Ana Griciuc, Ph.D.

Instructor in Neurology, Harvard Medical School;  Assistant in Neuroscience, Massachusetts General Hospital

Dr. Griciuc received her M.Eng. in biotechnology from INSA-Lyon and M.Sc. in biochemistry from the Max Planck Institute of Neurobiology (Munich) in 2006. She then became a fellow of the European Union research training network “Marie Curie-Neurotrain,” and received her Ph.D. in neuroscience from the Helmholtz Research Center Munich in 2010. Dr. Griciuc is the recipient of the 2011 Graduate Student Award in Environmental Health Research.

Dr. Griciuc began her postdoctoral research training in the laboratory of Dr. Rudolph Tanzi at Massachusetts General Hospital (MGH) and Harvard Medical School in 2011. She has been exploring how CD33, an innate immunity-related gene, serves as a pathogenetic risk factor in Alzheimer’s disease (AD). Dr. Griciuc showed that CD33 activity in microglia strongly impaired their ability to uptake and clear brain amyloid beta. Dr. Griciuc’s research uncovered a novel pathway for amyloid beta clearance in the aging brain and AD pathogenesis.

Dr. Griciuc was appointed as assistant professor of neurology at the Massachusetts General Hospital and Harvard Medical School in 2017. Her current research projects focus on investigating the function of CD33 and other innate immunity genes, and how mutations in these genes result in susceptibility to late-onset AD. Dr. Griciuc received several awards, including a two-year postdoctoral fellowship from the German Research Foundation, the Tosteson & Fund for Medical Discovery Fellowship from MGH/ECOR and the NIH Pathway to Independence Award (K99/R00).

Funded Research

Project Description Researchers Funding
Microglial Core/CD33 and Alzheimer’s Disease: From Biology to Therapy

Our current inability to prevent or delay Alzheimer’s disease (AD) and the expected increase in the prevalence of AD are predicted to give rise to a global AD pandemic. We recently have identified a novel pathway for amyloid beta (Abeta) clearance in the aging brain that is highly relevant to AD pathogenesis. In a very large family-based, genome-wide association study, we identified CD33 as a novel late-onset AD risk factor. CD33 encodes a transmembrane sialic acid-binding immunoglobulin-like lectin that regulates innate immunity.

2015 to 2016