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Neurotoxicity Research

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https://www.readbyqxmd.com/read/28643233/assessing-environmental-exposure-to-%C3%AE-n-methylamino-l-alanine-bmaa-in-complex-sample-matrices-a-comparison-of-the-three-most-popular-lc-ms-ms-methods
#1
Teesha C Baker, Fiona J M Tymm, Susan J Murch
β-N-Methylamino-L-alanine (BMAA) is a naturally occurring non-protein amino acid produced by cyanobacteria, accumulated through natural food webs, found in mammalian brain tissues. Recent evidence indicates an association between BMAA and neurological disease. The accurate detection and quantification of BMAA in food and environmental samples are critical to understanding BMAA metabolism and limiting human exposure. To date, there have been more than 78 reports on BMAA in cyanobacteria and human samples, but different methods give conflicting data and divergent interpretations in the literature...
June 22, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28643232/caffeine-protects-against-anticonvulsant-induced-neurotoxicity-in-the-developing-rat-brain
#2
Stefanie Endesfelder, Ulrike Weichelt, Cornelia Schiller, Marco Sifringer, Ivo Bendix, Christoph Bührer
Phenobarbital is the most commonly used drug for the treatment of neonatal seizures but may induce neurodegeneration in the developing brain. Methylxanthine caffeine is used for the treatment of apnea in newborn infants and appears to be neuroprotective, as shown by antiapoptotic and anti-inflammatory effects in oxidative stress models in newborn rodents and reduced rates of cerebral palsy in human infants treated with caffeine. We hypothesized that caffeine may counteract the proapoptotic effects of phenobarbital in newborn rats...
June 22, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28639241/huntington-s-disease-and-mitochondria
#3
REVIEW
Mohammad Jodeiri Farshbaf, Kamran Ghaedi
Huntington's disease (HD) as an inherited neurodegenerative disorder leads to neuronal loss in striatum. Progressive motor dysfunction, cognitive decline, and psychiatric disturbance are the main clinical symptoms of the HD. This disease is caused by expansion of the CAG repeats in exon 1 of the huntingtin which encodes Huntingtin protein (Htt). Various cellular and molecular events play role in the pathology of HD. Mitochondria as important organelles play crucial roles in the most of neurodegenerative disorders like HD...
June 21, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28634653/assessing-the-combined-toxicity-of-bmaa-and-its-isomers-2-4-dab-and-aeg-in-vitro-using-human-neuroblastoma-cells
#4
Brendan J Main, Kenneth J Rodgers
The non-protein amino acid (NPAA) ß-methylamino-L-alanine (BMAA) is produced by a diverse range of cyanobacteria, diatoms and dinoflagellates, and is present in both aquatic and terrestrial ecosystems globally. Exposure to BMAA has been implicated in the development of neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD) and Parkinson's disease (PD). BMAA is often found in nature along with its structural isomers 2,4-diaminobutyric acid (2,4-DAB) and aminoethylglycine (AEG); however, the toxicity of these NPAAs in combination has not been examined...
June 20, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28631256/vulnerability-to-a-metabolic-challenge-following-perinatal-asphyxia-evaluated-by-organotypic-cultures-neonatal-nicotinamide-treatment
#5
R Perez-Lobos, C Lespay-Rebolledo, A Tapia-Bustos, E Palacios, V Vío, D Bustamante, P Morales, M Herrera-Marschitz
The hypothesis of enhanced vulnerability following perinatal asphyxia was investigated with a protocol combining in vivo and in vitro experiments. Asphyxia-exposed (AS) (by 21 min water immersion of foetuses containing uterine horns) and caesarean-delivered control (CS) rat neonates were used at P2-3 for preparing triple organotypic cultures (substantia nigra, neostriatum and neocortex). At DIV 18, cultures were exposed to different concentrations of H2O2 (0.25-45 mM), added to the culture medium for 18 h...
