Articles tagged with Neurotoxicity
Researchers from the University of Rochester's TraCe-bMPS have developed tissue chips that can predict dangerous immune reactions to cancer therapies. The technology, which uses human cells and sensors, has been accepted into the FDA's Innovative Science and Technology Approaches for New Drugs pilot program.
Researchers found specific combinations of blood proteins from western diamondback rattlesnakes provided unprecedented neutralizing power against multiple dangerous snake species. Combining several FETUA proteins dramatically increased ability to neutralize venom's damaging effects.
Scientists at the University of Virginia Health System have developed a suite of AI-powered tools, called YuelDesign, YuelPocket and YuelBond, to transform how new drugs are created. These tools can design drug molecules tailored to fit their protein targets exactly, even accounting for protein flexibility.
Researchers used Caenorhabditis elegans to model chemotherapy-induced neurological dysfunction and tested two compounds for improved recovery. Both sildenafil citrate and Resveramorph-3 significantly reduced seizure-like behaviors and duration, suggesting their potential as therapeutic candidates.
A rare case of hyperammonemic encephalopathy caused by 5-fluorouracil (5-FU) chemotherapy has been reported, highlighting the importance of monitoring neurological symptoms in patients receiving 5-FU. The patient's symptoms resolved after stopping 5-FU and administering lactulose and intravenous fluids.
Researchers used integrated strategy to assess neurotoxicity of environmental chemicals, identifying six core proteins as targets. Exposure to low levels of nicotine stunted growth and triggered abnormal behaviors in zebrafish larvae.
Researchers will investigate how HIV and cancer drugs damage brain cells over time, identifying potential early biomarkers of neurotoxicity. They will use human brain organoids grown in the lab to mimic brain physiology.
The study found that S. birrea extract reversed behavioral alterations caused by monosodium glutamate, reduced oxidative stress parameters, and counteracted malondialdehyde levels. These results support the potential of S. birrea as a neuroprotective agent for preventing and treating cognitive deficits.
A study by Wake Forest University School of Medicine reveals that a stress response in immune cells contributes to chemotherapy-induced nerve damage. By blocking this pathway, researchers aim to develop new treatments to protect cancer patients from debilitating side effects.
Researchers develop efficient testing procedure to quickly detect neurotoxic effects in humans, closing the gap with traditional animal experiments. Chlorophene is identified as a substance that disrupts learning and memory processes, exhibiting paradoxical excitation, a previously unknown effect.
A team of researchers from Goethe University and Kiel University has discovered a way to prevent the formation of harmful protein aggregates in cultured cells. The study found that linking TDP-43 with SUMO prevents its aggregation, suggesting a potential new approach for treating ALS and other neurodegenerative diseases.
Research reveals the gut microbiota-metabolite-brain axis plays a critical role in Sevoflurane-induced neurotoxicity, particularly in neonatal mice. The study demonstrates that fecal microbiota transplantation and bile acid regulation can rescue social behavior deficits and improve synaptic function.
Researchers found that biotin supplementation reverses neurotoxicity in human nerve cells, improving mitochondrial function and reducing cell loss. Biotin metabolism was identified as a modifier of manganese-induced neurodegeneration, offering potential therapeutic strategy for Parkinson's disease
The study proposes a novel approach for simultaneous extraction of metabolites and lipids from zebrafish embryos to shed light on PFOS-induced neurotoxicity. The researchers found that sphingolipids are a reliable biomarker of PFOS-induced neurotoxicity, and the method can be expanded to various biomolecules.
Researchers have identified 11 genes affected by PFAS exposure, which could serve as markers to detect neurotoxicity. The study found distinct molecular structures within each type of PFAS drive changes in gene expression, highlighting the need for individual investigation.
Researchers have unveiled a critical mechanism linking cellular stress in the brain to Alzheimer's disease progression, highlighting microglia as central players in both protective and harmful responses. The study reveals that blocking a specific stress pathway reverses symptoms of Alzheimer's disease in preclinical models.
A new study by Thomas Jefferson University neuroscientist Jay Schneider suggests that high-quality maternal care and an enriched environment can reduce the toxic effects of lead exposure in rats. The findings provide hope for families with lead-poisoned children, particularly those from lower socioeconomic status.
A UFZ study found that individual chemicals can have additive effects on human health when combined with other chemicals, leading to increased neurotoxicity. The research analyzed blood samples from pregnant women and found that even low concentrations of chemicals could cause adverse effects on nerve-like cells.
