Fabrizio Gardoni

Summary

Affiliation: University of Milan
Country: Italy

Publications

  1. Mellone M, Zianni E, Stanic J, Campanelli F, Marino G, Ghiglieri V, et al. NMDA receptor GluN2D subunit participates to levodopa-induced dyskinesia pathophysiology. Neurobiol Dis. 2019;121:338-349 pubmed publisher
    ..Our findings support a role for GluN2D-NMDARs in LID, and they confirm that cell-type and subunit specific modifications of NMDARs underlie the pathophysiology of LID. ..
  2. Gardoni F, Morari M, Kulisevsky J, Brugnoli A, Novello S, Pisano C, et al. Safinamide Modulates Striatal Glutamatergic Signaling in a Rat Model of Levodopa-Induced Dyskinesia. J Pharmacol Exp Ther. 2018;367:442-451 pubmed publisher
  3. Gardoni F. MAGUK proteins: new targets for pharmacological intervention in the glutamatergic synapse. Eur J Pharmacol. 2008;585:147-52 pubmed publisher
  4. Gardoni F, Mauceri D, Malinverno M, Polli F, Costa C, Tozzi A, et al. Decreased NR2B subunit synaptic levels cause impaired long-term potentiation but not long-term depression. J Neurosci. 2009;29:669-77 pubmed publisher
    ..These data indicate that NR2B redistribution between synaptic and extrasynaptic membranes represents an important molecular disturbance of the glutamatergic synapse and affects the correct induction of LTP. ..
  5. Ploia C, Sclip A, Colombo A, Repici M, Gardoni F, Di Luca M, et al. Role of Glycogen Synthase Kinase-3? in APP Hyperphosphorylation Induced by NMDA Stimulation in Cortical Neurons. Pharmaceuticals (Basel). 2010;3:42-58 pubmed
    ..These data show a tight connection, in excitotoxic conditions, between APP metabolism and the GSK-3? signaling pathway. ..
  6. Mellone M, Gardoni F. Glutamatergic mechanisms in L-DOPA-induced dyskinesia and therapeutic implications. J Neural Transm (Vienna). 2018;125:1225-1236 pubmed publisher
    ..These results indicate that modulation of the glutamatergic system remains one of the most promising pharmacological strategies in the field. ..
  7. request reprint
    Gardoni F, Mauceri D, Fiorentini C, Bellone C, Missale C, Cattabeni F, et al. CaMKII-dependent phosphorylation regulates SAP97/NR2A interaction. J Biol Chem. 2003;278:44745-52 pubmed
    ..Our findings suggest that SAP97/NR2A interaction is regulated by CaMKII-dependent phosphorylation and provide a novel mechanism for the regulation of synaptic targeting of NMDA receptor subunits. ..
  8. request reprint
    Gardoni F, Bellone C, Cattabeni F, Di Luca M. Protein kinase C activation modulates alpha-calmodulin kinase II binding to NR2A subunit of N-methyl-D-aspartate receptor complex. J Biol Chem. 2001;276:7609-13 pubmed
    ..Thus, our data provide clues on understanding the molecular basis of a direct cross-talk between alphaCaMKII and PKC pathways in the postsynaptic compartment. ..
  9. request reprint
    Gardoni F, Schrama L, Kamal A, Gispen W, Cattabeni F, Di Luca M. Hippocampal synaptic plasticity involves competition between Ca2+/calmodulin-dependent protein kinase II and postsynaptic density 95 for binding to the NR2A subunit of the NMDA receptor. J Neurosci. 2001;21:1501-9 pubmed

More Information

Publications13

  1. Gardoni F, Saraceno C, Malinverno M, Marcello E, Verpelli C, Sala C, et al. The neuropeptide PACAP38 induces dendritic spine remodeling through ADAM10-N-cadherin signaling pathway. J Cell Sci. 2012;125:1401-6 pubmed publisher
  2. Stanic J, Mellone M, Cirnaru M, Perez Carrion M, Zianni E, Di Luca M, et al. LRRK2 phosphorylation level correlates with abnormal motor behaviour in an experimental model of levodopa-induced dyskinesias. Mol Brain. 2016;9:53 pubmed publisher
    ..Our findings support a close link between LRKK2 functional state and L-DOPA-induced abnormal motor behaviour and highlight that LRRK2 phosphorylation level may be implicated in LIDs, calling for novel therapeutic strategies. ..
  3. Borroni B, Stanic J, Verpelli C, Mellone M, Bonomi E, Alberici A, et al. Anti-AMPA GluA3 antibodies in Frontotemporal dementia: a new molecular target. Sci Rep. 2017;7:6723 pubmed publisher
    ..In conclusion, autoimmune mechanism might represent a new potentially treatable target in FTD and might open new lights in the disease underpinnings. ..
  4. Stanic J, Mellone M, Napolitano F, Racca C, Zianni E, Minocci D, et al. Rabphilin 3A: A novel target for the treatment of levodopa-induced dyskinesias. Neurobiol Dis. 2017;108:54-64 pubmed publisher
    ..Thus, we suggest that Rph3A/GluN2A complex could represent an innovative therapeutic target for those pathological conditions where NMDAR composition is significantly altered. ..