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Neurotoxicity Research

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
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
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
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
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
Abhishek Kumar Singh, Akalabya Bissoyi, Mahendra Pratap Kashyap, Pradeep Kumar Patra, Syed Ibrahim Rizvi
Autophagy is an evolutionary conserved catabolic process that ensures continuous removal of damaged cell organelles and long-lived protein aggregates to maintain cellular homeostasis. Although autophagy has been implicated in amyloid-β (Aβ) production and deposition, its role in pathogenesis of Alzheimer's disease remains elusive. Thus, the present study was undertaken to assess the cytoprotective and neuroprotective potential of autophagy on Aβ-induced oxidative stress, apoptosis and neurotoxicity in human neuroblastoma SH-SY5Y cells...
May 8, 2017: Neurotoxicity Research
Rebeca Alvariño, Eva Alonso, Marie-Aude Tribalat, Sandra Gegunde, Olivier P Thomas, Luis M Botana
Sarains are diamide alkaloids isolated from the Mediterranean sponge Haliclona (Rhizoniera) sarai that have previously shown antibacterial, insecticidal and anti-fouling activities. In this study, we examined for the first time the neuroprotective effects of sarains 1, 2 and A against oxidative stress in a human neuronal model. SH-SY5Y cells were co-incubated with sarains at concentrations ranging from 0.01 to 10 μM, and the well-known oxidant hydrogen peroxide at 150 μM for 6 h and the protective effects of the compounds were evaluated...
May 6, 2017: Neurotoxicity Research
Ariana Ern Schmitz, Luiz Felipe de Souza, Barbara Dos Santos, Pamela Maher, Fernanda Martins Lopes, Giovana Ferreira Londero, Fabio Klamt, Alcir Luiz Dafre
Thioredoxin (Trx) and glyoxalase (Glo) systems have been suggested to be molecular targets of methylglyoxal (MGO). This highly reactive endogenous compound has been associated with the development of neurodegenerative pathologies and cell death. In the present study, the glutathione (GSH), Trx, and Glo systems were investigated to understand early events (0.5-3 h) that may determine cell fate. It is shown for the first time that MGO treatment induces an increase in glutathione reductase (GR) protein in hippocampal slices (1 h) and HT22 nerve cells (0...
May 6, 2017: Neurotoxicity Research
Patricia S Muñoz, Juan Segura-Aguilar
Alpha-synuclein (SNCA) oligomers have been reported to inhibit autophagy. Aminochrome-induced SNCA oligomers are neurotoxic, but the flavoenzyme DT-diaphorase prevents both their formation and their neurotoxicity. However, the possible protective role of DT-diaphorase against autophagy impairment by aminochrome-induced SNCA oligomers remains unclear. To test this idea, we used the cell line RCSN-3NQ7SNCA, with constitutive expression of a siRNA against DT-diaphorase and overexpression SNCA, and RCSN-3 as control cells...
May 6, 2017: Neurotoxicity Research
Sandra Anne Banack, Paul Alan Cox
The theory that β-N-methylamino-L-alanine (BMAA), a cyanobacterial toxin, contaminates traditional food supplies of the Chamorro people of Guam is supported by the recent finding that chronic dietary exposure to L-BMAA in vervets (Chlorocebus sabaeus) triggers the formation of neurofibrillary tangles (NFT) and β-amyloid plaques in the brain. In the first experiment, we found that all four vervets receiving a 210 mg/kg dose for 140 days developed NFT and sparse amyloid deposits. In the second experiment, all eight vervets receiving a 210 mg/kg dose for 140 days developed NFT and amyloid deposits, as well as all eight vervets that received only 21 mg/kg...
May 6, 2017: Neurotoxicity Research
A R Bentivoglio, E Di Stasio, D Mulas, M L Cerbarano, T Ialongo, A Laurienzo, Martina Petracca
Botulinum toxin is considered as first-line therapy for cervical dystonia, but few papers have addressed these issues in the long term. Aim of this study was to investigate the long-term efficacy and safety of abobotulinumtoxin A (A/Abo) in patients with primary cervical dystonia. Consecutive patients who received at least six injections with A/Abo were included. Safety was assessed on patients' self-reports. Efficacy was assessed by recording the total duration of benefit, duration of maximum efficacy, disease severity measured by means of the Tsui score, and pain intensity evaluated by means of the visual analog scale (VAS)...
May 6, 2017: Neurotoxicity Research
Sandra Anne Banack, Susan J Murch
β-N-Methylamino-L-alanine (BMAA) is a non-canonical amino acid implicated as a cause for amyotrophic lateral sclerosis/parkinsonism dementia complex and potentially other neurodegenerative diseases. As interest in this molecule has increased, there has been a proliferation of methods along with a plethora of opinions as to the superiority of some methods over others. We analyzed the literature with reference to BMAA and its naturally occurring isomers, N-(2-aminoethyl) glycine (AEG) and 2,4 diaminobutyric acid (DAB)...
May 4, 2017: Neurotoxicity Research
Nathan Torbick, Beth Ziniti, Elijah Stommel, Ernst Linder, Angeline Andrew, Tracie Caller, Jim Haney, Walter Bradley, Patricia L Henegan, Xun Shi
Reoccurring seasonal cyanobacterial harmful algal blooms (CHABs) persist in many waters, and recent work has shown links between CHAB and elevated risk of amyotrophic lateral sclerosis (ALS). Quantifying the exposure levels of CHAB as a potential risk factor for ALS is complicated by human mobility, potential pathways, and data availability. In this work, we develop phycocyanin concentration (i.e., CHAB exposure) maps using satellite remote sensing across northern New England to assess relationships with ALS cases using a spatial epidemiological approach...
