Ceftriaxone blocks the polymerisation of alpha-synuclein and exerts neuroprotective effects in vitro. (Articolo in rivista)

Type
Label
  • Ceftriaxone blocks the polymerisation of alpha-synuclein and exerts neuroprotective effects in vitro. (Articolo in rivista) (literal)
Anno
  • 2014-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1021/cn400149k (literal)
Alternative label
  • Ruzza, P.; Siligardi, G.;Hussain, R.; Marchiani, A.; Islami, M.; Bubacco, L.; Delogu, G.; Fabbri, D.; Dettori, A.M.; Sechi, M.; Nicolino Pala, N.; Spissu, Y.; Migheli, R.; Serra, P.A.; Sechi, G.P. (2014)
    Ceftriaxone blocks the polymerisation of alpha-synuclein and exerts neuroprotective effects in vitro.
    in ACS chemical neuroscience
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Ruzza, P.; Siligardi, G.;Hussain, R.; Marchiani, A.; Islami, M.; Bubacco, L.; Delogu, G.; Fabbri, D.; Dettori, A.M.; Sechi, M.; Nicolino Pala, N.; Spissu, Y.; Migheli, R.; Serra, P.A.; Sechi, G.P. (literal)
Pagina inizio
  • 30 (literal)
Pagina fine
  • 38 (literal)
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  • 5 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
  • 9 (literal)
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  • 1 (literal)
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  • Institute of Biomolecular Chemistry of CNR, Padua Unit, Padua 35131, Italy Diamond Light Source Ltd., Harwell Science and Innovation Campus, Didcot, Oxfordshire OX11 0DE, United Kingdom Department of Biology, University of Padua, Padua 35121, Italy Institute of Biomolecular Chemistry of CNR, Sassari Unit, Sassari 07100, Italy Department of Chemistry and Pharmacy, University of Sassari, Sassari 07100, Italy Department of Clinical and Experimental Medicine, Medical School, University of Sassari, Sassari 07100, Italy. (literal)
Titolo
  • Ceftriaxone blocks the polymerisation of alpha-synuclein and exerts neuroprotective effects in vitro. (literal)
Abstract
  • The ?-lactam antibiotic ceftriaxone was suggested as a therapeutic agent in several neurodegenerative disorders, either for its ability to counteract glutamate-mediated toxicity, as in cerebral ischemia, or for its ability to enhance the degradation of misfolded proteins, as in Alexander's disease. Recently, the efficacy of ceftriaxone in neuroprotection of dopaminergic neurons in a rat model of Parkinson's disease was documented. However, which characteristics of ceftriaxone mediate its therapeutic effects remains unclear. Since, at the molecular level, neuronal ?-synuclein inclusions and pathological ?-synuclein transmission play a leading role in initiation of Parkinson-like neurodegeneration, we thought of investigating, by circular dichroism spectroscopy, the capability of ceftriaxone to interact with ?-synuclein. We found that ceftriaxone binds with good affinity to ?-synuclein and blocks its in vitro polymerization. Considering this finding, we also documented that ceftriaxone exerts neuroprotective action in an in vitro model of Parkinson's disease. Our data, in addition to the findings on neuroprotective activity of ceftriaxone on Parkinson-like neurodegeneration in vivo, indicates ceftriaxone as a potential agent in treatment of Parkinson's disease. (literal)
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