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Edaravone and Its Protective Effects against Disease Progression in Neurological Conditions Besides Strokes
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Letter to the Editor Edaravone and Its Protective Effects against Disease Progression in Neurological Conditions Besides Strokes Dear Editor, Edaravone (EDVN) exerts neuroprotection against a number of different1 neuronal pathologies. EDVN appears to have a protective effect against disease evolution in Alzheimer’s disease (AD). It mediates this role in part by suppressing Aβ aggregation.2 EDVN therapy attenuates and restricts AD associated memory deficits. Yang et al3 have recently demonstrated that this is associated with decreased acetylcholinesterase activity in the hippocampus. At the same time, EDVN mitigates Aβinduced intracranial oxidation. In addition, “spatial learning” defects seen in AD models are decreased.4 Besides the above changes, EDVN also alters “superoxide dismutase” activity. Overall, EDVN also enhances and augments α-secretase-derived APP fragments.5 Concurrently, EDVN modulates and ameliorates glial activation. In addition, Aβ-induced accentuation of I Ca is reversed by EDVN. Interestingly, Qiang et al have recently designed DL-3-n-butylphthalide-EDVN hybrids that act as dual inhibitors of amyloid-β aggregation as well as monoamine oxidases.6 Concurrently, EDVN restricts and reduces Tau hyperphosphorylation. This is accompanied by an attenuating effect on β-secretase-derived APP fragments. At the same time, EDVN alters and affects “glutathione peroxidase” activity.7 Besides the above-mentioned changes, EDVN also has a negative impact on intrahippocampal choline acetylase activity. EDVN also exhibits neuroprotection from the development and progression of the disease processes in Parkinson’s disease (PD).8 Cheng et al have recently demonstrated that EDVN mediates this role primarily by accentuating heme oxygenase-1 expression.9 In addition, EDVN suppresses dopaminergic neuron apoptosis. These neuroprotective effects of EDVN have been confirmed both in vivo as well as in vitro.10 At the same time, EDVN has a negative impact on intracranial ROS activity. Ahmadinejad et al 11 have recently shown that concurrently, EDVN modulates and affects the induction of peroxiredoxin-2, thereby further protecting neuronal tissue from PD. 1052-3057/$ - see front matter © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.
As is very well evident from the above examples, EDVN exhibits significant neuroprotective properties. Hopefully, the coming few years will see an increase in the clinical utilization of EDVN as a therapeutic agent for ameliorating the disease processes in both AD as well as PD. Shailendra Kapoor, MD Kaiser Permanente, Atlanta, Georgia. E-mail: [email protected] https://doi.org/10.1016/j.jstrokecerebrovasdis.2017.08.042
References 1. Yamaguchi T, Awano H, Matsuda H, et al. Edaravone with and without. 6 Mg/Kg alteplase within 4.5 hours after Ischemic Stroke: a prospective cohort study (PROTECT4. 5). J Stroke Cerebrovasc Dis 2017;26:756-765. 2. Jiao SS, Yao XQ, Liu YH, et al. Edaravone alleviates Alzheimer’s disease-type pathologies and cognitive deficits. Proc Natl Acad Sci USA 2015;112:5225-5230. 3. Yang R, Wang Q, Li F, et al. Edaravone injection ameliorates cognitive deficits in rat model of Alzheimer’s disease. Neurol Sci 2015;36:2067-2072. 4. He F, Cao YP, Che FY, et al. Inhibitory effects of edaravone in beta-amyloid-induced neurotoxicity in rats. Biomed Res Int 2014;2014:370368. 5. Zhou S, Yu G, Chi L, et al. Neuroprotective effects of edaravone on cognitive deficit, oxidative stress and tau hyperphosphorylation induced by intracerebroventricular streptozotocin in rats. Neurotoxicology 2013;38:136-145. 6. Qiang X, Li Y, Yang X, et al. DL-3-n-butylphthalideEdaravone hybrids as novel dual inhibitors of amyloid-β aggregation and monoamine oxidases with high antioxidant potency for Alzheimer’s therapy. Bioorg Med Chem Lett 2017;27:718-722. 7. Shen Y, Wang Y, Yu G, et al. Effects of edaravone on amyloid-β precursor protein processing in SY5Y-APP695 cells. Neurotox Res 2013;24:139-147. 8. Yuan WJ, Yasuhara T, Shingo T, et al. Neuroprotective effects of edaravone-administration on 6-OHDA-treated dopaminergic neurons. BMC Neurosci 2008;9:75. 9. Cheng B, Guo Y, Li C, et al. Edaravone protected PC12 cells against MPP (+)-cytoxicity via inhibiting oxidative stress and up-regulating heme oxygenase-1 expression. J Neurol Sci 2014;343:115-119. 10. Jami M, Salehi-Najafabadi Z, Ahmadinejad F, et al. Edaravone leads to proteome changes indicative of neuronal cell protection in response to oxidative stress. Neurochem Int 2015;90:134-141. 11. Ahmadinejad F, Geir Møller S, Hashemzadeh-Chaleshtori M, et al. Molecular mechanisms behind free radical scavengers function against oxidative stress. Antioxidants (Basel) 2017;6:51.
