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Alzheimer's disease (AD), a common neurodegenerative disease, is the main cause of dementia, with cognitive decline as the core symptom observed during diagnosis. Synaptic loss may be the main cause of early cognitive dysfunction in AD, but the detailed mechanism is still unclear. In this study, we investigated the role of abnormal miR-455–5p/CPEB1 pathway in AD mouse model. We found that miR-455–5p was upregulated, while its downstream target, cytoplasmic polyadenylation element-binding 1 (CPEB1), was downregulated in the hippocampus of APP/PS1 mice at the age of 9 m. Abnormal miR-455–5p/CPEB1 pathway mediated cognitive deficits in APP/PS1 mice through suppressing α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor expressions. And miR-455–5p suppression, CPEB1 overexpression or application of a peptide disrupting the miR-455–5p/CPEB1 interaction in CA1 of APP/PS1 mice rescued AD-like phenotypes in mice, including deficits in synaptic plasticity and memory. In conclusion, our results indicated that miRNA-455–5p/CPEB1 pathway mediated synaptic and memory deficits in Alzheimer's Disease through targeting on AMPARs, providing a potential therapeutic strategy for AD. • MiR-455–5p/CPEB1 pathway mediated synaptic and memory deficits in APP/PS1 mice. • MiR-455–5p suppression through antagomirs or CPEB1 overexpression rescued synaptic and memory deficits. • Application of peptides to disrupt interaction between miR-455–5p and CPEB1 rescued synaptic and memory deficiency. • CPEB1 decrease in APP/PS1 mice mediates Aβ-related synaptic failure through broadly suppressing AMPAR expressions. [ABSTRACT FROM AUTHOR]

• The Mo-doped Bi2S3 materials with nanorod-linked sphere were fabricated. • Doping and nanostructure synchronously improve the conductivity of Bi2S3. • The nanorod-crosslinked sphere delivers superior structure durability. Although zinc-ion batteries express superior advantages included great safety and cost-effectiveness for grid-level energy storage, the electrode materials are still suffering from structural collapse and depressed kinetics. Fortunately, these defects can be effectively improved by the combination of structure engineering and composition regulation, which is an effective strategy for improving electrochemical reaction kinetics and structure tolerance. Thereof, the Mo-doped Bi 2 S 3 materials with nanorod-linked spherical framework have been constructed in this work. The introduction of Mo-heteroatom can optimize the electronic structure of Bi 2 S 3 for strengthening its conductivity, which contributes to obtain the enhanced reaction kinetics. Furthermore, this trend can be boosted by the design of nanorod-assembled sphere, which effectually reduces the ion diffusion path. In addition, the shaggy sphere possesses the ability of stress dispersion, contributing to maintain the structure integrity during charging/discharging process. As expected, this designed electrode materials exhibit a superior reversibility capacity of 51.0 mA h g − 1 over 1000 cycles at 2000 mA g − 1, and a prominent high-rate capacity of 93.7 mA h g − 1 at the enlarged rate of 6000 mA g − 1. Importantly, this present research will enlighten the combined modification strategy to engineering metal sulfides for high-performance zinc-ion batteries. [Display omitted] The introduction of Mo-atom in Bi 2 S 3 can strengthen its reaction kinetics derived from the generated defect energy level and increased holes, and the designed nanorods will enhance the trend for further. Meanwhile, constructing nanorod-crosslinked sphere can effectively restrain the reaction-induced stress concentration, heightening the structure durability. Benefitting from the above advantages, the modified Bi 2 S 3 achieves a superior reversible capacity with prominent cycling stability. [ABSTRACT FROM AUTHOR]

Current clinical practice primarily relies on surgical intervention to remove hematomas in patients with intracerebral hemorrhage (ICH), given the lack of effective drug therapies. Previous research indicates that simvastatin (SIM) may enhance hematoma absorption and resolution in the acute phase of ICH, though the precise mechanisms remain unclear. Recent findings have highlighted the glymphatic system (GS) as a crucial component in intracranial cerebrospinal fluid circulation, playing a significant role in hematoma clearance post-ICH. This study investigates the link between SIM efficacy in hematoma resolution and the GS. Our experimental results show that SIM alleviates GS damage in ICH-induced rats, resulting in improved outcomes such as reduced brain edema, neuronal apoptosis, and degeneration. Further analysis reveals that SIM's effects are mediated through the VEGF-C/VEGFR3/PI3K-Akt pathway. This study advances our understanding of SIM's mechanism in promoting intracranial hematoma clearance and underscores the potential of targeting the GS for ICH treatment. • Simvastatin intervention accelerates hematoma resolution in intracerebral hemorrhage rats. • Simvastatin repairs the damaged glymphatic system post-intracerebral hemorrhage. • Glymphatic system protection is promising for intracerebral hemorrhage treatment. [ABSTRACT FROM AUTHOR]