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  1. Naoyuki Taniguchi, Yasuhiko Kizuka, Shinji Takamatsu, Eiji Miyoshi, Congxiao Gao, Keiichiro Suzuki, Shinobu Kitazume and Kazuaki Ohtsubo.
    Glyco-redox, a link between oxidative stress and changes of glycans: Lessons from research on glutathione, reactive oxygen and nitrogen species to glycobiology. Archives of Biochemistry and Biophysics 595:72–80, April 2016.
    Abstract Reduction-oxidation (redox) response is one of the most important biological phenomena. The concept introduced by Helmut Sies encouraged many researchers to examine oxidative stress under pathophysiological conditions. Our group has been interested in redox regulation under oxidative stress as well as glycobiology in relation to disease. Current studies by our group and other groups indicate that functional and structural changes of glycans are regulated by redox responses resulting from the generation of reactive oxygen species (ROS) or reactive nitrogen species (RNS) in various diseases including cancer, diabetes, neurodegenerative disease such as Parkinson disease, Alzheimer's disease and amyotrophic lateral sclerosis (ALS), and chronic obstructive pulmonary disease (COPD), even though very few investigators appear to be aware of these facts. Here we propose that the field "glyco-redox" will open the door to a more comprehensive understanding of the mechanism associated with diseases in relation to glycan changes under oxidative stress. A tight link between structural and functional changes of glycans and redox system under oxidative stress will lead to the recognition and interest of these aspects by many scientists. Helmut's contribution in this field facilitated our future perspectives in glycobiology.
    URL, DOI BibTeX

    @article{Taniguchi2016,
    	abstract = {Reduction-oxidation (redox) response is one of the most important biological phenomena. The concept introduced by Helmut Sies encouraged many researchers to examine oxidative stress under pathophysiological conditions. Our group has been interested in redox regulation under oxidative stress as well as glycobiology in relation to disease. Current studies by our group and other groups indicate that functional and structural changes of glycans are regulated by redox responses resulting from the generation of reactive oxygen species (ROS) or reactive nitrogen species (RNS) in various diseases including cancer, diabetes, neurodegenerative disease such as Parkinson disease, Alzheimer's disease and amyotrophic lateral sclerosis (ALS), and chronic obstructive pulmonary disease (COPD), even though very few investigators appear to be aware of these facts. Here we propose that the field "glyco-redox" will open the door to a more comprehensive understanding of the mechanism associated with diseases in relation to glycan changes under oxidative stress. A tight link between structural and functional changes of glycans and redox system under oxidative stress will lead to the recognition and interest of these aspects by many scientists. Helmut's contribution in this field facilitated our future perspectives in glycobiology.},
    	author = "Taniguchi, Naoyuki and Kizuka, Yasuhiko and Takamatsu, Shinji and Miyoshi, Eiji and Gao, Congxiao and Suzuki, Keiichiro and Kitazume, Shinobu and Ohtsubo, Kazuaki",
    	doi = "10.1016/j.abb.2015.11.024",
    	issn = 00039861,
    	journal = "Archives of Biochemistry and Biophysics",
    	month = "apr",
    	pages = "72--80",
    	pmid = 27095220,
    	title = "{Glyco-redox, a link between oxidative stress and changes of glycans: Lessons from research on glutathione, reactive oxygen and nitrogen species to glycobiology}",
    	url = "http://www.ncbi.nlm.nih.gov/pubmed/27095220",
    	volume = 595,
    	year = 2016
    }
    
