D Centonze

Summary

Affiliation: University of Rome Tor Vergata
Country: Italy

Publications

  1. request reprint
    Centonze D, Gubellini P, Rossi S, Picconi B, Pisani A, Bernardi G, et al. Subthalamic nucleus lesion reverses motor abnormalities and striatal glutamatergic overactivity in experimental parkinsonism. Neuroscience. 2005;133:831-40 pubmed
    ..Since neither l-DOPA treatment nor STN lesion affected sEPSCs kinetic properties, the reversal of these abnormalities in striatal excitatory synaptic transmission can be attributable to the normalization of glutamate release. ..
  2. Studer V, Rossi S, Motta C, Buttari F, Centonze D. Peripheral B cell depletion and central proinflammatory cytokine reduction following repeated intrathecal administration of rituximab in progressive Multiple Sclerosis. J Neuroimmunol. 2014;276:229-31 pubmed publisher
    ..Several central proinflammatory cytokines, and markers of neurodegeneration were markedly reduced. Central B cells modulation should be investigated in PMS. ..
  3. Stampanoni Bassi M, Iezzi E, Marfia G, Simonelli I, Musella A, Mandolesi G, et al. Platelet-derived growth factor predicts prolonged relapse-free period in multiple sclerosis. J Neuroinflammation. 2018;15:108 pubmed publisher
    ..Our results suggest that PDGF could promote a more prolonged relapse-free period during the course of RR-MS, without influencing inflammation reactivation and inflammation-driven neuronal damage and likely enhancing adaptive plasticity. ..
  4. Gentile A, Mori F, Bernardini S, Centonze D. Role of amyloid-β CSF levels in cognitive deficit in MS. Clin Chim Acta. 2015;449:23-30 pubmed publisher
  5. Rossi S, Motta C, Studer V, Macchiarulo G, Volpe E, Barbieri F, et al. Interleukin-1β causes excitotoxic neurodegeneration and multiple sclerosis disease progression by activating the apoptotic protein p53. Mol Neurodegener. 2014;9:56 pubmed publisher
    ..Inflammatory synaptopathy and neurodegeneration caused by IL-1β in RRMS patients involve the apoptotic cascade. Targeting IL-1β-p53 interaction might result in significant neuroprotection in MS. ..
  6. Centonze D, Floris R, Stefanini M, Rossi S, Fabiano S, Castelli M, et al. Proposed chronic cerebrospinal venous insufficiency criteria do not predict multiple sclerosis risk or severity. Ann Neurol. 2011;70:51-8 pubmed publisher
    ..Our results indicate that CCSVI has no role in either MS risk or MS severity. ..
  7. Gentile A, Fresegna D, Federici M, Musella A, Rizzo F, Sepman H, et al. Dopaminergic dysfunction is associated with IL-1β-dependent mood alterations in experimental autoimmune encephalomyelitis. Neurobiol Dis. 2015;74:347-58 pubmed publisher
  8. Centonze D, Mori F, Koch G, Buttari F, Codecà C, Rossi S, et al. Lack of effect of cannabis-based treatment on clinical and laboratory measures in multiple sclerosis. Neurol Sci. 2009;30:531-4 pubmed publisher
    ..This compound also failed to affect the synthesis and the degradation of the endocannabinoid anandamide, as well as the expression of both CB1 and CB2 cannabinoid receptors in various subpopulations of peripheral lymphocytes. ..
  9. request reprint
    Centonze D, Bari M, Rossi S, Prosperetti C, Furlan R, Fezza F, et al. The endocannabinoid system is dysregulated in multiple sclerosis and in experimental autoimmune encephalomyelitis. Brain. 2007;130:2543-53 pubmed
    ..Our study suggests that targeting the endocannabinoid system might be useful for the treatment of MS. ..

