Antonino Cattaneo

Dr. Antonino Cattaneo


Research Focus & Metrics

Academic Career Length

48Years (1979-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 February 2006 in Current Biology
Verified
Journal Article
Closed access
DVDario R. Valenzano
Dario R. Valenzano
Eva Terzibasi TozziniEva Terzibasi Tozzini
Eva Terzibasi Tozzini
TGTyrone Genade
Tyrone Genade
ACAntonino Cattaneo
Antonino Cattaneo
LDLuciano Domenici
Luciano Domenici
ACAlessandro Cellerino
Alessandro Cellerino

1 December 1993 in Nature
Verified
Journal Article
Closed access
PTParaskevi Tavladoraki
Paraskevi Tavladoraki
EBEugenio Benvenuto
Eugenio Benvenuto
STStefania Trinca
Stefania Trinca
DMDomenico De Martinis
Domenico De Martinis
ACAntonino Cattaneo
Antonino Cattaneo
PGPatrizia Galeffi
Patrizia Galeffi

15 December 1997 in Journal of Neuroscience
Verified
Journal Article
Open access
PDF file
Enrico TongiorgiEnrico Tongiorgi
Enrico Tongiorgi
MRMassimo Righi
Massimo Righi
ACAntonino Cattaneo
Antonino Cattaneo
The mechanisms underlying the subcellular localization of neurotrophins and their receptors are poorly understood. We show that in cultured hippocampal neurons, the mRNAs for BDNF and TrkB have a somatodendritic localization, and we quantify the extent of their dendritic mRNA localization. In the dendrites the labeling covers on average the proximal 30% of the total dendritic length. On high potassium depolarization, the labeling of BDNF and TrkB mRNA extends on average to 68% of the dendritic length. This increase does not depend on new RNA synthesis, is inhibited by the Na+channel blocker tetrodotoxin, and involves the activation of glutamate receptors. Extracellular Ca2+, partly flowing through L-type Ca2+channels, is absolutely required for this process to occur. At the protein level, a brief stimulation of hippocampal neurons with 10 mmKCl leads to a marked increase of BDNF and TrkB immunofluorescence density in the distal portion of dendrites, which also occurs, even if at lower levels, when transport is inhibited by nocodazole. The protein synthesis inhibitor cycloheximide abolishes this increase. The activity-dependent modulation of mRNA targeting and protein accumulation in the dendrites may provide a mechanism for achieving a selective local regulation of the activity of neurotrophins and their receptors, close to their sites of action.

22 August 2005 in Aging Cell
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Journal Article
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TGTyrone Genade
Tyrone Genade
MBMauro Benedetti
Mauro Benedetti
Eva Terzibasi TozziniEva Terzibasi Tozzini
Eva Terzibasi Tozzini
PRPaola Roncaglia
Paola Roncaglia
DVDario Riccardo Valenzano
Dario Riccardo Valenzano
ACAlessandro Cellerino
Alessandro Cellerino

23 February 2005 in Proceedings of the National Academy of Sciences
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Journal Article
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RRRoberta De Rosa
Roberta De Rosa
AGAddys Ancheta Garcia
Addys Ancheta Garcia
CBChiara Braschi
Chiara Braschi
SCSimona Capsoni
Simona Capsoni
LMLamberto Maffei
Lamberto Maffei
ACAntonino Cattaneo
Antonino Cattaneo
Nerve growth factor (NGF) delivery to the brain of patients appears to be an emerging potential therapeutic approach to neurodegenerative disease, such as Alzheimer's disease (AD). The intranasal route of administration could provide an alternative to intracere-broventricular infusion and gene therapy. We previously showed that intranasal administration of NGF determined an amelioration of cholinergic deficit and a decrease in the number of phosphotau-positive neurons and of β-amyloid accumulation in AD11 mice, which express transgenic antibodies neutralizing NGF action and exhibit a progressive Alzheimer-like neurodegeneration. In this study, we report that the Alzheimer-like neurodegeneration in AD11 mice is linked to progressive behavioral deficits in visual recognition memory and spatial memory starting from 4 months of age. To establish whether intranasal administration of NGF, started after the appearance of the first memory deficits, could revert the cognitive deficits in AD11 mice, we assessed the performance of NGF-treated or control AD11 mice in the object recognition test and in a test of memory for place and context. Deficits exhibited by untreated AD11 mice could be rescued by the intranasal administration of NGF. Thus, this route of administration provides a promising way to deliver NGF to the brain in a therapeutic perspective.

6 June 2000 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
PDF file
SCSimona Capsoni
Simona Capsoni
GUGabriele Ugolini
Gabriele Ugolini
ACAlessandro Comparini
Alessandro Comparini
FRFrancesca Ruberti
Francesca Ruberti
NBNicoletta Berardi
Nicoletta Berardi
ACAntonino Cattaneo
Antonino Cattaneo
Neurotrophin nerve growth factor (NGF) has been suggested to be involved in age-related neurodegenerative diseases, but no transgenic model is currently available to study this concept. We have obtained transgenic mice expressing a neutralizing anti-NGF recombinant antibody, in which the levels of antibodies are three orders of magnitude higher in adult than in newborn mice [F.R., S. C., A.C., E. Di Daniel, J. Franzot, S. Gonfloni, G. Rossi, N. B. & A. C. (2000) J. Neurosci. , 20, 2589–2601]. In this paper, we analyze the phenotype of aged anti-NGF transgenic mice and demonstrate that these mice acquire an age-dependent neurodegenerative pathology including amyloid plaques, insoluble and hyperphosphorylated τ, and neurofibrillary tangles in cortical and hippocampal neurons. Aged anti-NGF mice also display extensive neuronal loss throughout the cortex, cholinergic deficit in the basal forebrain, and behavioral deficits. The overall picture is strikingly reminiscent of human Alzheimer's disease. Aged anti-NGF mice represent, to our knowledge, the most comprehensive animal model for this severe neurodegenerative disease. Also, these results demonstrate that, in mice, a deficit in the signaling and/or transport of NGF leads to neurodegeneration.