/Bi2S3 photocatalyst displays a notable H2 production rate of 8012 μmol h–1 g–1, and 2,4-dichlorophenol is almost completely photocatalytically degraded in 150 min. This strategy and rational design offer a new path toward the design of specific nanocatalysts with enhanced activity and stability and challenging reactions.

Haploinsufficiency of the protein kinase Tbk1 has shown to cause both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD); however, the pathogenic mechanisms are unclear. Here we show that conditional neuronal deletion of Tbk1 in leads to cognitive and locomotor deficits in mice. Tbk1-NKO mice exhibited numerous neuropathological changes, including neurofibrillary tangles, abnormal dendrites, reduced dendritic spine density, and cortical synapse loss. The Purkinje cell layer of the cerebellum presented dendritic swelling, abnormally shaped astrocytes, and p62- and ubiquitin-positive aggregates, suggesting impaired autophagy. Inhibition of autophagic flux with bafilomycin A increased total Tkb1 levels in motor neuron-like cells in vitro , suggesting autophagy-dependent degradation of Tbk1. Although Tbk1 over-expression did not affect mutant SOD1 levels in SOD1 G93A -transfected cells, it increased the soluble/insoluble ratio and reduced the number and size of SOD1 G93A aggregates. Finally, in vivo experiments showed that Tkb1 expression was reduced in SOD1 G93A ALS transgenic mice, which showed decreased p62 protein aggregation and extended survival after ICV injection of adeno-associated viral vectors encoding Tbk1. These data shed light on the neuropathological changes that result from Tbk1 deficiency and hint at impaired autophagy as a contributing factor to the cognitive and locomotor deficits that characterize FTD-ALS in patients with Tkb1 haploinsufficiency.