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224 results for “neurotoxicity”
Identifying Unexpected Neurotoxicity Drivers with Acetylcholinesterase Inhibition by Virtual Effect-Directed Analysis in Nationwide Estuarine Waters
<p><span>Neurotoxicity is frequently observed in the global aquatic environment, </span><span>threatening aquatic ecosystems and human health</span><span>. </span><span>However, </span><span>a very limited proportion of neurotoxic effects (~1%) has been explained by known chemicals of concern. Here, we integrated</span><span> machine learning, nontargeted analysis, and <em>in vitro</em> biotesting</span><span> to identify neurotoxic drivers of acetylcholinesterase (AChE) inhibition in estuarine waters along the coastline of China. Machine learning was used as a virtual fractionation tool to reduce the complexity of chemical mixtures, thus guiding nontargeted screening of AChE inhibitors. Ultimately, sixty chemicals with diverse </span><span>known and presently unknown</span><span> structures were identified, explaining 82.1% of the observed AChE inhibition </span><span>in estuarine water samples</span><span>. Polyunsaturated fatty acids were unexpectedly found to be neurotoxic drivers, accounting for 80.5% of the overall effect. This proof-of-concept study demonstrates that our approach enables rapid and comprehensive screening of </span><span>causative organic pollutants</span><span> </span><span>associated with various <em>in vitro</em> endpoints </span><span>for large-scale monitoring of water quality</span><span>.</span></p>
The effects of PaPE-1 on amyloid beta-induced neurotoxicity
<p>Data related to the article Posttreatment with PaPE-1 Protects from Aβ-Induced Neurodegeneration Through Inhibiting the Expression of Alzheimer's Disease-Related Genes and Apoptosis Process That Involves Enhanced DNA Methylation of Specific Genes. These are biochemical, molecular and microscopic data. We aimed to verify the neuroprotective capacity of PaPE-1 against amyloid beta (Aβ)-induced toxicity. Fig 1 – the presence of amyloid beta in cellular cultures; Fig 2 – the effects of apoptosis inhibitors on amyloid beta-induced caspase-3 activity; Fig 3 – the effects of amyloid beta and PaPE-1 on caspase -3, -8, and -9 activities; Fig 4 – effects of amyloid beta and PaPE-1 on Calcein AM and Hoechst 33342 staining; Fig 5 – effects of amyloid beta and PaPE-1 on expression of apoptosis related factors; Fig 6 – effects of amyloid beta and PaPE-1 on methylation of specific genes; Fig 7 – effects of amyloid beta and PaPE-1 on the degree of neurodegeneration; Fig 8 - effects of amyloid beta and PaPE-1 on the membrane stain; Fig 9 - effects of amyloid beta and PaPE-1 on the expression of Alzheimer’s disease-related genes.</p>
A Phase 2 Trial of Anakinra for the Prevention of CAR-T Cell Mediated Neurotoxicity
ClinicalTrials.gov study NCT04150913. IPD Sharing: YES. Countries: 1. Publications: 1.
Comparison of physiologically based pharmacokinetic modeling platforms for developmental neurotoxicity in vitro to in vivo extrapolation
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The nuclear import receptor Kapβ2 modifies neurotoxicity mediated by poly(GR) in C9orf72-linked ALS/FTD
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Neurotoxicity of an HBV Transcript Inhibitor in 13-Week Rat and Monkey Studies
<p>Supplemental Tables 1-7 for the manuscript<br> "Neurotoxicity of an HBV Transcript Inhibitor in 13-Week Rat and Monkey Studies"</p>
Differences in neurotoxic outcomes of organophosphorus pesticides revealed via multi-dimensional screening in adult and regenerating planarians
<p>Organophosphorus pesticides (OPs) are a chemically diverse class of commonly used insecticides. Epidemiological studies suggest that low dose chronic prenatal and infant exposures can lead to life-long neurological damage and behavioral disorders. While inhibition of acetylcholinesterase (AChE) is the shared mechanism of acute OP neurotoxicity, OP-induced developmental neurotoxicity (DNT) can occur independently and/or in the absence of significant AChE inhibition, suggesting alternative targets. Moreover, different OPs can cause different adverse outcomes, suggesting that different OPs act through different mechanisms, emphasizing the importance of comparative studies of OP toxicity. Freshwater planarians are an invertebrate system that uniquely allows for automated, rapid and inexpensive testing of adult and developing organisms in parallel to differentiate neurotoxicity from DNT. Effects found only in regenerating planarians would be indicative of DNT, whereas shared effects may represent general neurotoxicity. We leverage this feature to investigate potential differential effects of these OPs on the adult and developing brain by performing a comparative high-throughput screen to test 7 OPs (acephate, chlorpyrifos, dichlorvos, diazinon, malathion, parathion and profenofos) across 