Marco Colonna, M.D.

Professor of Pathology & Immunology and Medicine

Robert Rock Belliveau M.D. Endowed Professor

Washington University School of Medicine

Dr. Marco Colonna was born in Parma, Italy. He received his medical degree from the School of Medicine at Parma University in 1983, and completed his specialization in Internal Medicine at Parma University in 1988. Dr. Colonna began his postdoctoral training as a Research Fellow at the Istituto Nazionale per la Ricerca sul Cancro in Genova, Italy, followed by work as a Research Fellow in Pathology at Dana Farber Cancer Institute and Harvard Medical School. He then became a scientific member of the Basel Institute for Immunology in Basel, Switzerland, a leading center for collaborative immunology research that helped to lay the groundwork for our understanding of immunology. Since 2001 he has been a Professor of Pathology & Immunology and Medicine at Washington University School of Medicine in St. Louis, MO.

Dr. Colonna’s laboratory is broadly interested in innate immunity. His team has discovered Triggering receptors expressed on myeloid cells (TREM), cell surface receptors encoded on human chromosome 6 that are differentially expressed on granulocytes, dendritic cells, macrophages and osteoclasts and regulate their functions. Human deficiency in TREM2 or the associated signaling adaptor DAP12 causes a progressive, early onset dementia known as Nasu-Hakola disease. Recently, a TREM2 polymorphism was implicated as a genetic risk for Alzheimer’s disease (AD). Dr. Colonna’s laboratory is currently exploring the capacity of TREM2 to promote microglial cell function and how TREM2 allelic variants result in susceptibility to AD.


Dr. Colonna has published 80 primary last-author studies in peer-reviewed journals, and holds editorial appointments for many publications, including European Journal of Immunology (Deputy Editor), Immunity, Journal of Experimental Medicine, Blood, Journal of Clinical Investigation, Journal of Biological Chemistry, Virology and Human Immunology

Funded Research

Project Description Researchers Funding
The Biological Impact of TREM Locus Mutations in Alzheimer’s Disease

Whole Genome Sequencing has identified certain polymorphisms affecting genes encoding triggering receptors expressed on myeloid cells (TREMs) with increased risk of non-familial (sporadic) Alzheimer's disease. TREM signaling is known to be important in the innate immune response, particularly in the inflammatory response. However, the relationship between the function of TREM receptors and Alzheimer's disease pathology is largely unresolved.

2015 to 2016

The Role of TREML2 in Alzheimer's Disease

Recent genetic studies have demonstrated that a nonsynonimous polymorphism of the cell surface receptor TREM-Like 2 (TREML2) is protective for Alzheimer's disease (AD)1, 2. However, the function of TREML2 and its relationship to AD remain largely unresolved. Studies proposed in this application will provide the initial characterization of the expression and function of TREML2 in the human brain in AD and normal aging.


Selected Publications

These published papers resulted from Cure Alzheimer’s Fund support.
Jason D. Ulrich, Tyler K. Ulland, Marco Colonna, and David M. Holtzman, Elucidating the Role of TREM2 in Alzheimer’s Disease, Neuron, 94, 19 Apr 2017, 237-248
Wilbur Song, Basavaraj Hooli, Kristina Mullin, Sheng Chih Jin, Marina Cella, Tyler K. Ulland, Yaming Wang, Rudolph Tanzi, Marco Colonna, Alzheimer's disease-associated TREM2 variants exhibit either decreased or increased ligand-dependent activation, Alzheimer's & Dementia, 9 Aug 2016