C Bendotti

Summary

Affiliation: Istituto di Ricerche Farmacologiche Mario Negri
Country: Italy

Publications

  1. ncbi New ideas for therapy in ALS: critical considerations
    Ettore Beghi
    Amyotroph Lateral Scler 7:126-7; discussion 127. 2006
  2. ncbi Early vacuolization and mitochondrial damage in motor neurons of FALS mice are not associated with apoptosis or with changes in cytochrome oxidase histochemical reactivity
    C Bendotti
    Laboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157, Milan, Italy
    J Neurol Sci 191:25-33. 2001
  3. ncbi Activated p38MAPK is a novel component of the intracellular inclusions found in human amyotrophic lateral sclerosis and mutant SOD1 transgenic mice
    Caterina Bendotti
    Laboratory of Molecular Neurobiology, Dept Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea, 62, 20157 Milano, Italy
    J Neuropathol Exp Neurol 63:113-9. 2004
  4. ncbi Inter- and intracellular signaling in amyotrophic lateral sclerosis: role of p38 mitogen-activated protein kinase
    C Bendotti
    Laboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy
    Neurodegener Dis 2:128-34. 2005
  5. ncbi Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression
    M Tortarolo
    Laboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy
    Mol Cell Neurosci 23:180-92. 2003
  6. ncbi Overexpression of S100beta in transgenic mice does not protect from serotonergic denervation induced by 5,7-dihydroxytryptamine
    C Bendotti
    Laboratory of Molecular Neurobiology, Mario Negri Institute for Pharmacological Research, Via Eritrea 62, 20157 Milan, Italy
    J Neurosci Res 67:501-10. 2002
  7. ncbi Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS
    P Veglianese
    Lab Molecular Neurobiology, Dept Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157 Milano, Italy
    Mol Cell Neurosci 31:218-31. 2006
  8. ncbi Unraveling the complexity of amyotrophic lateral sclerosis: recent advances from the transgenic mutant SOD1 mice
    M Peviani
    Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Milano, Italy
    CNS Neurol Disord Drug Targets 9:491-503. 2010
  9. ncbi Lack of changes in the PI3K/AKT survival pathway in the spinal cord motor neurons of a mouse model of familial amyotrophic lateral sclerosis
    M Peviani
    Lab Molecular Neurobiology, Dept Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157 Milano, Italy
    Mol Cell Neurosci 34:592-602. 2007
  10. ncbi Accumulation of human SOD1 and ubiquitinated deposits in the spinal cord of SOD1G93A mice during motor neuron disease progression correlates with a decrease of proteasome
    C Cheroni
    Laboratory Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea, 62 20157 Milan, Italy
    Neurobiol Dis 18:509-22. 2005

Collaborators

Detail Information

Publications48

  1. ncbi New ideas for therapy in ALS: critical considerations
    Ettore Beghi
    Amyotroph Lateral Scler 7:126-7; discussion 127. 2006
  2. ncbi Early vacuolization and mitochondrial damage in motor neurons of FALS mice are not associated with apoptosis or with changes in cytochrome oxidase histochemical reactivity
    C Bendotti
    Laboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157, Milan, Italy
    J Neurol Sci 191:25-33. 2001
    ..Activation of the mitochondrial permeability transition pore may be involved in this process, through excitotoxicity or other neurotoxic stimuli...
  3. ncbi Activated p38MAPK is a novel component of the intracellular inclusions found in human amyotrophic lateral sclerosis and mutant SOD1 transgenic mice
    Caterina Bendotti
    Laboratory of Molecular Neurobiology, Dept Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea, 62, 20157 Milano, Italy
    J Neuropathol Exp Neurol 63:113-9. 2004
    ..Our observations indicate that activation of p38MAPK might contribute significantly to the pathology of motor neurons in ALS...
  4. ncbi Inter- and intracellular signaling in amyotrophic lateral sclerosis: role of p38 mitogen-activated protein kinase
    C Bendotti
    Laboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy
    Neurodegener Dis 2:128-34. 2005
    ..Increased activation of p38MAPK may phosphorylate neuron-specific substrates altering their physiological properties and it may turn on responsive genes leading to neurotoxicity...
  5. ncbi Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression
    M Tortarolo
    Laboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy
    Mol Cell Neurosci 23:180-92. 2003
    ..These data suggest that 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...