June 19, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28623460/spreading-of-pathology-in-alzheimer-s-disease
#6
REVIEW
Zhong-Yue Lv, Chen-Chen Tan, Jin-Tai Yu, Lan Tan
The senile plaques (SPs) and neurofibrillary tangles (NFTs) are the two major pathological hallmarks of AD, which are composed of β-amyloid protein and Tau protein. So the β-amyloid protein (Aβ) and Tau oligomers (oTau) are the majority in the pathology of AD. Recently, the spreading of Aβ and oTau in the brain of AD patients has received heated value. In this review, we summarize recent research progress and aim to figure out the spreading mechanism of Aβ and Tau in AD via introduction of the formation, release, uptake, diffusion between different brain regions, and the propagation principle of Aβ and Tau...
June 16, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28612296/kinesin-5-blocker-monastrol-protects-against-bortezomib-induced-peripheral-neurotoxicity
#7
Ilja Bobylev, Dominik Peters, Maulik Vyas, Mohammed Barham, Ines Klein, Elke Pogge von Strandmann, Wolfram F Neiss, Helmar C Lehmann
Neurotoxicity is a relevant side effect of bortezomib treatment. Previous reports have shown that the development of peripheral neuropathy caused by anti-neoplastic agents may be a result of reduced axonal transport. Based on evidence from prior studies that the kinesin-5 inhibitor monastrol enhances axonal transport and improves neuronal regeneration, we focused on the neuroprotective role of monastrol during the chemotherapeutic treatment with bortezomib. Prolonged treatment of C57BL/6 mice with bortezomib induced a length-dependent small-fiber neuropathy with axonal atrophy and loss of sensory nerve fibers...
June 13, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28612295/neuroprotective-effect-of-creatine-and-pyruvate-on-enzyme-activities-of-phosphoryl-transfer-network-and-oxidative-stress-alterations-caused-by-leucine-administration-in-wistar-rats
#8
Elenara Rieger, Itiane Diehl de Franceschi, Thales Preissler, Clovis Milton Duval Wannmacher
Maple syrup urine disease is an autosomal metabolic disease caused by a deficiency of branched-chain α-keto acid dehydrogenase complex activity. In this disease occur the accumulation of the branched-chain amino acids leucine, isoleucine, and valine and their corresponding branched-chain α-keto acids in the tissues and body fluids. The affected patients may present psychomotor development delay and mental retardation. The pathophysiology of maple syrup urine disease is not entirely understood, but leucine seems to be the primary neurotoxic metabolite...
June 13, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28612294/the-potential-role-of-bmaa-in-neurodegeneration
#9
REVIEW
Tracie Caller, Patricia Henegan, Elijah Stommel
Neurodegenerative diseases are a major public health issue throughout the world with devastating effects on patients and families. Sporadic forms of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis are generally thought to develop as a consequence of genetic susceptibility and environmental influences. A number of environmental triggers have been identified in association with amyotrophic lateral sclerosis and Parkinson's disease. We discuss the role of β-methylamino-L-alanine in the development of neurodegeneration and the potential importance of this neurotoxin as a risk for neurodegeneration...
June 13, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28597409/progression-and-persistence-of-neurotoxicity-induced-by-mdma-in-dopaminergic-regions-of-the-mouse-brain-and-association-with-noradrenergic-gabaergic-and-serotonergic-damage
#10
Giulia Costa, Micaela Morelli, Nicola Simola
The amphetamine-related drug 3,4-methylenedioxymethamphetamine (MDMA) is known to induce neurotoxic damage in dopaminergic regions of the mouse brain. In order to characterize how the number of administrations influenced the severity of MDMA-induced dopaminergic damage and to describe the localization and persistence of this damage, we evaluated the changes in tyrosine hydroxylase (TH) and dopamine transporter (DAT) in different regions of the mouse brain. Moreover, we investigated whether dopaminergic damage was associated with noradrenergic, GABAergic, and serotonergic damage, by evaluating the changes in noradrenaline transporter (NET), glutamic acid decarboxylase-67 (GAD-67), and serotonin transporter (SERT)...