More Information

Publications25

  1. Rossi S, Motta C, Studer V, Macchiarulo G, Germani G, Finardi A, et al. Subclinical central inflammation is risk for RIS and CIS conversion to MS. Mult Scler. 2015;21:1443-52 pubmed publisher
    ..IL-8 might provide utility in determining the presence of active intrathecal inflammation, and could be important in diagnostically undefined cases. ..
  2. Centonze D, Rossi S, Rinaldi F, Gallo P. Severe relapses under fingolimod treatment prescribed after natalizumab. Neurology. 2012;79:2004-5 pubmed publisher
  3. Rossi S, Motta C, Musella A, Centonze D. The interplay between inflammatory cytokines and the endocannabinoid system in the regulation of synaptic transmission. Neuropharmacology. 2015;96:105-12 pubmed publisher
    ..In addition, the behavioral and clinical consequences of the modulation of synaptic transmission during neuroinflammation are discussed. This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'. ..
  4. request reprint
    Centonze D, Rossi S, Mercaldo V, Napoli I, Ciotti M, De Chiara V, et al. Abnormal striatal GABA transmission in the mouse model for the fragile X syndrome. Biol Psychiatry. 2008;63:963-73 pubmed
    ..Understanding the physiologic action of FMRP and the synaptic defects associated with GABA transmission might be useful to design appropriate pharmacologic interventions for FXS. ..
  5. request reprint
    Mori F, Nisticò R, Nicoletti C, Zagaglia S, Mandolesi G, Piccinin S, et al. RANTES correlates with inflammatory activity and synaptic excitability in multiple sclerosis. Mult Scler. 2016;22:1405-1412 pubmed
    ..RANTES correlates with inflammation and synaptic excitability in MS brains. ..
  6. Albanese M, Zagaglia S, Landi D, Boffa L, Nicoletti C, Marciani M, et al. Cerebrospinal fluid lactate is associated with multiple sclerosis disease progression. J Neuroinflammation. 2016;13:36 pubmed publisher
    ..A better understanding of the alterations of mitochondrial metabolic pathways associated to RRMS severity may pave the way to new therapeutic targets to contrast axonal damage and disease severity. ..
  7. Stampanoni Bassi M, Mori F, Buttari F, Marfia G, Sancesario A, Centonze D, et al. Neurophysiology of synaptic functioning in multiple sclerosis. Clin Neurophysiol. 2017;128:1148-1157 pubmed publisher
    ..Innate and adaptive immunity interact with the CNS in MS, in line with the concept that cytokines and chemokines, in concert with neurotransmitters and neuropeptides, represent a major communication system in the CNS. ..
  8. request reprint
    Centonze D, Koch G, Versace V, Mori F, Rossi S, Brusa L, et al. Repetitive transcranial magnetic stimulation of the motor cortex ameliorates spasticity in multiple sclerosis. Neurology. 2007;68:1045-50 pubmed
    ..No effect was obtained after a 2-week sham stimulation. Repetitive transcranial magnetic stimulation may improve spasticity in multiple sclerosis. ..
  9. Mango D, Nistico R, Furlan R, Finardi A, Centonze D, Mori F. PDGF Modulates Synaptic Excitability and Short-Latency Afferent Inhibition in Multiple Sclerosis. Neurochem Res. 2018;: pubmed publisher
    ..These findings show that PDGF affects GABAergic activity both in MS patients and in EAE hippocampus. ..
  10. Gentile A, Musella A, De Vito F, Fresegna D, Bullitta S, Rizzo F, et al. Laquinimod ameliorates excitotoxic damage by regulating glutamate re-uptake. J Neuroinflammation. 2018;15:5 pubmed publisher
    ..Overall, our results suggest that laquinimod protects against glutamate excitotoxicity of the cerebellum of EAE mice by bursting the expression of glial glutamate transporters, independently of its anti-inflammatory effects. ..
  11. Mori F, Ribolsi M, Kusayanagi H, Siracusano A, Mantovani V, Marasco E, et al. Genetic variants of the NMDA receptor influence cortical excitability and plasticity in humans. J Neurophysiol. 2011;106:1637-43 pubmed publisher
  12. Monteleone F, Nicoletti C, Stampanoni Bassi M, Iezzi E, Buttari F, Furlan R, et al. Nerve growth factor is elevated in the CSF of patients with multiple sclerosis and central neuropathic pain. J Neuroimmunol. 2018;314:89-93 pubmed publisher
    ..We found increased levels of NGF in the CSF of patients with CNP compared to patients without and to controls. This finding supports the hypothesis that NGF plays a role in MS related CNP. ..
  13. Musella A, Fresegna D, Rizzo F, Gentile A, Bullitta S, De Vito F, et al. A novel crosstalk within the endocannabinoid system controls GABA transmission in the striatum. Sci Rep. 2017;7:7363 pubmed publisher
  14. Mandolesi G, Bullitta S, Fresegna D, Gentile A, De Vito F, Dolcetti E, et al. Interferon-? causes mood abnormalities by altering cannabinoid CB1 receptor function in the mouse striatum. Neurobiol Dis. 2017;108:45-53 pubmed publisher
    ..A better understanding of the biological pathways underling the psychological disorders during neuroinflammatory conditions is crucial for developing effective therapeutic strategies. ..
  15. request reprint
    Centonze D, Prosperetti C, Barone I, Rossi S, Picconi B, Tscherter A, et al. NR2B-containing NMDA receptors promote the neurotoxic effects of 3-nitropropionic acid but not of rotenone in the striatum. Exp Neurol. 2006;202:470-9 pubmed