  6. ncbi Overexpression of S100beta in transgenic mice does not protect from serotonergic denervation induced by 5,7-dihydroxytryptamine
    C Bendotti
    Laboratory of Molecular Neurobiology, Mario Negri Institute for Pharmacological Research, Via Eritrea 62, 20157 Milan, Italy
    J Neurosci Res 67:501-10. 2002
    ....
  7. ncbi Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS
    P Veglianese
    Lab Molecular Neurobiology, Dept Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157 Milano, Italy
    Mol Cell Neurosci 31:218-31. 2006
    ..These findings highlight the activation of a selective intracellular signaling pathway in the motor neurons of SOD1 mutant mice, which is likely implicated in their death...
  8. ncbi Unraveling the complexity of amyotrophic lateral sclerosis: recent advances from the transgenic mutant SOD1 mice
    M Peviani
    Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Milano, Italy
    CNS Neurol Disord Drug Targets 9:491-503. 2010
    ..In particular it will focus on the contribution of multiple cell types in governing the disease development and progression...
  9. ncbi Lack of changes in the PI3K/AKT survival pathway in the spinal cord motor neurons of a mouse model of familial amyotrophic lateral sclerosis
    M Peviani
    Lab Molecular Neurobiology, Dept Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157 Milano, Italy
    Mol Cell Neurosci 34:592-602. 2007
    ..Thus, motor neurons in SOD1G93A mice do not lose the pro-survival PI3K/Akt signal nor increase it in order to suppress the cell death mechanisms...
  10. ncbi Accumulation of human SOD1 and ubiquitinated deposits in the spinal cord of SOD1G93A mice during motor neuron disease progression correlates with a decrease of proteasome
    C Cheroni
    Laboratory Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea, 62 20157 Milan, Italy
    Neurobiol Dis 18:509-22. 2005
    ..This provides further evidence for an involvement of proteasome impairment in the toxicity of mutant SOD1...
  11. ncbi Transgenic SOD1 G93A mice develop reduced GLT-1 in spinal cord without alterations in cerebrospinal fluid glutamate levels
    C Bendotti
    Department of Neuroscience Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy
    J Neurochem 79:737-46. 2001
    ..The lack of changes in GLT-1 at the presymptomatic stage suggests that glial glutamate transporter reduction is not a primary event leading to motor neurone loss...
  12. ncbi Evidence that central 5-HT2 receptors do not play an important role in the anorectic activity of D-fenfluramine in the rat
    R Samanin
    Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy
    Neuropharmacology 28:465-9. 1989
    ..The results suggest that 5-HT receptors, other than 5-HT2, possibly 5-HT1B, are involved in the anorectic effect of D-fenfluramine in food-deprived rats...
  13. ncbi S-100beta protein is upregulated in astrocytes and motor neurons in the spinal cord of patients with amyotrophic lateral sclerosis
    A Migheli
    Department of Neuroscience, University of Turin, Italy
    Neurosci Lett 261:25-8. 1999
    ..S-100beta expression was also unrelated to neuronal or glial apoptosis. S-100beta upregulation in ALS spinal cord suggests that the protein might be involved in cellular defense mechanisms against oxidative stress...
  14. ncbi Differential expression of S100beta and glial fibrillary acidic protein in the hippocampus after kainic acid-induced lesions and mossy fiber sprouting in adult rat
    C Bendotti
    Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, Milano, 20157, Italy
    Exp Neurol 161:317-29. 2000
    ..These data show for the first time that an increase in S100beta expression in subpopulations of reactive astrocytes may be involved in the structural reorganization of the hippocampus following KA-induced neurodegeneration...
  15. ncbi Erythropoietin does not preserve motor neurons in a mouse model of familial ALS
    Giuliano Grignaschi
    Department of Neuroscience, Mario Negri Institute, Milano, Italy
    Amyotroph Lateral Scler 8:31-5. 2007
    ..However, it did not prolong life span or reduce motor neuron loss in lumbar spinal cord. The effect on motor function may be due to the improvement of skeletal muscle oxygenation induced by chronic EPO administration...
