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32 results on '"Grigoletto, Jessica"'

5. The 5-HT4 receptor agonist, Velusetrag, rescues GI dysfunction, gut inflammation and dysbiosis in the A53T αS mouse model of Parkinson’s Disease.

Author

Colla, Emanuela, primary, Grigoletto, Jessica, additional, Miraglia, Fabiana, additional, Benvenuti, Laura, additional, Pellegrini, Carolina, additional, Soldi, Sara, additional, Galletti, Serena, additional, Cattaneo, Antonino, additional, Pich, Emilio Merlo, additional, Grimaldi, Maria, additional, and Vesci, Loredana, additional

Published
2023
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8. Additional file 4 of Ischemic stroke causes Parkinson���s disease-like pathology and symptoms in transgenic mice overexpressing alpha-synuclein

Author

Lohmann, Stephanie, Grigoletto, Jessica, Bernis, Maria Eugenia, Pesch, Verena, Ma, Liang, Reithofer, Sara, and Tamg��ney, G��ltekin

Abstract

Additional file 4. Quantification of phosphorylated ��-synuclein deposits in different brain regions of TgM83+/��� at 360 days after stroke. The number of phosphorylated ��-synuclein-positive cells per square millimeter was plotted for the ipsilateral and contralateral brain hemisphere for each quantified brain area of mice subjected to stroke. The coordinates of the quantified coronal tissue sections relative to the bregma were 0.74 mm (a), ���1.70 mm (b), ���2.92 mm (c), ���4.84 mm (d), and ���5.68 mm (e) as shown in the heat map in Fig. 7b. Data shown represent the mean �� standard deviation of four animals.

Published
2022
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10. Additional file 3 of Ischemic stroke causes Parkinson���s disease-like pathology and symptoms in transgenic mice overexpressing alpha-synuclein

Author

Lohmann, Stephanie, Grigoletto, Jessica, Bernis, Maria Eugenia, Pesch, Verena, Ma, Liang, Reithofer, Sara, and Tamg��ney, G��ltekin

Subjects
cardiovascular diseases
Abstract

Additional file 3. Spread of neuroinflammation to the contralateral brain hemisphere by 360 days after stroke. Staining of brain tissue sections of MCAO- and sham-treated TgM83+/��� mice with antibodies to Iba1 (a) and to GFAP (b) revealed that microgliosis and astrogliosis had spread to the contralateral brain hemisphere by 360 days after stroke. A higher amount of microglia was found throughout the entire contralateral brain hemisphere of MCAO-treated animals compared to sham-treated animals (a). Also, a higher amount of astrocytes was detected in the contralateral brain hemisphere of MCAO-treated animals compared to sham-treated animals, especially in the lower isocortical region and the upper part of the caudoputamen (b). Scale bars represent 1.0 mm.

Published
2022
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11. Additional file 2 of Ischemic stroke causes Parkinson���s disease-like pathology and symptoms in transgenic mice overexpressing alpha-synuclein

Author

Lohmann, Stephanie, Grigoletto, Jessica, Bernis, Maria Eugenia, Pesch, Verena, Ma, Liang, Reithofer, Sara, and Tamg��ney, G��ltekin

Subjects
nervous system
Abstract

Additional file 2. TgM83+/��� mice do not show any neuronal loss following sham surgery Immunohistochemical staining for NeuN showed that sham surgery did not cause any neuronal loss in the ipsilateral or contralateral brain hemispheres of TgM83+/��� mice at 14 (a), 30 (b), 90 (b), 180 (b), or 360 days (b) after sham surgery. The scale bar represents 0.5 mm.

Published
2022
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13. Additional file 2 of A role for α-Synuclein in axon growth and its implications in corticostriatal glutamatergic plasticity in Parkinson’s disease

Author

Schechter, Meir, Grigoletto, Jessica, Suaad Abd-Elhadi, Glickstein, Hava, Friedman, Alexander, Geidy E. Serrano, Beach, Thomas G., and Sharon, Ronit

Subjects
nervous system
Abstract

Additional file 2 Supplementary Fig. S1. α-Syn expression enhances axonal growth in primary hippocampal, mesencephalic and cortical neurons. A. Primary hippocampal cultures from α-Syn−/− (C57BL/6JOlaHsd) mouse brains, virally transduced either with WT α-Syn, A53T α-Syn, K10,12E α-Syn, or a mock-GFP vector. Cells were fixed at 4 DIV and immunoreacted with antibodies against α-Syn (MJFR1, green), α-tubulin (white) and PI4,5P2 (red). Direct fluorescence was captured for GFP (green). Bar = 25 μm. B. Graph showing the average length of the main extension designated as axons (in μm); C. Total length of collaterals per axon (in μm); and D. PI4,5P2 levels within the main axon and its collaterals (per μm2 area) quantified by Fiji (Image J) program. Mean ± SE; n > 17 cells; *, P 15 cells; *, P 20 cells; *, P

Published
2020
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14. Alpha-synuclein/synapsin III pathological interplay boosts the motor response to methylphenidate