  2. Negin Nouraei, Lauren Zarger, Justin N Weilnau, Jimin Han, Daniel M Mason and Rehana K Leak.
    Investigation of the therapeutic potential of N-acetyl cysteine and the tools used to define nigrostriatal degeneration in vivo.. Toxicology and applied pharmacology 296:19–30, April 2016.
    Abstract The glutathione precursor N-acetyl-l-cysteine (NAC) is currently being tested on Parkinson's patients for its neuroprotective properties. Our studies have shown that NAC can elicit protection in glutathione-independent manners in vitro. Thus, the goal of the present study was to establish an animal model of NAC-mediated protection in which to dissect the underlying mechanism. Mice were infused intrastriatally with the oxidative neurotoxicant 6-hydroxydopamine (6-OHDA; 4$\mu$g) and administered NAC intraperitoneally (100mg/kg). NAC-treated animals exhibited higher levels of the dopaminergic terminal marker tyrosine hydroxylase (TH) in the striatum 10d after 6-OHDA. As TH expression is subject to stress-induced modulation, we infused the tracer FluoroGold into the striatum to retrogradely label nigrostriatal projection neurons. As expected, nigral FluoroGold staining and cell counts of FluoroGold(+) profiles were both more sensitive measures of nigrostriatal degeneration than measurements relying on TH alone. However, NAC failed to protect dopaminergic neurons 3weeks following 6-OHDA, an effect verified by four measures: striatal TH levels, nigral TH levels, nigral TH(+) cell counts, and nigral FluoroGold levels. Some degree of mild toxicity of FluoroGold and NAC was evident, suggesting that caution must be exercised when relying on FluoroGold as a neuron-counting tool and when designing experiments with long-term delivery of NAC-such as clinical trials on patients with chronic disorders. Finally, the strengths and limitations of the tools used to define nigrostriatal degeneration are discussed.
    URL, DOI BibTeX

    @article{Nouraei2016,
    	abstract = "The glutathione precursor N-acetyl-l-cysteine (NAC) is currently being tested on Parkinson's patients for its neuroprotective properties. Our studies have shown that NAC can elicit protection in glutathione-independent manners in vitro. Thus, the goal of the present study was to establish an animal model of NAC-mediated protection in which to dissect the underlying mechanism. Mice were infused intrastriatally with the oxidative neurotoxicant 6-hydroxydopamine (6-OHDA; 4$\mu$g) and administered NAC intraperitoneally (100mg/kg). NAC-treated animals exhibited higher levels of the dopaminergic terminal marker tyrosine hydroxylase (TH) in the striatum 10d after 6-OHDA. As TH expression is subject to stress-induced modulation, we infused the tracer FluoroGold into the striatum to retrogradely label nigrostriatal projection neurons. As expected, nigral FluoroGold staining and cell counts of FluoroGold(+) profiles were both more sensitive measures of nigrostriatal degeneration than measurements relying on TH alone. However, NAC failed to protect dopaminergic neurons 3weeks following 6-OHDA, an effect verified by four measures: striatal TH levels, nigral TH levels, nigral TH(+) cell counts, and nigral FluoroGold levels. Some degree of mild toxicity of FluoroGold and NAC was evident, suggesting that caution must be exercised when relying on FluoroGold as a neuron-counting tool and when designing experiments with long-term delivery of NAC-such as clinical trials on patients with chronic disorders. Finally, the strengths and limitations of the tools used to define nigrostriatal degeneration are discussed.",
    	author = "Nouraei, Negin and Zarger, Lauren and Weilnau, Justin N and Han, Jimin and Mason, Daniel M and Leak, Rehana K",
    	doi = "10.1016/j.taap.2016.02.010",
    	issn = "1096-0333",
    	journal = "Toxicology and applied pharmacology",
    	month = "apr",
    	pages = "19--30",
    	pmid = 26879220,
    	title = "{Investigation of the therapeutic potential of N-acetyl cysteine and the tools used to define nigrostriatal degeneration in vivo.}",
    	url = "http://www.ncbi.nlm.nih.gov/pubmed/26879220",
    	volume = 296,
    	year = 2016
    }
    
  3. Ines Elbini Dhouib, Manel Jallouli, Alya Annabi, Najoua Gharbi, Saloua Elfazaa and Mohamed Montassar Lasram.
    A minireview on N-acetylcysteine: An old drug with new approaches.. Life sciences 151:359–63, 2016.
    Abstract N-acetylcysteine (NAC), a cysteine pro-drug and glutathione precursor has been used in therapeutic practices for several decades, as a mucolytic agent and for the treatment of numerous disorders including paracetamol intoxication. There is a growing interest concerning the beneficial effects of NAC against the early stages of toxicity-induced by pesticides. Nevertheless, the mechanisms underlying the therapeutic and clinical applications of NAC are not fully understood. In this review we aimed to focus on the protective effects of NAC against oxidative stress caused by pesticide in many organs. The possible mechanisms of action may be associated to its antioxidant properties. The anti-oxidative activity of NAC has been attributed to the fast reaction with free radicals as well as the restitution of reduced glutathione (GSH).
    URL, DOI BibTeX

