Dr. Bohr is Chief of the Laboratory of Molecular Gerontology at the U.S. National Institute of Aging in Baltimore and Affiliated Professor at the Center for Healthy Aging at the University of Copenhagen.

He received his MD, PhD and D.Sc. from the University of Copenhagen, and was trained in neurology and infectious diseases. He worked as a post-doctoral fellow with Dr. Hans Klenow in Copenhagen and as a research scholar with Dr. Philip Hanawalt in Stanford before he was appointed to the U.S. National Cancer Institute in Bethesda. Dr. Bohr´s research is focused on mechanisms of DNA damage processing by transcription-coupled repair as well as energy metabolism and mitochondrial biology. A main interest is how changes in these processes are involved in aging processes and contribute to the development age-associated neuro - de generative disorders such as Alzheimer’s disease. Lately, he has described a signaling pathway from damage in nuclear DNA to mitochondrial dysfunction, which involves translation.

Vilhelm A. Bohr
Chief of the Laboratory of Molecular Gerontology at the U.S. National Institute of Aging in Baltimore, Maryland, and Affiliated Professor at the Center for Healthy Aging at the University of Copenhagen, Denmark

Dr. Bohr is Chief of the Laboratory of Molecular Gerontology at the U.S. National Institute of Aging in Baltimore and Affiliated Professor at the Center for Healthy Aging at the University of Copenhagen. He received his MD, PhD and D.Sc. from the University of Copenhagen, and was trained in neurology and infectious diseases. He worked as a post-doctoral fellow with Dr. Hans Klenow in Copenhagen and as a research scholar with Dr. Philip Hanawalt in Stanford before he was appointed to the U.S. National Cancer Institute in Bethesda. Dr. Bohr´s research is focused on mechanisms of DNA damage processing by transcription-coupled repair as well as energy metabolism and mitochondrial biology. A main interest is how changes in these processes are involved in aging processes and contribute to the development age-associated neuro - de generative disorders such as Alzheimer’s disease. Lately, he has described a signaling pathway from damage in nuclear DNA to mitochondrial dysfunction, which involves translation.	Selected publications Fang EF, Hou Y, Palikaras K, Adriaanse BA, Kerr JS, Yang B, Lautrup S, Hasan-Olive MM, Caponio D, Dan X, Rocktäschel P, Croteau DL, Akbari M, Greig NH, Fladby T, Nilsen H, Cader MZ, Mattson MP, Tavernarakis N, Bohr VA (2019). Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer's disease. Nat. Neurosci. 22: 401-412. doi: 10.1038/s41593-018-0332-9 Hou Y, Lautrup S, Cordonnier S, Wang Y, Croteau DL, Zavala E, Zhang Y, Moritoh K, O'Connell JF, Baptiste BA, Stevnsner TV, Mattson MP, Bohr VA (2018). NAD+ supplementation normalizes key Alzheimer's features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency. Proc. Natl. Acad. Sci. U. S. A. 115: E1876-E1885. doi: 10.1073/pnas.1718819115 Lu H, Shamanna RA, de Freitas JK, Okur M, Khadka P, Kulikowicz T, Holland PP, Tian J, Croteau DL, Davis AJ, Bohr VA (2017). Cell cycle-dependent phosphorylation regulates RECQL4 pathway choice and ubiquitination in DNA double-strand break repair. Nat. Commun. 8: 2039. doi: 10.1038/s41467-017-02146-3 Sykora P, Kanno S, Akbari M, Kulikowicz T, Baptiste BA, Leandro GS, Lu H, Tian J, May A, Becker KA, Croteau DL, Wilson DM 3rd, Sobol RW, Yasui A, Bohr VA (2017). DNA Polymerase Beta Participates in Mitochondrial DNA Repair. Mol. Cell. Biol. 37: e00237-17. doi: 10.1128/MCB.00237-17 Shamanna RA, Lu H, de Freitas JK, Tian J, Croteau DL, Bohr VA (2016). WRN regulates pathway choice between classical and alternative non-homologous end joining. Nat. Commun. 7: 13785. doi: 10.1038/ncomms13785. Scheibye-Knudsen M, Tseng A, Borch Jensen M, Scheibye-Alsing K, Fang EF, Iyama T, Bharti SK, Marosi K, Froetscher L, Kassahun H, Eckley DM, Maul RW, Bastian P, De S, Ghosh S, Nilsen H, Goldberg IG, Mattson MP, Wilson DM 3rd, Brosh RM Jr, Gorospe M, Bohr VA (2016). Cockayne syndrome group A and B proteins converge on transcription-linked resolution of non-B DNA. Proc. Natl. Acad. Sci. U. S. A. 113: 12502-12507. doi: 10.1073/pnas.1610198113 Fang EF, Kassahun H, Croteau DL, Scheibye-Knudsen M, Marosi K, Lu H, Shamanna RA, Kalyanasundaram S, Bollineni RC, Wilson MA, Iser WB, Wollman BN, Morevati M, Li J, Kerr JS, Lu Q, Waltz TB, Tian J, Sinclair DA, Mattson MP, Nilsen H, Bohr VA (2016). NAD+ Replenishment Improves Lifespan and Healthspan in Ataxia Telangiectasia Models via Mitophagy and DNA Repair. Cell Metab. 24: 566-581. doi: 10.1016/j.cmet.2016.09.004 Lu H, Shamanna RA, Keijzers G, Anand R, Rasmussen LJ, Cejka P, Croteau DL, Bohr VA (2016). RECQL4 Promotes DNA End Resection in Repair of DNA Double-Strand Breaks. Cell Rep. 16: 161-173. doi: 10.1016/j.celrep.2016.05.079 Scheibye-Knudsen M, Mitchell SJ, Fang EF, Iyama T, Ward T, Wang J, Dunn CA, Singh N, Veith S, Hasan-Olive MM, Mangerich A, Wilson MA, Mattson MP, Bergersen LH, Cogger VC, Warren A, Le Couteur DG, Moaddel R, Wilson DM 3rd, Croteau DL, de Cabo R, Bohr VA (2014). A high-fat diet and NAD+ activate Sirt1 to rescue premature aging in cockayne syndrome. Cell Metab. 20: 840-855. doi: 10.1016/j.cmet.2014.10.005 Fang EF, Scheibye-Knudsen M, Brace LE, Kassahun H, SenGupta T, Nilsen H, Mitchell JR, Croteau DL, Bohr VA (2014). Defective mitophagy in XPA via PARP-1 hyperactivation and NAD+/SIRT1 reduction. Cell 157: 882-896. doi: 10.1016/j.cell.2014.03.026