Nicergoline, a drug used for age-dependent cognitive impairment, protects cultured neurons against β-amyloid toxicity (943 views)
Brain Res (ISSN: 0006-8993), 2005; 1047(1): 30-37.
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Paper type: Journal Article,
Impact factor: 2.296, 5-year impact factor: 2.957
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-20444391320&partnerID=40&md5=b32bdfa88209280ff987ec9c2110536d
Keywords: β-Amyloid Toxicity, Cortical Neurons, Glial-Neuronal Interaction, Nicergoline, Alpha Adrenergic Receptor Blocking Agent, Amyloid Beta Protein[25-35], Glial Cell Line Derived Neurotrophic Factor, Methysergide, Prazosin, Protein Bax, Protein Bcl 2, Serotonin Antagonist, Transforming Growth Factor Beta, Alzheimer Disease, Animal Experiment, Animal Tissue, Apoptosis, Article, Astrocyte, Brain Cortex, Brain Slice, Cell Culture, Cognitive Defect, Controlled Study, Culture Medium, Drug Withdrawal, Nerve Cell Necrosis, Nerve Degeneration, Neuroprotection, Neurotoxicity, Nonhuman, Priority Journal, Amyloid Beta-Protein, Bcl-2-Associated X Protein, Cell Communication, Cerebral Cortex, Coculture Techniques, Cognition Disorders, Memory Disorders, Nerve Growth Factors, Neuroprotective Agents, Peptide Fragments, Proto-Oncogene Proteins C-Bcl-2, Sprague-Dawley, Amyloid Beta Protein [25-35],
Affiliations:
*** IBB - CNR ***
Department of Pharmaceutical Sciences, University of Catania, Viale A. Doria, 6, 95125, Catania, Italy
Department of Experimental and Clinical Pharmacology, University of Catania, Viale A. Doria, 6, 95125, Catania, Italy
DISCAFF, University of Piemonte Orientale, Italy
CNS Medical Department, Pfizer Italia, Rome, Italy
I.N.M. Neuromed, Pozzilli, Italy
IRCCS Oasi Maria SS, Troina, Italy
Department of Human Physiology and Pharmacology, University of Rome La Sapienza, Italy
IBB, CNR, Catania, Italy
I. N. M. Neuromed, Pozzilli, Italy
References:
Not available.
Brain Res (ISSN: 0006-8993), 2005; 1047(1): 30-37.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 2.296, 5-year impact factor: 2.957
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-20444391320&partnerID=40&md5=b32bdfa88209280ff987ec9c2110536d
Keywords: β-Amyloid Toxicity, Cortical Neurons, Glial-Neuronal Interaction, Nicergoline, Alpha Adrenergic Receptor Blocking Agent, Amyloid Beta Protein[25-35], Glial Cell Line Derived Neurotrophic Factor, Methysergide, Prazosin, Protein Bax, Protein Bcl 2, Serotonin Antagonist, Transforming Growth Factor Beta, Alzheimer Disease, Animal Experiment, Animal Tissue, Apoptosis, Article, Astrocyte, Brain Cortex, Brain Slice, Cell Culture, Cognitive Defect, Controlled Study, Culture Medium, Drug Withdrawal, Nerve Cell Necrosis, Nerve Degeneration, Neuroprotection, Neurotoxicity, Nonhuman, Priority Journal, Amyloid Beta-Protein, Bcl-2-Associated X Protein, Cell Communication, Cerebral Cortex, Coculture Techniques, Cognition Disorders, Memory Disorders, Nerve Growth Factors, Neuroprotective Agents, Peptide Fragments, Proto-Oncogene Proteins C-Bcl-2, Sprague-Dawley, Amyloid Beta Protein [25-35],
Affiliations:
*** IBB - CNR ***
Department of Pharmaceutical Sciences, University of Catania, Viale A. Doria, 6, 95125, Catania, Italy
Department of Experimental and Clinical Pharmacology, University of Catania, Viale A. Doria, 6, 95125, Catania, Italy
DISCAFF, University of Piemonte Orientale, Italy
CNS Medical Department, Pfizer Italia, Rome, Italy
I.N.M. Neuromed, Pozzilli, Italy
IRCCS Oasi Maria SS, Troina, Italy
Department of Human Physiology and Pharmacology, University of Rome La Sapienza, Italy
IBB, CNR, Catania, Italy
I. N. M. Neuromed, Pozzilli, Italy
References:
Not available.