    @article{ElbiniDhouib2016,
    	abstract = "N-acetylcysteine (NAC), a cysteine pro-drug and glutathione precursor has been used in therapeutic practices for several decades, as a mucolytic agent and for the treatment of numerous disorders including paracetamol intoxication. There is a growing interest concerning the beneficial effects of NAC against the early stages of toxicity-induced by pesticides. Nevertheless, the mechanisms underlying the therapeutic and clinical applications of NAC are not fully understood. In this review we aimed to focus on the protective effects of NAC against oxidative stress caused by pesticide in many organs. The possible mechanisms of action may be associated to its antioxidant properties. The anti-oxidative activity of NAC has been attributed to the fast reaction with free radicals as well as the restitution of reduced glutathione (GSH).",
    	author = "{Elbini Dhouib}, Ines and Jallouli, Manel and Annabi, Alya and Gharbi, Najoua and Elfazaa, Saloua and Lasram, Mohamed Montassar",
    	doi = "10.1016/j.lfs.2016.03.003",
    	issn = "1879-0631",
    	journal = "Life sciences",
    	month = "",
    	pages = "359--63",
    	pmid = 26946308,
    	title = "{A minireview on N-acetylcysteine: An old drug with new approaches.}",
    	url = "http://www.ncbi.nlm.nih.gov/pubmed/26946308",
    	volume = 151,
    	year = 2016
    }
    
  4. Lina Du, Philip E Empey, Jing Ji, Honglu Chao, Patrick M Kochanek, Hülya Bayır and Robert S B Clark.
    Probenecid and N-Acetylcysteine Prevent Loss of Intracellular Glutathione and Inhibit Neuronal Death after Mechanical Stretch Injury In Vitro.. Journal of neurotrauma, 2016.
    Abstract Probenecid and N-acetylcysteine (NAC) can preserve intracellular levels of the vital antioxidant glutathione (GSH) via two distinct biochemical pathways. Probenecid inhibits transporter-mediated GSH efflux and NAC serves as a cysteine donor for GSH synthesis. We hypothesized that probenecid and NAC alone would maintain intracellular GSH concentrations and inhibit neuronal death after traumatic stretch injury, and that the drugs in combination would produce additive effects. Sex-segregated rat primary cortical neurons were treated with probenecid (100 $\mu$M) and NAC (50 $\mu$M), alone and in combination (Pro-NAC), then subjected to mechanical stretch (10s(-1) strain rate, 50% membrane deformation). At 24 h, both probenecid and NAC inhibited trauma-induced intracellular GSH depletion, lactate dehydrogenase (LDH) release, and propidium iodide (PI) uptake in both XY- and XX-neurons. Combined Pro-NAC treatment was superior to probenecid or NAC alone in maintenance of intracellular GSH and neuronal death assessed by PI uptake. Interestingly, caspase 3 activity 24 h after mechanical trauma was more prominent in XX-neurons, and treatment effects (probenecid, NAC, and Pro-NAC) were observed in XX- but not XY-neurons; however, XY-neurons were ultimately more vulnerable to mechanical stretch-induced injury than their XX counterparts, as was evidenced by more neuronal death detected by LDH release and PI uptake. In addition, after stretch injury in HT22 hippocampal cells, both NAC and probenecid were highly effective at reducing oxidative stress detected by dichlorofluorescein fluorescence. These in vitro data support further testing of this drug combination in models of traumatic neuronal injury in vivo.
    URL, DOI BibTeX