  16. doi Treatment with lithium carbonate does not improve disease progression in two different strains of SOD1 mutant mice
    Chiara Pizzasegola
    Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy
    Amyotroph Lateral Scler 10:221-8. 2009
    ..The present study does not identify any therapeutic or neuroprotective effect of lithium in SOD1G93A female mice...
  17. ncbi Kif1Bbeta isoform is enriched in motor neurons but does not change in a mouse model of amyotrophic lateral sclerosis
    Laura Conforti
    Mario Negri Research Institute for Pharmacological Research, Milan, Italy
    J Neurosci Res 71:732-9. 2003
    ..The absence of changes of Kif1Bbeta mRNA in transgenic SOD1G93A mice suggests that other molecular mechanisms may play a role in the disruption of axonal transport occurring in the motor neurons of these mice...
  18. pmc Functional alterations of the ubiquitin-proteasome system in motor neurons of a mouse model of familial amyotrophic lateral sclerosis
    Cristina Cheroni
    Laboratory of Molecular Neurobiology, Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Via La Masa, 19, 20156 Milan, Italy
    Hum Mol Genet 18:82-96. 2009
    ..These data suggest that UPS impairment occurs in motor neurons of mutant SOD1-linked ALS mice and may play a role in the disease progression...
  19. doi Intracerebroventricular administration of human umbilical cord blood cells delays disease progression in two murine models of motor neuron degeneration
    P Bigini
    Mario Negri Institute for Pharmacological Research, Milan, Italy
    Rejuvenation Res 14:623-39. 2011
    ..In particular, we show that HuCB-MNCs release a series of cytokines and chemokines with antiinflammatory properties that could be responsible of the functional improvement of mouse models of motor neuron degenerative disorders...
  20. ncbi Distribution of GAP-43 mRNA in the brain stem of adult rats as evidenced by in situ hybridization: localization within monoaminergic neurons
    C Bendotti
    Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy
    J Neurosci 11:600-7. 1991
    ....
  21. ncbi Distribution and cellular localization of high mobility group box protein 1 (HMGB1) in the spinal cord of a transgenic mouse model of ALS
    Daniele Lo Coco
    Lab Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157 Milano, Italy
    Neurosci Lett 412:73-7. 2007
    ....
  22. ncbi Insoluble mutant SOD1 is partly oligoubiquitinated in amyotrophic lateral sclerosis mice
    Manuela Basso
    Dulbecco Telethon Institute, Milan, Italy
    J Biol Chem 281:33325-35. 2006
    ..On the basis of these results, we propose that ubiquitination occurs only after SOD1 aggregation and that oligoubiquitination may underline alternative mechanisms in disease pathogenesis...
  23. ncbi Scientific and clinic highlights from the 15th International Symposium on MND
    C Bendotti
    Department of Neuroscience, Institute for Pharmacological Research Mario Negri, Milan
    Amyotroph Lateral Scler Other Motor Neuron Disord 6:187-91. 2005
  24. doi The small heat shock protein B8 (HspB8) promotes autophagic removal of misfolded proteins involved in amyotrophic lateral sclerosis (ALS)
    Valeria Crippa
    Dipartimento di Endocrinologia, Fisiopatologia e Biologia Applicata Center of Excellence on Neurodegenerative Diseases, CEND, Universita degli Studi di Milano, Milano, Italy
    Hum Mol Genet 19:3440-56. 2010
    ..Overall, these results indicate that the pharmacological modulation of HspB8 expression in motor neurons may have important implications to unravel the molecular mechanisms involved both in fALS and in sALS...
  25. ncbi Proteomic analysis of spinal cord of presymptomatic amyotrophic lateral sclerosis G93A SOD1 mouse
    Tania Massignan
    Dulbecco Telethon Institute, Milan, Italy
    Biochem Biophys Res Commun 353:719-25. 2007
    ..Moreover, we found a variation in the isoform pattern of cyclophilin A, a molecular chaperone that protects cells from the oxidative stress...
  26. ncbi 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
    Mario Negri Institute for Pharmacological Research, Milano, Italy
    J Neurosci Res 83:134-46. 2006
    ..In support of this, we showed that treatment with a new noncompetitive AMPA antagonist, ZK 187638, partially protected motor neurons, improved motor function, and prolonged the survival of SOD1(G93A) mice...