Author

Faustini, Gaia, primary, Longhena, Francesca, additional, Bruno, Agostino, additional, Bono, Federica, additional, Grigoletto, Jessica, additional, La Via, Luca, additional, Barbon, Alessandro, additional, Casiraghi, Andrea, additional, Straniero, Valentina, additional, Valoti, Ermanno, additional, Costantino, Gabriele, additional, Benfenati, Fabio, additional, Missale, Cristina, additional, Pizzi, Marina, additional, Spillantini, Maria Grazia, additional, and Bellucci, Arianna, additional

Published
2020
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17. Depletion of Progranulin Reduces GluN2B-Containing NMDA Receptor Density, Tau Phosphorylation, and Dendritic Arborization in Mouse Primary Cortical Neurons

Author

Longhena, Francesca, primary, Zaltieri, Michela, additional, Grigoletto, Jessica, additional, Faustini, Gaia, additional, La Via, Luca, additional, Ghidoni, Roberta, additional, Benussi, Luisa, additional, Missale, Cristina, additional, Spano, PierFranco, additional, and Bellucci, Arianna, additional

Published
2017
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19. Synapsin III alterations in Parkinson's disease

Author

Bellucci, Arianna, primary, Zaltieri, Michela, additional, Longhena, Francesca, additional, Faustini, Gaia, additional, Grigoletto, Jessica, additional, Favero, Gaia, additional, Castrezzati, Stefania, additional, Rezzani, Rita, additional, Pizzi, Marina, additional, Benfenati, Fabio, additional, Spillantini, Maria Grazia, additional, Missale, Cristina, additional, and Spano, PierFranco, additional

Published
2016
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23. α-synuclein and synapsin III cooperatively regulate synaptic function in dopamine neurons

Author

Zaltieri, Michela, primary, Grigoletto, Jessica, additional, Longhena, Francesca, additional, Navarria, Laura, additional, Favero, Gaia, additional, Castrezzati, Stefania, additional, Colivicchi, Maria Alessandra, additional, Della Corte, Laura, additional, Rezzani, Rita, additional, Pizzi, Marina, additional, Benfenati, Fabio, additional, Spillantini, Maria Grazia, additional, Missale, Cristina, additional, Spano, PierFranco, additional, and Bellucci, Arianna, additional

Published
2015
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28. α-Synuclein- and MPTP-Generated Rodent Models of Parkinsons Disease and the Study of Extracellular Striatal Dopamine Dynamics: A Microdialysis Approach

Author

Bazzu, Gianfranco, primary, Calia, Giammario, additional, Puggioni, Giulia, additional, Spissu, Ylenia, additional, Rocchitta, Gaia, additional, Debetto, Patrizia, additional, Grigoletto, Jessica, additional, Zusso, Morena, additional, Migheli, Rossana, additional, Andrea Serra, Pier, additional, Speranza Desole, Maria, additional, and Miele, Egidio, additional

Published
2010
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32. alpha-Synuclein- and MPTP-generated rodent models of Parkinson's disease and the study of extracellular striatal dopamine dynamics: a microdialysis approach.

Author

Bazzu G, Calia G, Puggioni G, Spissu Y, Rocchitta G, Debetto P, Grigoletto J, Zusso M, Migheli R, Serra PA, Desole MS, and Miele E

Subjects
Animals, Brain drug effects, Brain metabolism, Dopamine metabolism, Humans, Mice, Mice, Transgenic genetics, Mice, Transgenic metabolism, Parkinsonian Disorders chemically induced, Rats, Rats, Transgenic genetics, Rats, Transgenic metabolism, alpha-Synuclein physiology, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine pharmacology, Disease Models, Animal, Dopamine physiology, Microdialysis, Neurotoxins pharmacology, Parkinson Disease metabolism, Parkinsonian Disorders metabolism, alpha-Synuclein metabolism
Abstract

The classical animal models of Parkinson's disease (PD) rely on the use of neurotoxins, including 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 6-hydroxydopamine and, more recently, the agricultural chemicals paraquat and rotenone, to deplete dopamine (DA). These neurotoxins elicit motor deficits in different animal species although MPTP fails to induce a significant dopaminergic neurodegeneration in rats. In the attempt to better reproduce the key features of PD, in particular the progressive nature of neurodegeneration, alternative PD models have been developed, based on the genetic and neuropathological links between -synuclein ( -syn) and PD. In vivo microdialysis was used to investigate extracellular striatal DA dynamics in MPTP- and -syn-generated rodent models of PD. Acute and sub-acute MPTP intoxication of mice both induce prolonged release of striatal DA. Such DA release may be considered the first step in MPTP-induced striatal DA depletion and nigral neuron death, mainly through reactive oxygen species generation. Although MPTP induces DA reduction, neurochemical and motor recovery starts immediately after the end of treatment, suggesting that compensatory mechanisms are activated. Thus, the MPTP mouse model of PD may be unsuitable for closely reproducing the features of the human disease and predicting potential long-term therapeutic effects, in terms of both striatal extracellular DA and behavioral outcome. In contrast, the -syn-generated rat model of PD does not suffer from a massive release of striatal DA during induction of the nigral lesion, but rather is characterized by a prolonged reduction in baseline DA and nicotine-induced increases in dialysate DA levels. These results are suggestive of a stable nigrostriatal lesion with a lack of dopaminergic neurochemical recovery. The -syn rat model thus reproduces the initial stage and slow development of PD, with a time-dependent impairment in motor function. This article will describe the above experimental PD models and demonstrate the utility of microdialysis for their characterization.

Published
2010
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