May 3, 2017: Neurotoxicity Research
Rebecca Albano, Doug Lobner
The study of the mechanism of β-N-methylamino-L-alanine (BMAA) neurotoxicity originally focused on its effects at the N-methyl-D-aspartate (NMDA) receptor. In recent years, it has become clear that its mechanism of action is more complicated. First, there are certain cell types, such as motor neurons and cholinergic neurons, where the dominate mechanism of toxicity is through action at AMPA receptors. Second, even in cortical neurons where the primary mechanism of toxicity appears to be activation of NMDA receptors, there are other mechanisms involved...
May 3, 2017: Neurotoxicity Research
Laura Louise Scott, Simoné Downing, Timothy Grant Downing
Chronic inhalation of aerosolized β-N-methylamino-L-alanine (BMAA) could serve as potenital route for exposure to this cyanobacterial neurotoxin implicated in the development of neurodegenerative disease. We investigated environmental aerosol BMAA loads and the fate of inhaled isotopically labeled aerosolized BMAA in adult male Sprague Dawley rats, with doses corresponding to chronic aerosolized environmental BMAA exposure of over 65 days and up to 266 years. Environmental BMAA aerosol concentrations ranged from 6-39 pg L¯(1)...
May 3, 2017: Neurotoxicity Research
R van Onselen, L Venables, M van de Venter, T G Downing
The implication of β-N-methylamino-L-alanine (BMAA) in the development of neurodegenerative diseases worldwide has led to several investigations of the mechanism, or mechanisms, of toxicity of this cyanobacterially produced amino acid. The primary mechanism of toxicity that was identified is excitotoxicity, with a second possible mechanism, the misincorporation of BMAA into the primary protein structure and consequent cell damage, having been more recently reported. However, studies on excitotoxicity and misincorporation have been conducted independently and there are therefore no data available on the relative contribution of each of these mechanisms to the total toxicity of BMAA...
May 3, 2017: Neurotoxicity Research
Sebastian Castillo, Patricia Muñoz, Maria Isabel Behrens, Fernando Diaz-Grez, Juan Segura-Aguilar
To explore the possible influence of heavy metal mining on incidence of Parkinson's disease (PD), global DNA methylation was assessed in blood samples from a population of PD patients (n = 45) and control subjects (n = 52) in Antofagasta neighborhood, a Chilean city built for exclusive use of mining companies. Comparisons were made with PD subjects (n = 52) and control subjects (n = 59) from Santiago Chile, a city having little association with mining. All subjects were assessed by two neurologists and PD diagnosis was based on UK Parkinson's Disease Society Brain Bank Clinical Diagnostic Criteria...
April 29, 2017: Neurotoxicity Research
Jasna Lojk, Sonja Prpar Mihevc, Vladimir Boštjan Bregar, Mojca Pavlin, Boris Rogelj
Increased environmental pollution has been suggested as one of the possible causes for increased incidence of neurodegenerative and developmental disorders. Through the environmental pollution, everyday consumer products and nanomedical applications, we are also exposed to various nanoparticles (NPs). Specific types of NPs have been shown to be able to cause neural damage in vivo through processes such as disruption of the blood-brain barrier, induction of neuroinflammation, increase in oxidative stress and protein aggregation...
April 25, 2017: Neurotoxicity Research
Desanka Milanovic, Vesna Pesic, Natasa Loncarevic-Vasiljkovic, Vladimir Avramovic, Vesna Tesic, Vesna Jevtovic-Todorovic, Selma Kanazir, Sabera Ruzdijic
Propofol is a general anesthetic commonly used in pediatric clinical practices. Experimental findings demonstrate that anesthetics induce widespread apoptosis and cognitive decline in a developing brain. Although anesthesia-mediated neurotoxicity is the most prominent during intense period of synaptogenesis, the effects of an early anesthesia exposure on the synapses are not well understood. The aim of this study was to examine the effects of neonatal propofol anesthesia on the expression of key proteins that participate in synaptogenesis and synaptic plasticity and to evaluate long-term neurobehavioral abnormalities in the mature adult brain...
April 24, 2017: Neurotoxicity Research
Janaína Camacho da Silva, Alexandre Umpierrez Amaral, Cristiane Cecatto, Alessandro Wajner, Kálita Dos Santos Godoy, Rafael Teixeira Ribeiro, Aline de Mello Gonçalves, Ângela Zanatta, Mateus Struecker da Rosa, Samanta Oliveira Loureiro, Carmen Regla Vargas, Guilhian Leipnitz, Diogo Onofre Gomes de Souza, Moacir Wajner
Tissue accumulation of α-ketoadipic (KAA) and α-aminoadipic (AAA) acids is the biochemical hallmark of α-ketoadipic aciduria. This inborn error of metabolism is currently considered a biochemical phenotype with uncertain clinical significance. Considering that KAA and AAA are structurally similar to α-ketoglutarate and glutamate, respectively, we investigated the in vitro effects of these compounds on glutamatergic neurotransmission in the brain of adolescent rats. Bioenergetics and redox homeostasis were also investigated because they represent fundamental systems for brain development and functioning...
April 20, 2017: Neurotoxicity Research
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