2008
DOI: 10.1016/j.neulet.2008.05.003
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Acetaminophen attenuates dopamine neuron degeneration in animal models of Parkinson's disease

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Cited by 71 publications
(54 citation statements)
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“…In rats, APAP induces apoptosis of cortical neurons (Posadas et al, 2010), but significantly attenuates superoxide production by the neurotoxin quinolinic acid, a metabolite implicated in the pathogenesis of neurodegenerative diseases (Maharaj et al, 2006). In a C. elegans model of Parkinson’s disease APAP also protects dopaminergic neurons from oxidative damage evoked by exposure to 6-hydroxy dopamine or excessive levels of dopamine (Locke et al, 2008). Therefore, we can speculate that HEI-OC1 cells probably respond to APAP just as neurons, which seems reasonable given their neuro-epithelial origin.…”
Section: Discussionmentioning
confidence: 99%
“…In rats, APAP induces apoptosis of cortical neurons (Posadas et al, 2010), but significantly attenuates superoxide production by the neurotoxin quinolinic acid, a metabolite implicated in the pathogenesis of neurodegenerative diseases (Maharaj et al, 2006). In a C. elegans model of Parkinson’s disease APAP also protects dopaminergic neurons from oxidative damage evoked by exposure to 6-hydroxy dopamine or excessive levels of dopamine (Locke et al, 2008). Therefore, we can speculate that HEI-OC1 cells probably respond to APAP just as neurons, which seems reasonable given their neuro-epithelial origin.…”
Section: Discussionmentioning
confidence: 99%
“…Administration of the 6-hydroxydopamine (6-OHDA) neurotoxin to C. elegans produced specific degeneration of dopamine neurons (Nass et al, 2002). By performing forward genetic and high-throughput chemical screens, mutations within the dopamine transporter dat-1 were found to suppress 6-OHDA sensitivity (Nass et al, 2005) and bromocriptine, quinpirole, and acetaminophen, and plant extracts from Bacopa monnieri and Uncaria tomentosa were found to be neuroprotective (Marvanova and Nichols, 2007; Locke et al, 2008; Ruan et al, 2010; Jadiya et al, 2011; Shi et al, 2013). These data demonstrate that pathological characteristics of PD can be recapitulated in C. elegans models and used to investigate the mechanism by which α-synuclein and other PD proteins produce neurotoxicity and cause motor defects.…”
Section: Elegans As a Model For Other Neurodegenerative Diseasesmentioning
confidence: 99%
“…The genes encoding GRP78, ATF6 and XBP-1 of the nematode are orthologues of human genes, which makes the nematode an interesting model for the study of these particular stressors in relation to PD. In this respect, the neuroprotective capacity of acetaminophen (also known as paracetamol) was tested in C. elegans, observing that the compound was able to attenuate the loss of dopaminergic neuron by oxidative damage, but not from the stress of protein misfolding (Locke et al 2008).…”
Section: Parkinson's Diseasementioning
confidence: 99%