10 concentrations in quarter-log steps. Neurotoxicity was evaluated using a wide range of quantitative morphological and behavioral readouts. AChE activity was measured using an Ellman assay. The toxicological profiles of the 7 OPs differed across the OPs and between adult and regenerating planarians. Toxicological profiles were not correlated with levels of AChE inhibition. Twenty-two "mechanistic control compounds" known to target pathways suggested in the literature to be affected by OPs (cholinergic neurotransmission, serotonin neurotransmission, endocannabinoid system, cytoskeleton, adenyl cyclase and oxidative stress) and 2 negative controls were also screened. When compared with the mechanistic control compounds, the phenotypic profiles of the different OPs separated into distinct clusters. The phenotypic profiles of adult vs regenerating planarians exposed to the OPs clustered differently, suggesting some developmental-specific mechanisms. These results further support findings in other systems that OPs cause different adverse outcomes in the (developing) brain and build the foundation for future comparative studies focused on delineating the mechanisms of OP neurotoxicity in planarians.</p>
Transcriptomic characterization of 2D and 3D human induced pluripotent stem cell-based in vitro models as New Approach Methodologies for developmental neurotoxicity testing
<p><strong>Abstract:</strong> The safety and developmental neurotoxicity (DNT) potential of chemicals remain critically understudied due to limitations of current in vivo testing guidelines, which are low throughput, resource-intensive, and hindered by species differences that limit their relevance to human health. To address these issues, robust new approach methodologies (NAMs) using deeply characterized cell models are essential. This study presents the comprehensive transcriptomic characterization of two advanced human-induced pluripotent stem cell (hiPSC)-derived models: a 2D adherent and a 3D neurosphere model of human neural progenitor cells (hiNPCs) differentiated up to 21 days. Using high-throughput RNA sequencing, we compared gene expression profiles of 2D and 3D models at three developmental stages (3, 14, and 21 days of differentiation). Both models exhibit maturation towards post-mitotic neurons, with the 3D model maturing faster and showing a higher prevalence of GABAergic neurons, while the 2D model is enriched with glutamatergic neurons. Both models demonstrate broad applicability domains, including excitatory and inhibitory neurons, astrocytes, and key endocrine and especially the understudied cholinergic receptors. Comparison with human fetal brain samples confirms their physiological relevance. This study provides novel in-depth applicability insights into the temporal and dimensional aspects of hiPSC-derived neural models for DNT testing. The complementary use of these two models is highlighted: the 2D model excels in synaptogenesis assessment, while the 3D model is particularly suited for neural network formation as observed as well in previous functional studies with these models. This research marks a significant advancement in developing human-relevant, high-throughput DNT assays for regulatory purposes.</p> <p><strong>This data sets contains:</strong></p> <p><strong>Tab. S1</strong> - Significant genes results</p> <p><strong>Tab. S2</strong> - Enriched pathways_GO_Biological Processes</p> <p><strong>Tab. S3</strong> - Enriched pathways_GO_Cellular Components</p> <p><strong>Tab. S4</strong> - Enriched pathways_GO_Molecular Function</p> <p><strong>Tab. S5</strong> - Enriched pathways_KEGG</p> <p><strong>Tab. S6</strong> - EnrichEnriched pathways_Panther</p> <p><strong>Tab. S7</strong> - Enriched pathways_Reactome</p> <p><strong>Tab. S8</strong> - Gene counts</p> <p><strong>Tab. S9</strong> - Gene selection for targeted analysis</p>
Figure 6 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2-methoxyethanol
Figure 6. Treatment Group with resveratrol standard after induced by Beta-Amyloid (10 x10).
Figure 3 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2-methoxyethanol
Figure 3. Treatment group: 2- ME + Resveratrol isolated from Tempeh (10 x10).
Figure 8 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2-methoxyethanol
Figure 8. Treatment Group with resveratrol tempeh + 2-ME after induced by Beta-Amyloid (10 x10).
Figure 5 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2-methoxyethanol
Figure 5. Treatment group: 2- ME (10 x10).
Figure 9. Treatment Group with 2 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2-methoxyethanol
Figure 9. Treatment Group with 2-ME after induced by Beta-Amyloid (10 x10).
Figure 2 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2-methoxyethanol
Figure 2. Treatment group: 2- ME + Resveratrol Standard (10 x10).
Figure 1 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2-methoxyethanol
Figure 1. Control Group (10 x10).
