Ottavio Arancio

About

Ottavio Arancio, MD, PhD, is a Professor of Pathology and Cell Biology and of Medicine at Columbia University, affiliated with the Taub Institute for Research on Alzheimer's Disease and the Aging Brain. He received his MD and PhD from the University of Pisa in Italy and completed residency training in Neurology at the University of Verona. Dr. Arancio has held faculty appointments at Columbia University, NYU School of Medicine, and SUNY HSCB. Since 2004, he has been a faculty member at Columbia University, where he is involved in research and teaching. His research focuses on the mechanisms of synaptic plasticity, particularly how oligomeric proteins such as amyloid-beta and tau interfere with memory formation and hippocampal long-term potentiation, which are models of learning and memory. Dr. Arancio is a cellular neurobiologist who has contributed to understanding the cellular and molecular mechanisms underlying learning in both healthy brains and in neurodegenerative diseases, especially Alzheimer's disease. Over the past decade, he has pioneered research into synaptic dysfunction in Alzheimer’s disease and has established a mouse model for traumatic brain injury using shockwave exposure. His laboratory investigates how changes in gene activation, post-translational mechanisms, ion channel activity, calcium signaling, and transmitter release contribute to synaptic function and dysfunction. Dr. Arancio has published extensively, raised significant grant funding, and is…

Research topics

• Neuroscience
• Cell biology
• Medicine
• Biochemistry
• Biology
• Internal medicine
• Immunology
• Psychology
• Pharmacology
• Chemistry

Selected publications

• Involvement of p38 MAPK in Synaptic Function and Dysfunction

  International Journal of Molecular Sciences · 2020 · 221 citations

  Many studies have revealed a central role of p38 MAPK in neuronal plasticity and the regulation of long-term changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). However, p38 MAPK is classically known as a responsive element to stress stimuli, including neuroinflammation. Specific to the pathophysiology of Alzheimer's disease (AD), several studies have shown that the p38 MAPK cascade is activated either in response to the Aβ peptide or in the presenc…

  DOI

• Development of novel phosphodiesterase 5 inhibitors for the therapy of Alzheimer’s disease

  Biochemical Pharmacology · 2020 · 89 citations

  DOI

• Alzheimer's disease as an autoimmune disorder of innate immunity endogenously modulated by tryptophan metabolites

  Alzheimer s & Dementia Translational Research & Clinical Interventions · 2022 · 79 citations

  Introduction: Alzheimer's disease (AD) is characterized by neurotoxic immuno-inflammation concomitant with cytotoxic oligomerization of amyloid beta (Aβ) and tau, culminating in concurrent, interdependent immunopathic and proteopathic pathogeneses. Methods: We performed a comprehensive series of in silico, in vitro, and in vivo studies explicitly evaluating the atomistic-molecular mechanisms of cytokine-mediated and Aβ-mediated neurotoxicities in AD. Next, 471 new chemical entities were designed…

  DOI

• Genetic and pharmacologic enhancement of SUMO2 conjugation prevents and reverses cognitive impairment and synaptotoxicity in a preclinical model of Alzheimer's disease

  Alzheimer s & Dementia · 2025-03-01 · 6 citations

  articleOpen access

  INTRODUCTION: Amyloid beta oligomers (Aβos) are toxic to synapses and key to the progression of Alzheimer's disease (AD) and amyloid pathology, representing a target for therapeutic strategies. METHODS: Amyloid and small ubiquitin modifier 2 (SUMO2) transgenics were analyzed by electrophysiology and behavioral testing. A recombinant analogue of SUMO2, SBT02, was generated and assessed for brain penetration and the ability to mitigate amyloid pathology. RESULTS: Elevated SUMO2 expression prevents…

  PublisherOA PDFDOI

• SUMO2 rescues neuronal and glial cells from the toxicity of P301L Tau mutant

  Frontiers in Cellular Neuroscience · 2024-12-12 · 4 citations

  articleOpen access

  Introduction: Abnormal intracellular accumulation of Tau aggregates is a hallmark of Alzheimer's disease (AD) and other Tauopathies, such as Frontotemporal dementia (FTD). Tau deposits primarily affect neurons, but evidence indicates that glial cells may also be affected and contribute distinctively to disease progression. Cells can respond to toxic insults by orchestrating global changes in posttranslational modifications of their proteome. Previous studies suggest that SUMOylation, a posttrans…

  PublisherDOI

Recent grants

• NIH Grant RF1AG055125

  NIH · $2.0M · 2023

• Chaperome networks in Alzheimer's disease

  NIH · $5.9M · 2021–2027

• NIH Grant U01AG032973

  NIH · $1.1M · 2014

Frequent coauthors

• Daniela Puzzo

  Istituti di Ricovero e Cura a Carattere Scientifico

  70 shared

• Fortunato Battaglia

  Hackensack Meridian Health

  48 shared

• Fabrizio Trinchese

  42 shared

• Agnieszka Staniszewski

  Columbia University

  41 shared

• Michael L. Shelanski

  Columbia University

  38 shared

• Bing Gong

  33 shared

• Mauro Fà

  Columbia University

  33 shared

• Agostino Palmeri

  University of Catania

  32 shared

Labs

• Digital and Computational Pathology LaboratoryPI

  The Digital and Computational Pathology Laboratory focuses on the development and application of computational methods to improve the diagnosis and treatment of diseases.

Education

• M.D., Medicine

  Columbia University

• Ph.D.

  Columbia University

Awards & honors

• G. Moruzzi Fellowship (1987)
• Anna Villa Rusconi Foundation Prize (1990)
• INSERM Poste Vert Fellowship (1991)
• Fellowship, University of Bologna (1994)
• Whitehead Fellowship (2001-2003)

Similar researchers at Columbia University

• Jonathan M. Baraschh-79
• Rando L. Allikmetsh-79
• Bachir Alobeidh-37