Title: Faculty & research interests

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Ottavio  Arancio
Ottavio Arancio, MD, PhD
Associate Professor
Associate Member

Department: Pathology and Cell Biology

P&S 12-420D
212-342-0533
oa1@columbia.edu


Personal Website

Disease Models: Neurodegenerative Diseases

Stem Cell Categories: Adult stem cells, iPS cells

Model Organisms: Human, Rodent

Themes: Neurodegeneration

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). He is Faculty member of the Dept of Pathology & Cell Biology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University. 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 ten years he has pioneered the field of mechanisms of synaptic dysfunction in Alzheimer's disease. These studies, which have suggested new links between synaptic dysfunction and oligomeric 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. Arancio's interest in stem cell research derives from the need to develop an iPSC model that recapitulates alterations of synaptic function in Alzheimer’s disease. Arancio’s honors include the “G. Moruzzi Fellowship” (Georgetown University), the “Anna Villa Rusconi Foundation Prize” (Italy), and the “INSERM Poste vert Fellowship” (France), Fidia Fellowship, Italy; Speaker's Fund for Biomedical Research Award; Investigator Initiated Research Award from the Alzheimer Association; AHAF centennial Award, Zenith Award, Margaret Cahn Research Award (2008), and Thome Award (2010).



Publications:

Puzzo, D.,Staniszewisky, A.,Deng, S-X, Privitera, L., Leznik, E.,Liu, S.,Zhang, H.,Feng, Y.,Palmeri, A.,Landry, D.W.,Arancio, O.
Phosphodiesterase 5 inhibition improves synaptic function, memory and Amyloid-beta load in an Alzheimer's Disease Mouse Model J. Neuroscience 29:8075-86. (2009)

Puzzo, D., Privitera, L., Leznik, E., Fa’, M., Staniszewski, A., Palmeri, A., Arancio, O.
Picomolar amyloid-beta positively modulates synaptic plasticity and memory in hippocampus J. Neurosci. 28:14537-45. (2008)

Trinchese, F.,Fa', M., Liu, S.,Zhang, H.,Hidalgo, A.,Schmidt, S.,Yamaguchi, H.,Yoshii, N.,Matthews, P., Nixon, R.,Arancio,O .
Calpains Contribute to the impairment of synaptic transmission and memory in an Alzheimer mouse model. J. Clin. Invest. 118:2796-807. (2008)

Gong, B., Cao, Z.,Zheng, P.,Vitolo, O.V.,Liu, S.,Staniszewski, A.,Zhang, H.,Moolman, D.,Zhang, H.,Shelanski, M., Arancio, O.
Ubiquitine Hydroloase Uch-L1 Rescues b-Amyloid-Induced Decreases in Synaptic Function and Contextual Memory Cell 126:775-788. (2006)

Ninan, I.,Arancio, O.
Presynaptic CaMKII is necessary for synaptic plasticity in cultured hippocampal neurons. Neuron 42:129-141. (2004)

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