Table 4 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2 - methoxyethanol
<p><b>Table 4.</b> Cytotoxic effect of various concentrations of Resveratrol and 2-Methoxyethanol Against Primary Neuron cell viability in MTT assay (570 nm).</p><table><tbody><tr><th><b>% Inhibition</b></th></tr></tbody><tbody><tr><th><b>Concentration of 2-Methoxyethanol</b></th><td><b>2-ME (10mM)</b></td><td><b>2-ME (10mM)</b></td><td><b>2-ME (10mM)</b></td></tr><tr><th><b>and Resveratrol</b></th><td><b>Resveratrol (Standard)</b></td><td><b>Resveratrol (Tempeh)</b></td><td><b>Resveratrol (Soybean Seed Coat)</b></td></tr><tr><th>IC50</th><td>(17.38 ± 0.99 µg/mL)</td><td>(31.14 ± 0.02 µg/mL)</td><td>(13.40 ± 0.30 µg/mL)</td></tr><tr><th>1.4 (µg/mL)</th><td>12.57</td><td>0</td><td>11.98</td></tr><tr><th>2.8 (µg/mL)</th><td>4.59</td><td>1.75</td><td>17.03</td></tr><tr><th>4.2 (µg/mL)</th><td>0</td><td>0</td><td>0</td></tr></tbody></table>
Table 3 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2 - methoxyethanol
<p><b>Table 3.</b> Cytotoxic effect of various concentrations of Resveratrol and 2-Methoxyethanol Against Primary Neuron cell viability in MTT assay (540 nm).</p><table><tbody><tr><th><b>% Inhibition</b></th></tr></tbody><tbody><tr><th><b>Concentration of 2-Methoxyethanol</b></th><td><b>2-ME (10mM)</b></td><td><b>2-ME (10mM)</b></td><td><b>2-ME (10mM)</b></td></tr><tr><th><b>and Resveratrol</b></th><td><b>Resveratrol (Standard)</b></td><td><b>Resveratrol (Tempeh)</b></td><td><b>Resveratrol (Soybean Seed Coat)</b></td></tr><tr><th>IC50</th><td>(17.64 ± 0.99 µg/mL)</td><td>(32.22 ± 1.18 µg/mL)</td><td>(17.43 ± 0.16 µg/mL)</td></tr><tr><th>1.4 (µg/mL)</th><td>11.8</td><td>0</td><td>7.95</td></tr><tr><th>2.8 (µg/mL)</th><td>5.27</td><td>0</td><td>14.41</td></tr><tr><th>4.2 (µg/mL)</th><td>0</td><td>0</td><td>0</td></tr></tbody></table>
Table 2 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2 - methoxyethanol
<p><b>Table 2.</b> Effect of Various concentrations of Resveratrol and 2-Methoxyethanol against Primary Neuron cell viability (570 nm).</p><table><tbody><tr><th><b>% Cell Viability</b></th></tr></tbody><tbody><tr><th><b>Concentration of 2-Methoxyethanol</b></th><td><b>2-ME (10mM)</b></td><td><b>2-ME (10mM)</b></td><td><b>2-ME (10mM)</b></td></tr><tr><th><b>and Resveratrol</b></th><td><b>Resveratrol (Standard)</b></td><td><b>Resveratrol (Tempeh)</b></td><td><b>Resveratrol (Soybean Seed Coat)</b></td></tr><tr><th>1.4 (µg/mL)</th><td>87.43</td><td>100</td><td>88.02</td></tr><tr><th>2.8 (µg/mL)</th><td>95.41</td><td>98.25</td><td>82.97</td></tr><tr><th>4.2 (µg/mL)</th><td>100</td><td>100</td><td>100</td></tr></tbody></table>
Table 1 in Potential neuroprotective of trans-resveratrol a promising agent tempeh and soybean seed coats-derived against beta-amyloid neurotoxicity on primary culture of nerve cells induced by 2 - methoxyethanol
<p><b>Table 1.</b> Effect of Various concentrations of Resveratrol and 2-Methoxyethanol against Primary Neuron cell viability (540 nm).</p><table><tbody><tr><th><b>% Cell Viability</b></th></tr></tbody><tbody><tr><th><b>Concentration of 2-Methoxyethanol</b></th><td><b>2-ME (10mM)</b></td><td><b>2-ME (10mM)</b></td><td><b>2-ME (10mM)</b></td></tr><tr><th><b>and Resveratrol</b></th><td><b>Resveratrol (Standard)</b></td><td><b>Resveratrol (Tempeh)</b></td><td><b>Resveratrol (Soybean Seed Coat)</b></td></tr><tr><th>1.4 (µg/mL)</th><td>88.2</td><td>100</td><td>92.05</td></tr><tr><th>2.8 (µg/mL)</th><td>94.73</td><td>100</td><td>85.59</td></tr><tr><th>4.2 (µg/mL)</th><td>100</td><td>100</td><td>100</td></tr></tbody></table>
Calcium Gluconate and Magnesium Sulfate in Preventing Neurotoxicity Caused By Oxaliplatin in Patients Receiving Combination Chemotherapy for Stage II, Stage III, or Stage IV Colorectal Cancer That Has
ClinicalTrials.gov study NCT00316914. IPD Sharing: Not stated. Countries: 1. Publications: 2.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.