An oriented single-crystalline TiO 2 nanorod or wire array on transparent conductive substrates would be the most desirable nanostructure in preparing photoelectrochemical solar cells because of its efficient charge separation and transport properties as well as superior light harvesting efficiency. In this study, a TiO 2 nanorod array film grown directly on transparent conductive glass (FTO) was prepared by a simple hydrothermal method. The formation of CdS quantum dots (QDs) on the vertically aligned TiO 2 nanorods photoelectrode was carried out by chemical bath deposition. The as-prepared materials were characterized by scanning electron microscopy, transmission electron microscopy (TEM), high-resolution TEM, and X-ray diffraction. The results indicate that CdS QDs with a diameter smaller than 10 nm are uniformly covered on the surface of the single-crystalline TiO 2 nanorods. Under AM 1.5 G illumination, the photoelectrode was found with a photocurrent intensity of 5.778 mA/cm 2 at a potential of 0 V versus Ag/AgCl and an open-circuit photovoltage of 1.292 V versus Ag/AgCl. The photocurrent is 28.6 times higher than that of a bare TiO 2 nanorod array, and the photoelectrochemical properties are comparable to those of a CdS QDs-sensitized TiO 2 nanotube array, suggesting that the CdS QDs-sensitized TiO 2 nanorod array on FTO photoelectrodes has a potential application in solar cells.
Tau pathology was recently identified as a key driver of disease progression and an attractive therapeutic target in Alzheimer's disease (AD). Selenomethionine (Se-Met), a major bioactive form of selenium (Se) in organisms with significant antioxidant capacity, reduced the levels of total tau and hyperphosphorylated tau and ameliorated cognitive deficits in younger triple transgenic AD (3xTg-AD) mice. Whether Se-Met has a similar effect on tau pathology and the specific mechanism of action in older 3xTg-AD mice remains unknown. Autophagy is a major self-degradative process to maintain cellular homeostasis and function. Autophagic dysfunction has been implicated in the pathogenesis of multiple age-dependent diseases, including AD. Modulation of autophagy has been shown to retard the accumulation of misfolded and aggregated proteins and to delay the progression of AD. Here, we found that 3xTg-AD mice showed significant improvement in cognitive ability after a 3-month treatment with Se-Met beginning at 8 months of age. In addition to attenuating the hyperphosphorylation of tau by modulating the activity of Akt/glycogen synthase kinase-3 and protein phosphatase 2A, Se-Met-induced reduction of tau was also mediated by an autophagy-based pathway. Specifically, Se-Met improved the initiation of autophagy via the AMP-activated protein kinase-mTOR (mammalian target of rapamycin) signaling pathway and enhanced autophagic flux to promote the clearance of tau in 3xTg-AD mice and primary 3xTg neurons. Thus, our results demonstrate for the first time that Se-Met mitigates cognitive decline by targeting both the hyperphosphorylation of tau and the autophagic clearance of tau in AD mice. These data strongly support Se-Met as a potent nutraceutical for AD therapy.
Disruption of the intracellular balance between free radicals and the antioxidant system is a prominent and early feature in the neuropathology of Alzheimer's disease (AD). Selenium, a vital trace element with known antioxidant potential, has been reported to provide neuroprotection through resisting oxidative damage but its therapeutic effect on AD remains to be investigated. The objective of our study was to investigate the potential of selenomethionine (Se-Met), an organic form of selenium, in the treatment of cognitive dysfunction and neuropathology of triple transgenic AD (3 × Tg-AD) mice. 3 × Tg-AD mice, which were four months old, were treated with Se-Met for 3 months and demonstrated significant improvements in cognitive deficit along with an increased selenium level compared with the untreated control mice. Se-Met treatment significantly reduced the level of total tau and phosphorylated tau, mitigated the decrease of synaptic proteins including synaptophysin and postsynaptic density protein 95 in the hippocampus and cortex of the 3 × Tg-AD mice. Meanwhile, glial activation in AD mice was inhibited and the level of reduced glutathione was increased in the treated mice compared with control mice. Additionally, the expression and activity of glycogen synthase kinase 3β and protein phosphatase 2A, two important enzymes involved in tau phosphorylation, were markedly decreased and increased respectively by Se-Met treatment. Thus Se-Met improves cognitive deficit in a murine model of AD, which is associated with reduction in tau expression and hyperphosphorylation, amelioration of inflammation, and restoration of synaptic proteins and antioxidants. This study provides a novel therapeutic approach for the prevention of AD.
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