M
Massimo Tortarolo
Researcher at Mario Negri Institute for Pharmacological Research
Publications - 40
Citations - 2015
Massimo Tortarolo is an academic researcher from Mario Negri Institute for Pharmacological Research. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Motor neuron. The author has an hindex of 23, co-authored 38 publications receiving 1822 citations. Previous affiliations of Massimo Tortarolo include King's College London.
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Journal ArticleDOI
Mutant Copper-Zinc Superoxide Dismutase (SOD1) Induces Protein Secretion Pathway Alterations and Exosome Release in Astrocytes IMPLICATIONS FOR DISEASE SPREADING AND MOTOR NEURON PATHOLOGY IN AMYOTROPHIC LATERAL SCLEROSIS
Manuela Basso,Silvia Pozzi,Massimo Tortarolo,Fabio Fiordaliso,Cinzia Bisighini,Laura Pasetto,Gabriella Spaltro,D. Lidonnici,Francesco Gensano,Elisa Battaglia,Caterina Bendotti,Valentina Bonetto +11 more
TL;DR: The expression of mutant SOD1 has a substantial impact on astrocyte protein secretion pathways, contributing to motor neuron pathology and disease spread and new therapeutic approaches should target exosomes to contain disease progression.
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Transgenic SOD1 G93A mice develop reduced GLT-1 in spinal cord without alterations in cerebrospinal fluid glutamate levels.
Caterina Bendotti,Massimo Tortarolo,Sachin K. Suchak,Novella Calvaresi,Lucia Carvelli,Antonio Bastone,T. Massimo Rizzi,Marcus Rattray,Tiziana Mennini +8 more
TL;DR: Findings indicate that the loss of GLT‐1 protein in ALS mice selectively occurs in the areas affected by neurodegeneration and reactive astrocytosis and it is not associated with increases of glutamate levels in CSF.
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Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression
Massimo Tortarolo,Pietro Veglianese,Novella Calvaresi,Andrea Botturi,Cosmo Rossi,A Giorgini,Antonio Migheli,Caterina Bendotti +7 more
TL;DR: Activation of p38MAPK in motor neurons and then in reactive glial cells may contribute, respectively, to the development and progression of motor neuron pathology in SOD1G93A mice.
Journal ArticleDOI
Functional alterations of the ubiquitin-proteasome system in motor neurons of a mouse model of familial amyotrophic lateral sclerosis†
Cristina Cheroni,Marianna Marino,Massimo Tortarolo,Pietro Veglianese,Silvia De Biasi,Elena Fontana,Laura Vitellaro Zuccarello,Christa J. Maynard,Nico P. Dantuma,Caterina Bendotti +9 more
TL;DR: Findings suggest that UPS impairment occurs in motor neurons of mutant SOD1-linked ALS mice and may play a role in the disease progression, and support the existence of proteasome modifications in ALS vulnerable tissues.
Journal ArticleDOI
Glutamate AMPA receptors change in motor neurons of SOD1G93A transgenic mice and their inhibition by a noncompetitive antagonist ameliorates the progression of amytrophic lateral sclerosis-like disease
Massimo Tortarolo,Giuliano Grignaschi,Novella Calvaresi,Eleonora Zennaro,Gabriella Spaltro,Milena Colovic,Claudia Fracasso,Giovanna Guiso,Bernd Elger,Herbert Schneider,Bernd Seilheimer,Silvio Caccia,Caterina Bendotti +12 more
TL;DR: Treatment with a new noncompetitive AMPA antagonist, ZK 187638, partially protected motor neurons, improved motor function, and prolonged the survival of SOD1G93A mice.