Dr. Ottavio Arancio received his Ph.D and M.D. from the University of Pisa (Italy).   From 1981 to 1986 he took residency training in Neurology at the University of Verona (Italy).  Dr. Arancio has held Faculty appointments at Columbia University, NYU School of Medicine and at SUNY HSCB.  In 2004 he became Faculty member of the Dept of Pathology and Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University.  His honors include the “G. Moruzzi Fellowship” (Georgetown University), the “Anna Villa Rusconi Foundation Prize” (Italy), and the “INSERM Poste vert Fellowship” (France).

Dr Arancio is a cellular neurobiologist who has contributed to the characterization of the mechanisms of learning in both normal conditions and during neurodegenerative diseases.   During the last seven years he has pioneered the field of mechanisms of synaptic dysfunction in Alzheimer’s disease.  Dr. Arancio’s laboratory has focused primarily on events triggered by amyloid protein.  These studies, which have suggested new links between synaptic dysfunction and amyloid protein, are of a general relevance to the field of Alzheimer’s disease both for understanding the etiopathogenesis of the disease and for developing therapies aiming to improve the cognitive symptoms. 

Select Recent Publications:

• Vitolo, O.V., Sant’Angelo A., Costanzo, V., Battaglia, F., Arancio, O., Shelanski, M.  Amyloid b peptide inhibition of the PKA/CREB pathway and long-term potentiation: reversibility by drugs that enhance cAMP signaling.  Proc. Natl. Acad. Sci. U S A, 2002; 99: 13217-13221.
  
  
• Ninan, I., Arancio, O. Presynaptic CaMKII is necessary for synaptic plasticity in cultured hippocampal neurons.  Neuron, 2004; 42:129-141. Faculty of 1000 Top 10 Neuroscience. http://invention.swmed.edu/frisc/faculty/sudhof/profile_this_year.shtml. 
  
  
• Trinchese, F., Liu, S., Battaglia, F., Walter, S., Mathews, P., Arancio, O.  Progressive age-related development of Alzheimer-like pathology in APP/PS1 mice. Ann. Neurol., 2004; 55: 801-814.
  
  
• Liu, S., Ninan, I., Antonova, I., Battaglia, F., Trinchese, F., Narasanna, A., Kholodilov, N., Dauer, W., Hawkins, R.D., Arancio, O.  a-synuclein produces a long-lasting increase in neurotransmitter release.  EMBO J., 2004, 23:4506-16.
  
  
• Arancio, O., Zhang, H.P., Chen, X., Lin, C., Trinchese, F., Puzzo, D., Liu, S., Hegde, A., Yan, S.F., Stern, A., Luddy, J.S., Lue, L-F., Walker, D., Roher, A., Buttini, M., Mucke, L., Li, W., Schmidt, A.M., Kindy, M., Hyslop, P., Stern, D.M., Yan S.S-D.  RAGE potentiates Aß-induced perturbation of neuronal function in transgenic mice.  EMBO J., 2004; 23:4096-105. Faculty of 1000 Top 10 Neuroscience.
  
  
• Gong, B., Vitolo, O.V., Trinchese, F., Liu, S., Shelanski, M., Arancio, O. Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model following rolipram treatment.  J. Clin. Invest ., 2004; 114:1624-1634.  Highlighted in the "In This Issue" section of the journal. See also  http://www.alzforum.org/new/detail.asp?id=1118
  
  
• Puzzo, D., Vitolo, O.V., Trinchese, F., Jacob, J.P., Palmeri, A., Arancio, O. Amyloid-β-peptide inhibits activation of the nitric oxide/cGMP/CREB pathway during  hippocampal synaptic plasticity. J. Neurosci. 2005; 25: 6887-6897.
  
  
• Gong, B., Cao, Z., Zheng, P., Vitolo, O.V., Liu, S., Staniszewski, A.,  Zhang, H., Moolman, D., Zhang, H., Shelanski, M., Arancio, O. Ubiquitin Hydrolase Uch-L1 Rescues b-Amyloid-Induced Decreases in Synaptic Function and Contextual Memory. Cell 2006; 126: 775-788.
  
  
• Ninan, I., Liu, S., Rabinowitz, D., Arancio, O. Early Presynaptic Changes during Plasticity in Cultured Hippocampal Neurons. EMBO J. In press.