22 results for “Developmental Neurotoxicity”. Showing 22 of 39,449.
Fenobucarb-induced developmental neurotoxicity and mechanisms in zebrafish.
developmental neurotoxicity and the underlying mechanisms have not been well
Maresin 1 alleviates sevoflurane-induced neuroinflammation in neonatal rats via JAK2/STAT3/IL-6 pathways.
Developmental neurotoxicity is a serious consequence of repeated exposure to sevoflurane
PM2.5 induces developmental neurotoxicity in cortical organoids.
developmental neurotoxicity in humans remain obscure. To address this research
Developmental neurotoxicity of PFOA exposure on hiPSC-derived cortical neurons.
developmental stages, with increased risks of neurodegenerative diseases (NDs). The neurotoxic
Boosting Microglial Lipid Metabolism via TREM2 Signaling by Biomimetic Nanoparticles to Attenuate the Sevoflurane-Induced Developmental Neurotoxicity.
neurotoxicity that can potentially affect the learning and memory function in the developmental
Organophosphates modulate tissue transglutaminase activity in differentiated C6 neural cells.
developmental neurotoxicity and neurodegeneration. However, the underlying mechanism remains unclear
Sevoflurane exposure triggers ferroptosis of neuronal cells initiated by the activation of ATM/p53 in the neonatal mouse brain via JNK/p38 MAPK-mediated oxidative DNA damage.
developmental neurotoxicity caused by the volatile anesthetic sevoflurane in the neonatal
Late effect of developmental exposure to glycidol on hippocampal neurogenesis in mice: Loss of parvalbumin-expressing interneurons.
developmental exposure to the same neurotoxic substances. In the present
The synergistic effects of UV-328 and polystyrene microplastics on zebrafish embryos: developmental toxicity, oxidative stress, and neurotoxicity.
developmental toxicity in zebrafish larvae and triggered oxidative stress responses. Transcriptome analysis and qRT-PCR validation showed co-activation of the peroxisome pathway and FoxO signaling pathway as compensatory antioxidant
Dose-dependent developmental fluoride exposure leads to neurotoxicity and impairs excitatory synapse development
Long-Term Neuropsychiatric Developmental Defects after Neonatal Organophosphate Exposure: Mitigation by Synthetic Neurosteroids.
neurotoxic effects of organophosphate (OP) pesticides and nerve agents than adults. OP poisoning in children leads to acute seizures and neuropsychiatric sequela, including the development of long-term disabilities
Brain Endothelial Cells in Blood-Brain Barrier Regulation and Neurological Therapy.
neurotoxic effects in the brain parenchyma and exacerbating neurodegeneration and disease progression. This review systematically summarizes the developmental
Integrated Behavioral and Proteomic Characterization of MPP+-Induced Early Neurodegeneration and Parkinsonism in Zebrafish Larvae.
neurotoxicity in zebrafish larvae, supporting its use as a relevant in vivo system to investigate early-stage Parkinson's disease mechanisms and shared neurodegenerative pathways, as well as for screening
Presenilins, the endoplasmic reticulum, and neuronal apoptosis in Alzheimer's disease.
developmental role for PSs in the nervous system. When expressed in cultured cells and transgenic mice, mutant PSs promote increased production of a long form of amyloid beta-peptide
Cell Biology and Pathophysiology of α-Synuclein.
developmental expression pattern, its cellular and subcellular localization, and its function in neurons. We also discuss recent progress on secretion of α-synuclein, which may contribute to its interneuronal spread
Autophagy and ethanol neurotoxicity.
developmentally regulated; their levels are much lower during an ethanol-sensitive period than during an ethanol-resistant period. Ethanol may stimulate autophagy through multiple mechanisms; these include induction of oxidative
Linking particulate matter exposure and neurological disorders: Evidence from epidemiology, biomarkers and mechanistic studies.
neurotoxic metals (e.g., lead, cadmium, vanadium) and understudied organic toxicants (e.g., PAHs, pesticides), amplifying its pathogenic potential. Exposure occurs through the olfactory route, systemic circulation, and gut-brain axis, highlighting
Analyzing different aging theories in the context of the brain: DNA damage, inflammation, redox imbalance, and neurodevelopment intertwine.
developmental process. Key points include (i) the resilience of the neuronal tissue to oxidative stress; (ii) the neuron's efficiency in repairing learning-induced DNA damage, even with fewer repair
Predifferentiation Neurotoxicity of GenX Exposure on hiPSC-Derived Cortical Neurons.
neurotoxic effects utilizing human induced pluripotent stem cell (hiPSC)-derived cortical neurons. Neurons exposed to 0.4 and 4 ppb GenX prior to differentiation possess altered neuronal characteristics including synaptic density
CD11c+ microglia: From basic research to clinical application.
neurotoxicity and promoting a repair environment. The current consensus is that specific microenvironmental cues, particularly hazard signaling molecules (DAMPs) and cytokines (such as interferon-γ), are the main drivers
A review of the putative antiseizure and antiepileptogenic mechanisms of action for soticlestat.
developmental and epileptic encephalopathies, and two phase III studies evaluating the safety and efficacy of soticlestat in Dravet syndrome (SKYLINE) and Lennox-Gastaut syndrome (SKYWAY) have recently been completed
β-Secretase BACE1 Is Required for Normal Cochlear Function.
neurotoxic amyloid-β peptides, which is widely considered an essential pathogenic mechanism in Alzheimer's disease (AD). Here, we report that BACE1 is essential for normal auditory function. Compared with