    @article{Du2016,
    	abstract = "Probenecid and N-acetylcysteine (NAC) can preserve intracellular levels of the vital antioxidant glutathione (GSH) via two distinct biochemical pathways. Probenecid inhibits transporter-mediated GSH efflux and NAC serves as a cysteine donor for GSH synthesis. We hypothesized that probenecid and NAC alone would maintain intracellular GSH concentrations and inhibit neuronal death after traumatic stretch injury, and that the drugs in combination would produce additive effects. Sex-segregated rat primary cortical neurons were treated with probenecid (100 $\mu$M) and NAC (50 $\mu$M), alone and in combination (Pro-NAC), then subjected to mechanical stretch (10s(-1) strain rate, 50\% membrane deformation). At 24 h, both probenecid and NAC inhibited trauma-induced intracellular GSH depletion, lactate dehydrogenase (LDH) release, and propidium iodide (PI) uptake in both XY- and XX-neurons. Combined Pro-NAC treatment was superior to probenecid or NAC alone in maintenance of intracellular GSH and neuronal death assessed by PI uptake. Interestingly, caspase 3 activity 24 h after mechanical trauma was more prominent in XX-neurons, and treatment effects (probenecid, NAC, and Pro-NAC) were observed in XX- but not XY-neurons; however, XY-neurons were ultimately more vulnerable to mechanical stretch-induced injury than their XX counterparts, as was evidenced by more neuronal death detected by LDH release and PI uptake. In addition, after stretch injury in HT22 hippocampal cells, both NAC and probenecid were highly effective at reducing oxidative stress detected by dichlorofluorescein fluorescence. These in vitro data support further testing of this drug combination in models of traumatic neuronal injury in vivo.",
    	author = {Du, Lina and Empey, Philip E and Ji, Jing and Chao, Honglu and Kochanek, Patrick M and Bayır, H\"{u}lya and Clark, Robert S B},
    	doi = "10.1089/neu.2015.4342",
    	issn = "1557-9042",
    	journal = "Journal of neurotrauma",
    	month = "",
    	pmid = 26830358,
    	title = "{Probenecid and N-Acetylcysteine Prevent Loss of Intracellular Glutathione and Inhibit Neuronal Death after Mechanical Stretch Injury In Vitro.}",
    	url = "http://www.ncbi.nlm.nih.gov/pubmed/26830358",
    	year = 2016
    }
    
  5. Reza Bavarsad Shahripour, Mark R Harrigan and Andrei V Alexandrov.
    N-acetylcysteine (NAC) in neurological disorders: mechanisms of action and therapeutic opportunities.. Brain and behavior 4(2):108–22, March 2014.
    Abstract BACKGROUND: There is an expanding field of research investigating the benefits of medicines with multiple mechanisms of action across neurological disorders. N-acetylcysteine (NAC), widely known as an antidote to acetaminophen overdose, is now emerging as treatment of vascular and nonvascular neurological disorders. NAC as a precursor to the antioxidant glutathione modulates glutamatergic, neurotrophic, and inflammatory pathways. AIM AND DISCUSSION: Most NAC studies up to date have been carried out in animal models of various neurological disorders with only a few studies completed in humans. In psychiatry, NAC has been tested in over 20 clinical trials as an adjunctive treatment; however, this topic is beyond the scope of this review. Herein, we discuss NAC molecular, intracellular, and systemic effects, focusing on its potential applications in neurodegenerative diseases including spinocerebellar ataxia, Parkinson's disease, tardive dyskinesia, myoclonus epilepsy of the Unverricht-Lundbor type as well as multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease. CONCLUSION: Finally, we review the potential applications of NAC to facilitate recovery after traumatic brain injury, cerebral ischemia, and in treatment of cerebrovascular vasospasm after subarachnoid hemorrhage.
    URL, DOI BibTeX

    @article{BavarsadShahripour2014,
    	abstract = "BACKGROUND: There is an expanding field of research investigating the benefits of medicines with multiple mechanisms of action across neurological disorders. N-acetylcysteine (NAC), widely known as an antidote to acetaminophen overdose, is now emerging as treatment of vascular and nonvascular neurological disorders. NAC as a precursor to the antioxidant glutathione modulates glutamatergic, neurotrophic, and inflammatory pathways. AIM AND DISCUSSION: Most NAC studies up to date have been carried out in animal models of various neurological disorders with only a few studies completed in humans. In psychiatry, NAC has been tested in over 20 clinical trials as an adjunctive treatment; however, this topic is beyond the scope of this review. Herein, we discuss NAC molecular, intracellular, and systemic effects, focusing on its potential applications in neurodegenerative diseases including spinocerebellar ataxia, Parkinson's disease, tardive dyskinesia, myoclonus epilepsy of the Unverricht-Lundbor type as well as multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease. CONCLUSION: Finally, we review the potential applications of NAC to facilitate recovery after traumatic brain injury, cerebral ischemia, and in treatment of cerebrovascular vasospasm after subarachnoid hemorrhage.",
    	author = "{Bavarsad Shahripour}, Reza and Harrigan, Mark R and Alexandrov, Andrei V",
    	doi = "10.1002/brb3.208",
    	file = ":C$\backslash$:/Users/riku/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Bavarsad Shahripour, Harrigan, Alexandrov - 2014 - N-acetylcysteine (NAC) in neurological disorders mechanisms of action and therapeutic.pdf:pdf",
    	issn = "2162-3279",
    	journal = "Brain and behavior",
    	keywords = "Acetylcysteine,Acetylcysteine: pharmacology,Animals,Free Radical Scavengers,Free Radical Scavengers: pharmacology,Humans,Nervous System Diseases,Nervous System Diseases: drug therapy",
    	month = "mar",
    	number = 2,
    	pages = "108--22",
    	pmid = 24683506,
    	title = "{N-acetylcysteine (NAC) in neurological disorders: mechanisms of action and therapeutic opportunities.}",
    	url = "http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3967529\&tool=pmcentrez\&rendertype=abstract",
    	volume = 4,
    	year = 2014
    }
    