A study from Goethe University Frankfurt reveals that venomous crustaceans, specifically remipede crabs in Mexican cenote caves, contain a variety of toxins with pharmacological potential. The xibalbines peptides effectively inhibit potassium channels and activate signaling pathways involved in pain sensitization.
Industrial fishing practices in tropical and subtropical waters release high levels of methylmercury into the ocean. The majority of this mercury is found in large pelagic fish like tuna, which are then consumed by humans. This can lead to developmental delays in children and impaired cardiovascular health in adults.
A study of 74 children in rural Ethiopian villages found that higher exposure to fluoride was linked to more errors on drawing and memory tests. The results suggest a potential association between high fluoride levels and cognitive impairment, particularly during early brain development and childhood.
Researchers at Chalmers University of Technology have shown that graphene oxide nanoflakes can reduce the accumulation of misfolded amyloid peptides in yeast cells, which are similar to human neurons affected by Alzheimer's disease. This suggests that graphene oxide may hold great potential for treating neurodegenerative diseases.
Researchers from Indiana University School of Medicine identified the protein bassoon as a key contributor to tau neurotoxicity in Alzheimer's disease. The study found that bassoon stabilizes the tau seed, allowing it to propagate in the brain and exacerbate neurodegeneration.
An international research team developed an animal-free testing battery to detect developmental neurotoxicity, using human cells instead of animals. The results show that the testing battery is technically feasible and already has a measurement sensitivity comparable to animal experiments.
A recent study published in Environmental Health Perspectives found that exposure to low levels of organophosphate esters can harm brain development in children, affecting IQ, attention, and memory. The chemicals, used as flame retardants and plasticizers in electronics and baby products, have been widely misassumed to be safe.
A study by University of South Florida Health researchers suggests that fenchol, a natural compound in basil, can help reduce neurotoxic amyloid-beta in the brain. Fenchol stimulates FFAR2 signaling, reducing senescent neuronal cells and increasing Aβ degradation.
Researchers develop VICE biosensor to assess toxicity of substances on human cells, providing a non-invasive method for early detection. The technology aims to address limitations of current toxicological assessments, which often fail to detect long-term side effects.
Researchers reprogrammed whale cells into neuronal cells to investigate the neurotoxic effects of an environmental pollutant. The study found that exposure to the pollutant led to apoptosis and disrupted cellular signaling pathways, ultimately causing neurodegeneration.
A study has identified potential biomarkers to predict patients at increased risk of severe neurotoxicity after receiving CD19 CAR T-cell therapy. Patients with early onset of CRS were found to be more susceptible to severe neurotoxicity.
Researchers at Fred Hutchinson Cancer Center identified potential biomarkers and created algorithms to identify patients at risk of severe side effects from CAR T-cell therapy. The studies found that most patients with these toxicities experienced reversible or no harm, but severe cases were associated with endothelial cell activation.
A study published in JAMA Pediatrics found that very-low-birth-weight (VLBW) babies who undergo major surgery have an increased risk of death or subsequent neurodevelopmental impairment. The study included 12,111 infants and found a 50% increase in risk for VLBW infants who underwent major surgery compared to those who did not.
Researchers found that zinc supplementation exhibited an antioxidant capacity, potentially reducing neurotoxic effects of aluminum on learning and memory function. The optimal dose of zinc for preventing aluminum-induced neurotoxicity was also identified.
Ketamine use in pediatric anesthesia may lead to long-term cognitive and behavioral problems in young children. Research suggests that ketamine's neurotoxic effects, particularly tau phosphorylation, can damage developing neurons and microtubule function.
A study published in Neural Regeneration Research found that paeonol, a natural compound, attenuates inflammation-mediated neurotoxicity and microglial activation. This suggests that paeonol may be effective in treating neurodegenerative diseases such as Alzheimer's and Parkinson's.
Recent studies have elucidated the mechanisms of lanthanide biological actions, indicating that these metals can alter neural functions. High doses and chronic exposure are associated with neural system damage, particularly in pregnant and lactating animals.
A recent study published in European Journal of Neuroscience reveals that prostaglandin E2 (PGE2) can provide protection against brain cell death by stimulating receptors EP2 and EP4. This stimulation results in increased cyclic-AMP (cAMP) levels, which reduces the toxic effects of amyloid-beta 1-42, a hallmark of Alzheimer's disease.
A new validated method measures HHMA in body fluids, establishing it as a likely contributor to Ecstasy's side effects. The detection of HHMA may provide new insights into the drug's effects and long-term toxicity.