Matthew C. Havrda, PhD
Assistant Professor of Molecular and Systems Biology
Molecular and Systems Biology
University of Maine: Graduate School of Biomedical Sciences and Engineering, Ph.D.
Norris Cotton Cancer Center
Program in Experimental and Molecular Medicine
Glial Cell Biology
Rotations and Thesis Projects:
Target Validation Award: The Michael J. Fox Foundation for Parkinson's Disease Research
Dartmouth SYNERGY Scholars Award
The Hitchcock Foundation
NIH-NIEHS 1R01ES024745: Mechanisms of rotenone-induced neuroinflammation and Parkinsonism in aging mice
Course Co-Director, Neurobiology of Disease (PEMM 211)
Dr. Havrda is a neurobiologist interested in characterizing the molecular basis of brain disorders, especially Parkinson’s disease and its various pathologic manifestations. He received his Ph.D. in 2006 from the Graduate School of Biomedical Science and Engineering of the University of Maine at the Maine Medical Center Research Institute. Dr. Havrda is an Assistant Professor at the Geisel School of Medicine at Dartmouth affiliated with the Parkinson’s Center at Dartmouth working at the Dartmouth-Hitchcock Medical Center in Lebanon, New Hampshire. Throughout his career he has published numerous research reports and book chapters while receiving academic awards including the Ian Sinclair Scholarship, the Apollon Valakis Scholarship and the Doris G. Alexander Memorial Scholarship. More recently Dr. Havrda has received prestigious young investigator awards including the Ruth L. Kirschstein National Research Service Award, the Dartmouth SYNERGY Scholar Award for Clinical and Translational Research, and a Target Validation Award from the Michael J. Fox Foundation. Dr. Havrda’s research program is focused on characterizing the molecular basis of neuroinflammation during the progression of Parkinson’s disease both in cellular and animal models as well as in biofluids and post-mortem tissues obtained from Parkinson’s patients. Such studies are expected to provide new platforms from which to discover, monitor and evaluate diagnostic indicators and therapeutic targets.
Secretion-mediated STAT3 activation promotes self-renewal of glioma stem-like cells during hypoxia.
Editor's Highlight: Nlrp3 Is Required for Inflammatory Changes and Nigral Cell Loss Resulting From Chronic Intragastric Rotenone Exposure in Mice.
ID2 promotes survival of glioblastoma cells during metabolic stress by regulating mitochondrial function.
Insulin-Mediated Signaling Facilitates Resistance to PDGFR Inhibition in Proneural hPDGFB-Driven Gliomas.
Phosphorylation Regulates Id2 Degradation and Mediates the Proliferation of Neural Precursor Cells.
Inhibitor of differentiation 4 (ID4): From development to cancer.
Id2 mediates oligodendrocyte precursor cell maturation arrest and is tumorigenic in a PDGF-rich microenvironment.
Id4 deficiency attenuates prostate development and promotes PIN-like lesions by regulating androgen receptor activity and expression of NKX3.1 and PTEN.
Behavioral abnormalities and Parkinson's-like histological changes resulting from Id2 inactivation in mice.
p53 directly represses Id2 to inhibit the proliferation of neural progenitor cells.