BTVT ameliorates offspring bloodbrain barrier damage induced by prenatal and lactational neodymium oxide exposure via the gutbrain axis.

Objectives: Exposure to rare earth elements (REEs) has been linked to various systemic diseases, but their impact on the offspring blood-brain barrier (BBB) via the gut-brain axis remains unclear. This study aims to investigate the effects of maternal exposure to neodymium oxide (NdO) on the BBB integrity of offspring rats, and to evaluate the potential protective role of bifidobacterium tetrad viable tablets (BTVT) against NdO-induced intestinal and BBB damage.

Methods: Healthy adult SD rats were mated at a 1:1 male-to-female ratio, with the day of vaginal plug detection marked as gestational day 0.

Vps34 knockdown attenuated AlNPs-induced neurodevelopmental toxicity in zebrafish larvae and adults by inhibiting mitophagy.

Nano-alumina (AlNPs) are susceptible to inducing neurotoxicity, mainly through excessive autophagy/mitophagy. Vacuolar protein sorting 34 (Vps34) is a target for modulating autophagy. This study aimed to investigate whether Vps34 knockdown could reduce AlNPs' neurodevelopmental toxicity.

A bidirectional pedestrian macroscopic speed model construction based on pedestrian microscopic simulation experiments.

Studies of macroscopic speed modeling of bidirectional pedestrian cross-flows have relied heavily on scenario experiments, but the data itself may be deficient because large-scale scenario experiments are not easy to organize and subjects may not be walking under normal conditions. In order to explore the possibility of using microscopic pedestrian flow simulations for macroscopic speed modeling of pedestrian flows, a series of two-way pedestrian cross-flow simulation experiments were designed. Bidirectional pedestrian flows are defined as Peds1 and Peds2.

The downregulation of TREM2 exacerbates toxicity of development and neurobehavior induced by aluminum chloride and nano-alumina in adult zebrafish.

To investigate the difference in the development and neurobehavior between aluminum chloride (AlCl) and nano-alumina (AlNPs) in adult zebrafish and the role of triggering receptor expressed on myeloid cells (TREM2) in this process. Zebrafish embryos were randomly administered with control, negative control, TREM2 knockdown, AlCl, TREM2 knockdown + AlCl, AlNPs, and TREM2 knockdown + AlNPs, wherein AlCl and AlNPs were 50 mg/L and TREM2 knockdown was achieved by microinjecting lentiviral-containing TREM2 inhibitors into the yolk sac. We assessed development, neurobehavior, histopathology, ultrastructural structure, neurotransmitters (AChE, DA), SOD, genes of TREM2 and neurodevelopment (α1-tubulin, syn2a, mbp), and AD-related proteins and genes.

Simultaneous effects of aluminum exposure on the homeostasis of essential metal content in rat brain and perturbation of gut microbiota.

The theory of the brain-gut axis has confirmed that gut microbiota and metabolites are involved in the progression of neurodegenerative diseases through multiple pathways. However, few studies have highlighted the role of gut microbiota in cognitive impairment induced by aluminum (Al) exposure and its correlations with the homeostasis of essential metal content in the brain. To explore the relationship between alterations in the content of essential metals in the brain and relative abundance changes in gut microbiota induced by Al exposure, the Al, zinc (Zn), copper (Cu), iron (Fe), chromium (Cr), manganese (Mn), and cobalt (Co) content level in the hippocampus, olfactory bulb, and midbrain tissue were measured by inductively coupled plasma mass spectrometry (ICP-MS) methods after Al maltolate was intraperitoneally injected every other day for exposed groups.

Involvement of Mitophagy in Primary Cultured Rat Neurons Treated with Nanoalumina.

The aim of this study was to explore the influence of the neurotoxicity of nanoalumina on primarily cultured neurons. Normal control, particle size control, aluminum, micron-alumina, and nanoalumina at 50-nm and 13-nm particle sizes were included as subjects to evaluate the level of apoptosis, necrosis, and autophagy in primarily cultured neurons and further explore the mitophagy induced by nanoalumina. The results demonstrated that nanoalumina could induce neuronal cell apoptosis, necrosis, and autophagy, among which autophagy was the most notable.

Necrostatin-1 Relieves Learning and Memory Deficits in a Zebrafish Model of Alzheimer's Disease Induced by Aluminum.

Aluminum (Al) is considered one of the environmental risk factors for Alzheimer's disease (AD). The present study aims to establish a zebrafish AD model induced by Al and explore if necrostation-1 (Nec-1), a specific inhibitor of necroptosis, is effective in relieving learning and memory deficits in the zebrafish AD models. We treated adult zebrafish with aluminum trichloride at various doses for 1 month, followed by a T-maze test to evaluate learning and memory performance.

Neurodevelopmental toxicity of alumina nanoparticles to zebrafish larvae: Toxic effects of particle sizes and ions.

The aim of this study was to explore the mechanism of neurodevelopmental toxicity of alumina nanoparticles (AlNPs) on zebrafish larvae, specifically, the toxic effects of AlNPs of different particle sizes and of dissolved aluminum ions. AlNPs with sizes of 13 nm (13 nm-Al) and 50 nm (50 nm-Al) were used as the main research objects; while nanocarbon particles with sizes of 13 nm (13 nm-C) and 50 nm (50 nm-C) as particle-size controls; and an aluminum chloride solution (Al) as an ion control. Zebrafish embryos were exposed to different treatments from 6 h post-fertilization (hpf) to 168 hpf.

Increased aluminum and lithium and decreased zinc levels in plasma is related to cognitive impairment in workers at an aluminum factory in China: A cross-sectional study.

Background: Previous studies have shown that multiple imbalances of metal ions in the brain are closely associated with the neurodegenerative disorders. Our studies have shown that long-term working exposure to aluminum induces increased plasma aluminum levels and causes cognitive impairment in workers at aluminum factories.

Objective: To explore the levels of nine metals in plasma and the effect on cognitive function among in-service workers.

Involvement of Mitophagy in Aluminum Oxide Nanoparticle-Induced Impairment of Learning and Memory in Mice.

Aluminum oxide nanoparticles (nano-aluminum) have been known to be widespread in the environment for decades. Exposure to nano-aluminum may impair learning and memory, but the potential mechanism has not yet been elucidated. In neurons, efficient clearance of damaged mitochondria through mitophagy plays an important role in mitochondrial energy supply, neuronal survival, and health.