  6. Tz-Chuen Ju, Hui-Mei Chen, Yu-Chen Chen, Ching-Pang Chang, Chen Chang and Yijuang Chern.
    AMPK-$\alpha$1 functions downstream of oxidative stress to mediate neuronal atrophy in Huntington's disease.. Biochimica et biophysica acta 1842(9):1668–80, 2014.
    Abstract Huntington's disease (HD) is an autosomal dominant neurological disorder that is induced by a CAG trinucleotide expansion in exon 1 of the Huntingtin (HTT) gene. We previously reported that the abnormal activation of an important energy sensor, AMP-activated protein kinase $\alpha$1 (AMPK-$\alpha$1), occurs in the brains of mice and patients with HD, which suggests that this abnormal activation may contribute to neuronal degeneration in HD. In the present study, we demonstrated that the elevated oxidative stress that was evoked by a polyQ-expanded mutant HTT (mHTT) caused the abnormal activation of AMPK-$\alpha$1 and, subsequently, resulted in neurotoxicity in a striatal progenitor cell line (STHdh(Q109)) and in the striatum of a transgenic mouse model of HD (R6/2). The systematic administration of an antioxidant (N-acetyl-cysteine, NAC) to R6/2 mice suppressed the activation of AMPK-$\alpha$1, reduced neuronal toxicity, which was assessed by the activation of caspases, increased neuronal density, ameliorated ventricle enlargement, and improved motor dysfunction. This beneficial effect of NAC in vivo appears to be direct because NAC also reduced the activation of AMPK-$\alpha$1 and the death of STHdh(Q109) cells upon elevated oxidative stress. Moreover, the activation of AMPK enhanced the level of oxidative stress in STHdh(Q109) cells, in primary neurons of R6/2 mice, and in the striatum of two different HD mouse models (R6/2 and Hdh(150Q/+)), whereas the inhibition of AMPK reduced the level of oxidative stress. Collectively, our findings suggest that positive feedback regulation between the elevated oxidative stress and the activation of AMPK-$\alpha$1 contributes to the progression of HD.
    URL, DOI BibTeX

    @article{Ju2014,
    	abstract = "Huntington's disease (HD) is an autosomal dominant neurological disorder that is induced by a CAG trinucleotide expansion in exon 1 of the Huntingtin (HTT) gene. We previously reported that the abnormal activation of an important energy sensor, AMP-activated protein kinase $\alpha$1 (AMPK-$\alpha$1), occurs in the brains of mice and patients with HD, which suggests that this abnormal activation may contribute to neuronal degeneration in HD. In the present study, we demonstrated that the elevated oxidative stress that was evoked by a polyQ-expanded mutant HTT (mHTT) caused the abnormal activation of AMPK-$\alpha$1 and, subsequently, resulted in neurotoxicity in a striatal progenitor cell line (STHdh(Q109)) and in the striatum of a transgenic mouse model of HD (R6/2). The systematic administration of an antioxidant (N-acetyl-cysteine, NAC) to R6/2 mice suppressed the activation of AMPK-$\alpha$1, reduced neuronal toxicity, which was assessed by the activation of caspases, increased neuronal density, ameliorated ventricle enlargement, and improved motor dysfunction. This beneficial effect of NAC in vivo appears to be direct because NAC also reduced the activation of AMPK-$\alpha$1 and the death of STHdh(Q109) cells upon elevated oxidative stress. Moreover, the activation of AMPK enhanced the level of oxidative stress in STHdh(Q109) cells, in primary neurons of R6/2 mice, and in the striatum of two different HD mouse models (R6/2 and Hdh(150Q/+)), whereas the inhibition of AMPK reduced the level of oxidative stress. Collectively, our findings suggest that positive feedback regulation between the elevated oxidative stress and the activation of AMPK-$\alpha$1 contributes to the progression of HD.",
    	author = "Ju, Tz-Chuen and Chen, Hui-Mei and Chen, Yu-Chen and Chang, Ching-Pang and Chang, Chen and Chern, Yijuang",
    	doi = "10.1016/j.bbadis.2014.06.012",
    	issn = "0006-3002",
    	journal = "Biochimica et biophysica acta",
    	keywords = "AMP-Activated Protein Kinases,AMP-Activated Protein Kinases: metabolism,Animals,Apoptosis,Atrophy,Atrophy: metabolism,Atrophy: pathology,Blotting, Western,Cell Proliferation,Cells, Cultured,Corpus Striatum,Corpus Striatum: metabolism,Corpus Striatum: pathology,Disease Models, Animal,Humans,Huntington Disease,Huntington Disease: metabolism,Huntington Disease: pathology,Immunoenzyme Techniques,Mice,Mice, Transgenic,Nerve Degeneration,Nerve Tissue Proteins,Nerve Tissue Proteins: physiology,Neurons,Neurons: metabolism,Neurons: pathology,Oxidative Stress",
    	month = "",
    	number = 9,
    	pages = "1668--80",
    	pmid = 24946181,
    	title = "{AMPK-$\alpha$1 functions downstream of oxidative stress to mediate neuronal atrophy in Huntington's disease.}",
    	url = "http://www.ncbi.nlm.nih.gov/pubmed/24946181",
    	volume = 1842,
    	year = 2014
    }
    