Journal of Stroke and Cerebrovascular Diseases, Vol. ■■, No. ■■ (■■), 2017: p ■■
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Letter to the Editor Edaravone and Its Protective Effects against Disease Progression in Neurological Conditions Besides Strokes Dear Editor, Edaravone (EDVN) exerts neuroprotection against a number of different1 neuronal pathologies. EDVN appears to have a protective effect against disease evolution in Alzheimer’s disease (AD). It mediates this role in part by suppressing Aβ aggregation.2 EDVN therapy attenuates and restricts AD associated memory deficits. Yang et al3 have recently demonstrated that this is associated with decreased acetylcholinesterase activity in the hippocampus. At the same time, EDVN mitigates Aβinduced intracranial oxidation. In addition, “spatial learning” defects seen in AD models are decreased.4 Besides the above changes, EDVN also alters “superoxide dismutase” activity. Overall, EDVN also enhances and augments α-secretase-derived APP fragments.5 Concurrently, EDVN modulates and ameliorates glial activation. In addition, Aβ-induced accentuation of I Ca is reversed by EDVN. Interestingly, Qiang et al have recently designed DL-3-n-butylphthalide-EDVN hybrids that act as dual inhibitors of amyloid-β aggregation as well as monoamine oxidases.6 Concurrently, EDVN restricts and reduces Tau hyperphosphorylation. This is accompanied by an attenuating effect on β-secretase-derived APP fragments. At the same time, EDVN alters and affects “glutathione peroxidase” activity.7 Besides the above-mentioned changes, EDVN also has a negative impact on intrahippocampal choline acetylase activity. EDVN also exhibits neuroprotection from the development and progression of the disease processes in Parkinson’s disease (PD).8 Cheng et al have recently demonstrated that EDVN mediates this role primarily by accentuating heme oxygenase-1 expression.9 In addition, EDVN suppresses dopaminergic neuron apoptosis. These neuroprotective effects of EDVN have been confirmed both in vivo as well as in vitro.10 At the same time, EDVN has a negative impact on intracranial ROS activity. Ahmadinejad et al 11 have recently shown that concurrently, EDVN modulates and affects the induction of peroxiredoxin-2, thereby further protecting neuronal tissue from PD. 1052-3057/$ - see front matter © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.
As is very well evident from the above examples, EDVN exhibits significant neuroprotective properties. Hopefully, the coming few years will see an increase in the clinical utilization of EDVN as a therapeutic agent for ameliorating the disease processes in both AD as well as PD. Shailendra Kapoor, MD Kaiser Permanente, Atlanta, Georgia. E-mail: [email protected] https://doi.org/10.1016/j.jstrokecerebrovasdis.2017.08.042
References 1. Yamaguchi T, Awano H, Matsuda H, et al. Edaravone with and without. 6 Mg/Kg alteplase within 4.5 hours after Ischemic Stroke: a prospective cohort study (PROTECT4. 5). J Stroke Cerebrovasc Dis 2017;26:756-765. 2. Jiao SS, Yao XQ, Liu YH, et al. Edaravone alleviates Alzheimer’s disease-type pathologies and cognitive deficits. Proc Natl Acad Sci USA 2015;112:5225-5230. 3. Yang R, Wang Q, Li F, et al. Edaravone injection ameliorates cognitive deficits in rat model of Alzheimer’s disease. Neurol Sci 2015;36:2067-2072. 4. He F, Cao YP, Che FY, et al. Inhibitory effects of edaravone in beta-amyloid-induced neurotoxicity in rats. Biomed Res Int 2014;2014:370368. 5. Zhou S, Yu G, Chi L, et al. Neuroprotective effects of edaravone on cognitive deficit, oxidative stress and tau hyperphosphorylation induced by intracerebroventricular streptozotocin in rats. Neurotoxicology 2013;38:136-145. 6. Qiang X, Li Y, Yang X, et al. DL-3-n-butylphthalideEdaravone hybrids as novel dual inhibitors of amyloid-β aggregation and monoamine oxidases with high antioxidant potency for Alzheimer’s therapy. Bioorg Med Chem Lett 2017;27:718-722. 7. Shen Y, Wang Y, Yu G, et al. Effects of edaravone on amyloid-β precursor protein processing in SY5Y-APP695 cells. Neurotox Res 2013;24:139-147. 8. Yuan WJ, Yasuhara T, Shingo T, et al. Neuroprotective effects of edaravone-administration on 6-OHDA-treated dopaminergic neurons. BMC Neurosci 2008;9:75. 9. Cheng B, Guo Y, Li C, et al. Edaravone protected PC12 cells against MPP (+)-cytoxicity via inhibiting oxidative stress and up-regulating heme oxygenase-1 expression. J Neurol Sci 2014;343:115-119. 10. Jami M, Salehi-Najafabadi Z, Ahmadinejad F, et al. Edaravone leads to proteome changes indicative of neuronal cell protection in response to oxidative stress. Neurochem Int 2015;90:134-141. 11. Ahmadinejad F, Geir Møller S, Hashemzadeh-Chaleshtori M, et al. Molecular mechanisms behind free radical scavengers function against oxidative stress. Antioxidants (Basel) 2017;6:51.
Journal of Stroke and Cerebrovascular Diseases, Vol. ■■, No. ■■ (■■), 2017: p ■■
1