Florian Eichler received his M.D. from the University of Vienna Medical School. After graduating from medical school in 1997, he entered residency in Pediatrics and pursued studies on cerebral blood flow and metabolism at the University of Vienna. In 1999 he won a scholarship to study in vivo MR spectroscopy in pediatric patients with metabolic and neurometabolic conditions at Johns Hopkins (Stipendium Metabolicum 1999) and joined the laboratory of Dr. Hugo Moser dedicated to peroxisomal disorders at the Kennedy Krieger Institute. Following his research fellowship at Johns Hopkins he underwent residency training in Child Neurology at the Massachusetts General Hospital (MGH). After completing residency in 2005 he joined the staff at MGH.
Now an Associate Professor of Neurology at Harvard Medical School he is extending his research into animal models of neurodegenerative disorders. His research focus is on the genetics of peroxisomal disorders, lipid metabolism, and spatial aspects of nuclear magnetic resonance spectroscopy. As director of the leukodystrophy clinic at the Massachusetts General Hospital he sees patients with a variety of white matter disorders. He currently holds several NIH awards funding studies to analyze metabolic changes seen in the brain by MR measures and to determine the neurotoxicity of newly discovered atypical sphingolipids.
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Mass General Neurology
55 Fruit St.
Boston, MA 02114
Phone: 855-644-6387
Mass General for Children: Pediatric Neurology
55 Fruit St.
Suite 6B
Boston, MA 02114
Phone: 617-724-6400
Medical Education
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My expertise lies in neurogenetics and translational neuroscience. The topic of my research is unraveling the disease mechanisms of monogenetic disorders affecting the nervous system. This allows my lab to explore the relationship of mutant genes to specific biochemical defects and their contribution to neurodegeneration. As director of the leukodystrophy service at MGH I see patients with a variety of neurogenetic disorders and am actively studying abnormal accumulation of lipids such as very long chain fatty acids and desoxysphingoid bases in both my clinic and my laboratory. My clinical research studies have defined disease progression in adrenoleukodystrophy, metachromatic leukodystrophy and Tay Sachs Disease. Recently we were able to show that levels of desoxysphingoid bases in mice and humans with an inherited form of neuropathy contribute to disease and can be lowered by supplementation with L-serine.