June 9, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28593525/lithium-chloride-facilitates-autophagy-following-spinal-cord-injury-via-erk-dependent-pathway
#11
Peilin Liu, Zijuan Zhang, Qingde Wang, Rundong Guo, Wei Mei
Spinal cord injury (SCI) is one major cause of death and results in long-term disability even in the most productive periods of human lives with few efficacious drugs. Autophagy is a potential therapeutic target for SCI. In the present study, we examined the role of lithium in functional recovery in the rat model of SCI and explored the related mechanism. Locomotion tests were employed to assess the functional recovery after SCI, Western blotting and RT-PCT to determine the level of p-ERK and LC3-II as well as p62, immunofluorescence imaging to localize LC3 and p62...
June 8, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28585115/cyanobacterial-neurotoxins-their-occurrence-and-mechanisms-of-toxicity
#12
Kenneth J Rodgers, Brendan J Main, Kate Samardzic
Cyanobacteria are some of the oldest organisms on earth, and have evolved to produce a battery of toxic metabolites, including hepatotoxins, dermatoxins, and neurotoxins. In this review, we focus on the occurrence and mechanisms of toxicity of a number of neurotoxins synthesised by these ancient photosynthetic prokaryotes. We discuss the evidence linking β-methylamino-L-alanine (BMAA), a non-protein amino acid, to an unusual neurological disease complex reported on the island of Guam in the 1950s, and how 60 years later, the role that BMAA plays in human disease is still unclear...
June 5, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28578480/acute-neuroinflammation-promotes-cell-responses-to-1800%C3%A2-mhz-gsm-electromagnetic-fields-in-the-rat-cerebral-cortex
#13
Julie Lameth, Annie Gervais, Catherine Colin, Philippe Lévêque, Thérèse M Jay, Jean-Marc Edeline, Michel Mallat
Mobile phone communications are conveyed by radiofrequency (RF) electromagnetic fields, including pulse-modulated global system for mobile communications (GSM)-1800 MHz, whose effects on the CNS affected by pathological states remain to be specified. Here, we investigated whether a 2-h head-only exposure to GSM-1800 MHz could impact on a neuroinflammatory reaction triggered by lipopolysaccharide (LPS) in 2-week-old or adult rats. We focused on the cerebral cortex in which the specific absorption rate (SAR) of RF averaged 2...
June 3, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28577066/comparison-of-the-psychopharmacological-effects-of-tiletamine-and-ketamine-in-rodents
#14
Piotr Popik, Małgorzata Hołuj, Tomasz Kos, Gabriel Nowak, Tadeusz Librowski, Kinga Sałat
The glutamate N-methyl-D-aspartate (NMDA) receptor antagonist ketamine (KET) produces rapid and sustained antidepressant effects in patients. Tiletamine (TIL; 2-ethylamino-2-thiophen-2-yl-cyclohexan-1-one) is another uncompetitive NMDA receptor antagonist, used in a medical (veterinary) setting as an anesthetic tranquilizer. Here, we compared the behavioral actions of KET and TIL in a variety of tests, focusing on antidepressant-like and dissociative-like effects in mice and rats. The minimum effective doses of KET and TIL were 10 mg/kg to reduce mouse forced swim test immobility and 15 mg/kg to reduce marble-burying behavior...
June 2, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28555260/serum-copeptin-predicts-severity-and-recurrent-stroke-in-ischemic-stroke-patients
#15
Wan-Zhong Tang, Xiao-Bo Wang, Huan-Ting Li, Mei Dong, Xiang Ji
Several studies investigated the prognostic role of copeptin in stroke. The aim of this study is to assess copeptin levels in serum, and investigate their associations with risk of recurrent stroke in a 1-year follow-up study in patients with ischemic stroke. In this post hoc analysis, serum levels of copeptin and NIH stroke scale (NIHSS) were measured at the time of admission in a cohort of 316 patients with ischemic stroke. The end point was stroke recurrence after 1-year follow-up. We used logistic regression model to assess the relationship between copeptin levels and risk recurrent stroke...