Nicergoline, a drug used for age-dependent cognitive impairment, protects cultured neurons against β-amyloid toxicity
Nicergoline, a drug used for the treatment of Alzheimer's disease and other types of dementia, was tested for its ability to protect neurons against β-amyloid toxicity. Pure cultures of rat cortical neurons were challenged with a toxic fragment of β-amyloid peptide (βAP25-35) and toxicity was assessed after 24 h. Micromolar concentrations of nicergoline or its metabolite, MDL, attenuated βAP25-35-induced neuronal death, whereas MMDL (another metabolite of nicergoline), the α1- adrenergic receptor antagonist, prazosin, or the serotonin 5HT-2 receptor antagonist, methysergide, were inactive. Nicergoline increased the basal levels of Bcl-2 and reduced the increase in Bax levels induced by β-amyloid, indicating that the drug inhibits the execution of an apoptotic program in cortical neurons. In mixed cultures of rat cortical cells containing both neurons and astrocytes, nicergoline and MDL were more efficacious than in pure neuronal cultures in reducing β-amyloid neurotoxicity. Experiments carried out in pure cultures of astrocytes showed that a component of neuroprotection was mediated by a mechanism of glial-neuronal interaction. The conditioned medium of cultured astrocytes treated with nicergoline or MDL for 72-96 h (collected 24 h after drug withdrawal) was neuroprotective when transferred to pure neuronal cultures challenged with β-amyloid. In cultured astrocytes, nicergoline increased the intracellular levels of transforming-growth factor-β and glial-derived neurotrophic factor, two trophic factors that are known to protect neurons against β-amyloid toxicity. These results raise the possibility that nicergoline reduces neurodegeneration in the Alzheimer's brain. © 2005 Elsevier B.V. All rights reserved.
Nicergoline, a drug used for the treatment of Alzheimer's disease and other types of dementia, was tested for its ability to protect neurons against β-amyloid toxicity. Pure cultures of rat cortical neurons were challenged with a toxic fragment of β-amyloid peptide (βAP25-35) and toxicity was assessed after 24 h. Micromolar concentrations of nicergoline or its metabolite, MDL, attenuated βAP25-35-induced neuronal death, whereas MMDL (another metabolite of nicergoline), the α1- adrenergic receptor antagonist, prazosin, or the serotonin 5HT-2 receptor antagonist, methysergide, were inactive. Nicergoline increased the basal levels of Bcl-2 and reduced the increase in Bax levels induced by β-amyloid, indicating that the drug inhibits the execution of an apoptotic program in cortical neurons. In mixed cultures of rat cortical cells containing both neurons and astrocytes, nicergoline and MDL were more efficacious than in pure neuronal cultures in reducing β-amyloid neurotoxicity. Experiments carried out in pure cultures of astrocytes showed that a component of neuroprotection was mediated by a mechanism of glial-neuronal interaction. The conditioned medium of cultured astrocytes treated with nicergoline or MDL for 72-96 h (collected 24 h after drug withdrawal) was neuroprotective when transferred to pure neuronal cultures challenged with β-amyloid. In cultured astrocytes, nicergoline increased the intracellular levels of transforming-growth factor-β and glial-derived neurotrophic factor, two trophic factors that are known to protect neurons against β-amyloid toxicity. These results raise the possibility that nicergoline reduces neurodegeneration in the Alzheimer's brain. © 2005 Elsevier B.V. All rights reserved.
Nicergoline, a drug used for age-dependent cognitive impairment, protects cultured neurons against β-amyloid toxicity
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Nicergoline, a drug used for age-dependent cognitive impairment, protects cultured neurons against β-amyloid toxicity
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Impact Factor: 5.275
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Caraci F, Molinaro G, Battaglia G, Giuffrida ML, Riozzi B, Traficante A, Bruno V, Cannella M, Merlo S, Wang X, Heinz BA, Nisenbaum ES, Britton TC, Drago F, Sortino MA, Copani A, Nicoletti F
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Mol Pharmacol (ISSN: 0026-895x), 2011 Mar; 79(3): 618-626.
Impact Factor: 4.883
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* Probing the Ca2+ Mobilizing Properties on Primary Cortical Neurons of a New Stable cADPR Mimic (105 views)
Bioorg Chem (ISSN: 0045-2068linking, 1090-2120electronic), 2021 Oct 2; 117: 105401-105411.
Impact Factor: 5.275
View Export to BibTeX Export to EndNote
Caraci F, Tascedda F, Merlo F, Benatti C, Spampinato S, Munafò A, Leggio GM, Nicoletti F, Brunello N, Drago F, Sortino MA, Copani A
* Fluoxetine Prevents Ab1-42-Induced Toxicity via a Paracrine Signaling Mediated by Transforming-Growth- Factor-b1 (334 views) (PDF 218 views)
Frontiers In Pharmacology, 2016 Oct; 7: 1-11.
Impact Factor: 4.418
View Export to BibTeX Export to EndNote
Caraci F, Molinaro G, Battaglia G, Giuffrida ML, Riozzi B, Traficante A, Bruno V, Cannella M, Merlo S, Wang X, Heinz BA, Nisenbaum ES, Britton TC, Drago F, Sortino MA, Copani A, Nicoletti F
* Targeting group II Metabotropic Glutamate (mGlu) receptors for the treatment of psychosis associated with alzheimer's disease: Selective activation of mGlu2 receptors amplifies β-amyloid toxicity in cultured neurons, whereas dual activation of mGlu2 and mGlu3 receptors is neuroprotective (825 views)
Mol Pharmacol (ISSN: 0026-895x), 2011 Mar; 79(3): 618-626.
Impact Factor: 4.883
View Export to BibTeX Export to EndNote
3 Records (3 excluding Abstracts).
Total impact factor: 14.576 (14.576 excluding Abstracts).
Total 5 year impact factor: 7.97 (7.97 excluding Abstracts).
Total impact factor: 14.576 (14.576 excluding Abstracts).
Total 5 year impact factor: 7.97 (7.97 excluding Abstracts).
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