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Antonio Federico
Researcher at University of Siena
Publications - 578
Citations - 17424
Antonio Federico is an academic researcher from University of Siena. The author has contributed to research in topics: CADASIL & Leukoencephalopathy. The author has an hindex of 56, co-authored 566 publications receiving 15624 citations. Previous affiliations of Antonio Federico include University of Porto & National Research Council.
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Journal ArticleDOI
Accurate, Robust, and Automated Longitudinal and Cross-Sectional Brain Change Analysis
Stephen M. Smith,Yongyue Zhang,Mark Jenkinson,Jacqueline T. Chen,Paul M. Matthews,Antonio Federico,Nicola De Stefano +6 more
TL;DR: Improvements to this method are described, and an extension of SIENA is extended to a new method for cross-sectional (single time point) analysis, which provides easy manual review of their output by the automatic production of summary images.
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Mitochondria, oxidative stress and neurodegeneration.
Antonio Federico,Elena Cardaioli,Paola Da Pozzo,Patrizia Formichi,Gian Nicola Gallus,Elena Radi +5 more
TL;DR: There is strong evidence that mitochondrial dysfunction occurs early and has a primary role in pathogenesis, and several mitochondrial diseases as models of neurodegeneration are discussed.
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Evidence of early cortical atrophy in MS Relevance to white matter changes and disability
N. De Stefano,Paul M. Matthews,Massimo Filippi,Federica Agosta,M De Luca,Maria Letizia Bartolozzi,Leonello Guidi,Angelo Ghezzi,E. Montanari,A. Cifelli,Antonio Federico,Stephen M. Smith +11 more
TL;DR: The extent of the changes suggests that neocortical GM pathology may occur early in the course of the disease in both RR and PP MS patients and contribute significantly to neurologic impairment.
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Apoptosis and oxidative stress in neurodegenerative diseases.
TL;DR: An overview of the involvement of neuronal apoptosis and oxidative stress in the most important neurodegenerative diseases is presented, mainly focusing the attention on several genetic disorders, discussing the interaction between primary genetic abnormalities and the apoptotic pathways.
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Mutations in SLC30A10 Cause Parkinsonism and Dystonia with Hypermanganesemia, Polycythemia, and Chronic Liver Disease
Marialuisa Quadri,Antonio Federico,Tianna Zhao,Guido J. Breedveld,Carla Battisti,Cathérine C.S. Delnooz,Lies Anne Severijnen,Lara Di Toro Mammarella,Andrea Mignarri,Lucia Monti,Antioco Sanna,Peng Lu,Francesca Punzo,Francesca Punzo,Giovanni Cossu,Rob Willemsen,Fabrizio Rasi,Ben A. Oostra,Bart P.C. van de Warrenburg,Vincenzo Bonifati +19 more
TL;DR: The SLC30A10 mutations cause a treatable recessive disease with pleomorphic phenotype with broad implications for understanding of the manganese biology and pathophysiology in multiple human organs and compelling evidence that SLC 30A10 plays a pivotal role inManganese transport is provided.