May 30, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28540665/different-molecular-mechanisms-mediate-direct-or-glia-dependent-prion-protein-fragment-90-231-neurotoxic-effects-in-cerebellar-granule-neurons
#16
Stefano Thellung, Elena Gatta, Francesca Pellistri, Valentina Villa, Alessandro Corsaro, Mario Nizzari, Mauro Robello, Tullio Florio
Glia over-stimulation associates with amyloid deposition contributing to the progression of central nervous system neurodegenerative disorders. Here we analyze the molecular mechanisms mediating microglia-dependent neurotoxicity induced by prion protein (PrP)90-231, an amyloidogenic polypeptide corresponding to the protease-resistant portion of the pathological prion protein scrapie (PrP(Sc)). PrP90-231 neurotoxicity is enhanced by the presence of microglia within neuronal culture, and associated to a rapid neuronal [Ca(++)] i increase...
May 25, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28540664/tnf-%C3%AE-mediates-the-intrinsic-and-extrinsic-pathway-in-propofol-induced-neuronal-apoptosis-via-pi3k-akt-signaling-pathway-in-rat-prefrontal-cortical-neurons
#17
Xiaoyuan Deng, Bo Chen, Bin Wang, Junfang Zhang, Hongliang Liu
Propofol can cause developing neuronal apoptosis in both in vivo and in vitro studies, and the mechanism is unclear till now. Our previous study has demonstrated that propofol can increase the TNF-α expression in the prefrontal cortex in rat developing brain, the TNF-α antagonist, etanercept, can inhibit propofol-induced neuronal apoptosis, but little is known about how TNF-α mediates that process. This study reveals that propofol at clinically relevant concentrations increases the TNF-α synthesis and release in neurons, and induces neuronal apoptosis; etanercept significantly reduces neuronal apoptosis, the elevation of cleaved caspase-8 and cleaved caspase-9, or the Akt phosphorylation induced by propofol, while the selective PI3K antagonist blocks the neuroprotection of etanercept...
May 24, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28540663/bmaa-and-neurodegenerative-illness
#18
Paul Alan Cox, Richard M Kostrzewa, Gilles J Guillemin
The cyanobacterial toxin β-N-methylamino-L-alanine (BMAA) now appears to be a cause of Guamanian amyotrophic lateral sclerosis/parkinsonism dementia complex (ALS/PDC). Its production by cyanobacteria throughout the world combined with multiple mechanisms of BMAA neurotoxicity, particularly to vulnerable subpopulations of motor neurons, has significantly increased interest in investigating exposure to this non-protein amino acid as a possible risk factor for other forms of neurodegenerative illness. We here provide a brief overview of BMAA studies and provide an introduction to this collection of scientific manuscripts in this special issue on BMAA...
May 24, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28540662/methamidophos-an-organophosphorus-insecticide-induces-pro-aggressive-behaviour-in-mice
#19
Cristina Paula do Nascimento, Gabriella Xavier Maretto, Graziany Leite Moreira Marques, Luciana Mesquita Passamani, Ana Paula Abdala, Luiz Carlos Schenberg, Vanessa Beijamini, Karla Nívea Sampaio
Although evidence indicates that exposure to organophosphorus (OP) pesticides induces neurobehavioral disorders, little is known about the effects of OP on aggressive behaviour. Our study investigated the effects of repeated exposure to an OP pesticide, methamidophos, on the isolation-induced aggressive behaviour in mice. Forty seven male mice were individually housed for a month. Socially isolated animals were then confronted with a standard non-isolated opponent for 15 min (pre-treatment trial), and the latency and frequency of aggressive and general exploratory behaviours were recorded...
May 24, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28527102/studies-of-environmental-risk-factors-in-amyotrophic-lateral-sclerosis-als-and-a-phase-i-clinical-trial-of-l-serine
#20
Walter G Bradley, R X Miller, T D Levine, E W Stommel, P A Cox
β-N-Methylamino-L-alanine (BMAA) has been linked to Guam ALS/PDC and shown to produce neurodegeneration in vitro and in vivo (Drosophila, mice, rats, primates). BMAA misincorporation into neuroproteins produces protein misfolding and is inhibited by L-serine. Case-control studies in Northern New England indicate that living near to water-bodies with cyanobacterial blooms increases the risk of developing amyotrophic lateral sclerosis (ALS). The distribution of addresses of ALS cases in New Hampshire, Vermont, and Florida was compared to that of controls...
May 19, 2017: Neurotoxicity Research
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