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International Journal of Clinical Pharmacology Research|January 1, 1988
Randomized double-blind study of flunarizine versus placebo in patients with chronic cerebrovascular disordersA Agnoli, V Manna, N Martucci, et al.
Acta Neurologica Scandinavica|December 1, 1991
Continuous intravenous infusion of TRH-T: clinical, cardiovascular and endocrinological effectsR Formisano, S Ruggieri, R Cerbo, et al.
Acta Otorhinolaryngologica Italica : Organo Ufficiale Della Societa Italiana Di Otorinolaringologia E Chirurgia Cervico-Facciale|May 1, 1992
[The definition of a reference protocol for the clinical study of vertigo drugs]F Drago, A Agnoli, G Avanzini, et al.
Italian Journal of Neurological Sciences|June 1, 1993
Botulinum toxin treatment in patients with focal dystonia and hemifacial spasm. A multicenter study of the Italian Movement Disorder GroupA Berardelli, A Formica, B Mercuri, et al.
Neurology|September 15, 2004
A family with Alzheimer disease and strokes associated with A713T mutation of the APP geneG Rossi, G Giaccone, R Maletta, et al.
The Journal of Biological Chemistry|November 23, 2000
A 7-kDa prion protein (PrP) fragment, an integral component of the PrP region required for infectivity, is the major amyloid protein in Gerstmann-Sträussler-Scheinker disease A117VF Tagliavini, P M Lievens, C Tranchant, et al.
The American Journal of Pathology|January 1, 1996
beta PP and Tau interaction. A possible link between amyloid and neurofibrillary tangles in Alzheimer's diseaseG Giaccone, B Pedrotti, A Migheli, et al.
Journal of Neuropathology and Experimental Neurology|June 22, 1999
Frontotemporal dementia and corticobasal degeneration in a family with a P301S mutation in tauO Bugiani, J R Murrell, G Giaccone, et al.
Proceedings of the National Academy of Sciences of the United States of America|January 23, 1996
Vascular variant of prion protein cerebral amyloidosis with tau-positive neurofibrillary tangles: the phenotype of the stop codon 145 mutation in PRNPB Ghetti, P Piccardo, M G Spillantini, et al.
The American Journal of Pathology|June 8, 2001
Prion proteins with different conformations accumulate in Gerstmann-Sträussler-Scheinker disease caused by A117V and F198S mutationsP Piccardo, J J Liepnieks, A William, et al.
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