Phone: +45 6550 3806
E-mail: klambertsen@health.sdu.dk
Department:
Neurobiology Research, Department of Molecular Medicine, 海角社区 & Department of Neurology, Odense University Hospital
Biography:
Kate Lykke Lambertsen is a professor of Neurobiology at Neurobiology Research, Department of Molecular Medicine, 海角社区 and Department of Neurology, Odense University Hospital. After obtaining her PhD in Neuroscience from the 海角社区, she did her first post doc funded by the Danish Medical Research Council at the Medical Biotechnology Center, 海角社区. In 2008-2009 she obtained a grant from Carlsbergfondet to do her second post doc at the Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL. In 2009, she started her independent research lab.
2004: 海角社区, Odense, Denmark
PhD, Neuroscience
1999: Odense University, Odense, Denmark
MSc, Biomedicine
2008: The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL
Post-Doctoral Fellowship, Neuroscience
2005: 海角社区, Odense, Denmark
Post-Doctoral Fellowship, Neuroscience
2004: 海角社区, Odense, Denmark
Research assistant, Neuroscience
10th Annual Certificate Course in Translational Medicine, EUREKA Institute for Translational Medicine (2018)
Dr. Lambertsen’s main interest is understanding the role of neuroinflammation in the pathophysiology of neurological disorders, such as stroke, spinal cord injury, and multiple sclerosis, with a specific focus on the contribution of glial cells.
In recent years she has devoted her efforts to investigating the function of tumor necrosis factor (TNF), both membrane-bound and soluble forms, in neuroimmune disease. Within this context, she is exploring the protective signaling initiated by the blocking the interaction of soluble TNF with TNFR1, taking advantage of cell-specific conditional knockout mice and different therapeutic approaches in vitro and in vivo using animal models and patient-derived samples.
Another important research topic being developed in her lab is understanding how sexual dimorphism might play a role in stroke etiopathogenesis. She is investigating this hypothesis using transgenic and normal mouse strains, as well as human microglia and monocyte cultures and post-mortem stroke brain tissue.
More recently, she has become interested in understanding how cardiometabolic diseases may participate in the pathogenesis and progression of neurological disease, specifically stroke. She is studying how obesity may affect post-stroke neuroinflammation and how different treatment approaches may contribute to neurorepair.