National Institute on Aging
National Institutes of Health
|Vilhelm A. Bohr, M.D., Ph.D., Senior Investigator
Chief, Section on DNA Repair
Oxidative DNA Damage Processing & Mitochondrial Functions Unit
Laboratory of Molecular Gerontology
|Biography: Dr. Bohr received his M.D. in 1978, Ph.D. in 1987, and D.Sc. in 1987 from the University of Copenhagen, Denmark. After training in neurology and infectious diseases at the University Hospital in Copenhagen, Dr. Bohr did a postdoctoral fellowship with Dr. Hans Klenow at the University of Copenhagen, Denmark. He then worked with Dr. Philip Hanawalt at Stanford University as a research scholar from 1982-1986. In 1986, he joined the National Cancer Institute (NCI) as an investigator and become a tenured Senior Investigator in 1988. Dr. Bohr developed a research section on DNA repair at the NCI. In 1992, he moved to the National Institute on Aging to become Chief of the Laboratory of Molecular Genetics, renamed Laboratory of Molecular Gerontology in February 2001.|
The Section on DNA Repair. Our studies focus on the molecular functions and protein interactions of proteins that are defective in premature aging syndromes such as: Werner syndrome protein (WRN) and Cockayne syndrome B protein (CSB). We are investigating the molecular mechanisms involved in DNA repair and in genomic instability in normal, senescent and cancer cells. We are comparing the functions of all five human RecQ helicases with special emphasis towards delineating why only three out of the five human enzymes are associated with disease. Additionally, we are examining the role of increased DNA damage accumulation in aging and during the induction of cellular senescence. The goal is to understand the underlying mechanisms involved in DNA damage formation and it's processing as well as the changes that take place with aging that make aging cells susceptible to cancer.
We are also investigating BER activities in different brain regions of normal mice, and in mouse models of age-associated neurodegenerative diseases. Specifically, we are investigating how a BER-deficiency impacts neurodegenerative diseases like Alzheimer disease (AD) and stroke. Our previous work suggests that Base Excision Repair (BER) may be deficient in human AD patients relative to controls. The goal of our present work is to investigate whether there is differential oxidative DNA repair capacity in a subset of neuronal cells and whether DNA repair insufficiency correlates with cell death in brain regions susceptible to neuronal loss in AD. In models of stroke, we have shown that a BER-deficiency leads to worse functional recovery after stoke. Therefore, our working hypothesis is that efficient BER is necessary for full recovery after acute oxidative stress. We have also found that deficient BER may play a role in normal memory and learning, therefore we are expanding our studies on how BER impacts these endpoints. These studies may provide valuable insights into the mechanisms that lead to neuronal loss with age.The Unit on Oxidative DNA Damage Processing and Mitochondrial Functions focuses on mitochondrial DNA, and the studies seek to investigate the basis for the mitochondrial theory of aging which states that accumulation of DNA damage with aging leads to the phenotypical changes that we observe in senescence and age-associated disease. The mechanisms of removal of oxidative DNA damage from mitochondria are investigated and how they are affected by increasing age or disease processes.
|DNA Repair Section Oxidative DNA Damage Processing & Mitochondrial Functions Unit (left to right). Top Row: Huiming Lu, Takashi Tadokoro, Joseph Hsu, Cindy Kasmer, Lale Dawut, Deb Croteau, Raghu Shamanna, Evandro Fang, Venkat Popuri, Will bohr
Bottom Row: Sonya Dorsey, Leslie Ferrarelli, Jane Tian, Tom Kulikowicz, Magda Misiak, Chandrika Canugovi, Chris Dunn, Morten Scheibye-Knudsen, Al May
Not Shown: Lorraine Oliver, Peter Sykora, Martin Borch Jensen
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