  27. ncbi Protein nitration in a mouse model of familial amyotrophic lateral sclerosis: possible multifunctional role in the pathogenesis
    Filippo Casoni
    Dulbecco Telethon Institute, Milan, Italy
    J Biol Chem 280:16295-304. 2005
    ....
  28. ncbi Glial activation and TNFR-I upregulation precedes motor dysfunction in the spinal cord of mnd mice
    Tiziana Mennini
    Department Molecular Biochemistry and Pharmacology, Mario Negri Institute for Pharmacological Research, Via Eritrea, 62, 20157, Milan, Italy
    Cytokine 25:127-35. 2004
    ..The role of TNF and TNFR-I on motor neurons is still to be demonstrated...
  29. ncbi Expression of glutamate receptor subtypes in the spinal cord of control and mnd mice, a model of motor neuron disorder
    Tiziana Mennini
    Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy
    J Neurosci Res 70:553-60. 2002
    ..These changes in ionotropic glutamate receptors may alter glutamatergic neurotransmission and play some role in the pathology of mnd mice...
  30. ncbi The heterogeneity of amyotrophic lateral sclerosis: a possible explanation of treatment failure
    Ettore Beghi
    Istituto di Ricerche Farmacologiche Mario Negri, Via La Masa 19, 20156 Milano, Italy
    Curr Med Chem 14:3185-200. 2007
    ....
  31. ncbi Androgen 5-alpha-reductase type 2 is highly expressed and active in rat spinal cord motor neurones
    P Pozzi
    Institute of Endocrinology, Center of Excellence on Neurodegenerative Diseases, University of Milan, Milano, Italy
    J Neuroendocrinol 15:882-7. 2003
    ..Because of the close association of androgen receptor and 5-alpha alpha-reductase type 2, motoneuronal cells should be considered as target cells for androgens...
  32. ncbi Mutation of SOD1 in ALS: a gain of a loss of function
    Daniela Sau
    Institute of Endocrinology, Center of Excellence on Neurodegenerative Diseases, Division of Human Nutrition, University of Milan, Milan, Italy
    Hum Mol Genet 16:1604-18. 2007
    ..The toxicity of mutant SOD1 might, therefore, arise from an initial misfolding (gain of function) reducing nuclear protection from the active enzyme (loss of function in the nuclei), a process that may be involved in ALS pathogenesis...
  33. pmc Characterization of detergent-insoluble proteins in ALS indicates a causal link between nitrative stress and aggregation in pathogenesis
    Manuela Basso
    Dulbecco Telethon Institute, Milan, Italy
    PLoS ONE 4:e8130. 2009
    ..However, the aggregate protein constituents are poorly characterized so knowledge on the role of aggregation in pathogenesis is limited...
  34. ncbi A single high dose of cocaine induces behavioural sensitization and modifies mRNA encoding GluR1 and GAP-43 in rats
    Giuliano Grignaschi
    Istituto di Ricerche Farmacologiche Mario Negri Via Eritrea 62, 20157 Milan, Italy
    Eur J Neurosci 20:2833-7. 2004
    ..These results further strengthen the involvement of NAc and VTA in the behavioural sensitization and suggest a role of GAP-43 in the synaptic reorganization associated to drug abuse...
  35. ncbi Low levels of ALS-linked Cu/Zn superoxide dismutase increase the production of reactive oxygen species and cause mitochondrial damage and death in motor neuron-like cells
    Milena Rizzardini
    Laboratory of Molecular Pathology, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157 Milan, Italy
    J Neurol Sci 232:95-103. 2005
    ..In conclusion, even a small amount of mutant SOD1 put motor neurons in a condition of oxidative stress and mitochondrial damage that causes cell vulnerability and death...
  36. ncbi Lessons from models of SOD1-linked familial ALS
    Caterina Bendotti
    Laboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri, Via Eritrea 62, 20157 Milan, Italy
    Trends Mol Med 10:393-400. 2004
    ..Recent data demonstrate that, although motoneurons are lost in patients, other cell types are also affected and actively contribute to the pathogenesis of the disease...
  37. ncbi Selective localization of mouse aldehyde oxidase mRNA in the choroid plexus and motor neurons
    C Bendotti
    Laboratory of Neuropharmacology, Centro Catullo e Daniela Borgomainerio, Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy
    Neuroreport 8:2343-9. 1997
    ..This localization is consistent with a possible role of AO in the pathogenesis of ALS...