  7. O A Andreassen, A Dedeoglu, P Klivenyi, M F Beal and A I Bush.
    N-acetyl-L-cysteine improves survival and preserves motor performance in an animal model of familial amyotrophic lateral sclerosis.. Neuroreport 11(11):2491–3, 2000.
    Abstract Increasing evidence implicates oxidative damage as a major mechanism in the pathogenesis of amyotrophic lateral sclerosis (ALS). We examined the effect of preventative treatment with N-acetyl-L-cysteine (NAC), an agent that reduces free radical damage, in transgenic mice with a superoxide dismutase (SODI) mutation (G93A), used as an animal model of familial ALS. NAC was administered at 1% concentration in the drinking water from 4-5 weeks of age. The treatment caused a significantly prolonged survival and delayed onset of motor impairment in G93A mice treated with NAC compared to control mice. These results provide further evidence for the involvement of free radical damage in the G93A mice, and support the possibility that NAC, an over-the-counter antioxidant, could be explored in clinical trials for ALS.
    URL BibTeX

    @article{Andreassen2000,
    	abstract = "Increasing evidence implicates oxidative damage as a major mechanism in the pathogenesis of amyotrophic lateral sclerosis (ALS). We examined the effect of preventative treatment with N-acetyl-L-cysteine (NAC), an agent that reduces free radical damage, in transgenic mice with a superoxide dismutase (SODI) mutation (G93A), used as an animal model of familial ALS. NAC was administered at 1\% concentration in the drinking water from 4-5 weeks of age. The treatment caused a significantly prolonged survival and delayed onset of motor impairment in G93A mice treated with NAC compared to control mice. These results provide further evidence for the involvement of free radical damage in the G93A mice, and support the possibility that NAC, an over-the-counter antioxidant, could be explored in clinical trials for ALS.",
    	author = "Andreassen, O A and Dedeoglu, A and Klivenyi, P and Beal, M F and Bush, A I",
    	issn = "0959-4965",
    	journal = "Neuroreport",
    	keywords = "Acetylcysteine,Acetylcysteine: pharmacology,Age Factors,Amyotrophic Lateral Sclerosis,Amyotrophic Lateral Sclerosis: drug therapy,Amyotrophic Lateral Sclerosis: genetics,Amyotrophic Lateral Sclerosis: physiopathology,Amyotrophic Lateral Sclerosis: prevention \& contro,Animals,Disease Models, Animal,Mice,Mice, Transgenic,Motor Activity,Motor Activity: drug effects,Motor Activity: physiology,Mutation,Mutation: physiology,Superoxide Dismutase,Superoxide Dismutase: genetics,Survival Rate",
    	month = "",
    	number = 11,
    	pages = "2491--3",
    	pmid = 10943709,
    	title = "{N-acetyl-L-cysteine improves survival and preserves motor performance in an animal model of familial amyotrophic lateral sclerosis.}",
    	url = "http://www.ncbi.nlm.nih.gov/pubmed/10943709",
    	volume = 11,
    	year = 2000
    }