  38. doi Nitroproteomics of peripheral blood mononuclear cells from patients and a rat model of ALS
    Giovanni Nardo
    Department of Molecular Biochemistry and Pharmacology, Mario Negri Institute for Pharmacological Research, Milano, Italy
    Antioxid Redox Signal 11:1559-67. 2009
    ....
  39. ncbi Cell culture models to investigate the selective vulnerability of motoneuronal mitochondria to familial ALS-linked G93ASOD1
    Andrea Raimondi
    Department of Pharmacology, School of Medicine, Center of Excellence on Neurodegenerative Diseases, University of Milano, Consiglio Nazionale delle Ricerche, CNR, Institute of Neuroscience, Milano, Italy
    Eur J Neurosci 24:387-99. 2006
    ..Our results suggest that mitochondrial vulnerability of motoneurons to G93ASOD1 is recapitulated in NSC-34 cells, and that peculiar features in network dynamics may account for the selective alterations of motoneuronal mitochondria...
  40. ncbi Studies on the role of 5-HT receptors in satiation and the effect of d-fenfluramine in the runway test
    J C Neill
    Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy
    Eur J Pharmacol 190:105-12. 1990
    ..In addition, blockade of 5-HT1 receptors can attenuate the development of satiation normally observed under control conditions in the runway test...
  41. pmc The epidemiology and treatment of ALS: focus on the heterogeneity of the disease and critical appraisal of therapeutic trials
    Ettore Beghi
    Istituto di Ricerche Farmacologiche Mario Negri, Via G La Masa 19, 20156 Milano, Italy
    Amyotroph Lateral Scler 12:1-10. 2011
    ..Further understanding of these factors will lead to improvements in patient stratification, and in the design of future clinical trials...
  42. ncbi Guidelines for the preclinical in vivo evaluation of pharmacological active drugs for ALS/MND: report on the 142nd ENMC international workshop
    Albert C Ludolph
    Department of Neurology, University of Ulm, Ulm, Germany
    Amyotroph Lateral Scler 8:217-23. 2007
    ..In this workshop, clinical and preclinical researchers established in the field of ALS/MND met in Holland in March 2006 in order to establish guidelines for the community for drug testing in mouse models...
  43. ncbi Does excitotoxic cell death of motor neurons in ALS arise from glutamate transporter and glutamate receptor abnormalities?
    Marcus Rattray
    King s College London, Wolfson Centre for Age Related Diseases, Guy s Hospital Campus, London SE1 1UL, UK
    Exp Neurol 201:15-23. 2006
  44. ncbi The densitometric physical fractionator for counting neuronal populations: application to a mouse model of familial amyotrophic lateral sclerosis
    Giuseppe Luca Ciavarro
    Bioengineering Department, Politecnico di Milano, Piazza L da Vinci, 32, I 20133 Milan, Italy
    J Neurosci Methods 129:61-71. 2003
    ..Furthermore, it has been applied to calculate the loss of spinal motor neurons during pathology progression in transgenic mice for superoxide-dismutase Cu/Zn dependent (SOD1) mutants, a model of amyotrophic lateral sclerosis (ALS)...
  45. ncbi Expression of SOD1 G93A or wild-type SOD1 in primary cultures of astrocytes down-regulates the glutamate transporter GLT-1: lack of involvement of oxidative stress
    Massimo Tortarolo
    Biochemical Neuropharmacology Group, GKT Centre for Neuroscience Research, King s College London, Guy s Hospital Campus, London, UK
    J Neurochem 88:481-93. 2004
    ....
  46. ncbi Merits of a new drug trial for ALS?
    Ettore Beghi
    Science 308:632-3; author reply 632-3. 2005
  47. ncbi Report from the Italian Ministerial Committee regarding the diagnosis, care and assistance of patients with ALS
    Caterina Bendotti
    Amyotroph Lateral Scler Other Motor Neuron Disord 6:5-7. 2005
  48. ncbi SCIENTIFIC HIGHLIGHTS from the 13th International Symposium on MND
    Caterina Bendotti
    Dept Neuroscience, Institute for Pharmacological Research Mario Negri, Milano, Itlay
    Amyotroph Lateral Scler Other Motor Neuron Disord 4:118-20. 2003