Contact us

MARK P. BURNS

Ph.D. (2000) National University of Ireland, Galway, Ireland
Phone: 202.687.4735 (office) or 202.687.0107 (lab)
Fax: 202.687.0617
E-mail:mpb37@georgetown.edu

 

In Alzheimer’s disease, genetics and lifestyle both play a part. There is one major genetic risk factor for developing late-onset Alzheimer’s disease, a mutant form of a cholesterol transporting protein in our blood (apoE). In addition, people with high cholesterol have increased risk of Alzheimer’s disease, suggesting that balancing cholesterol levels is vital for maintaining a healthy brain. Because of this, much of the work we do focuses on the role of cholesterol on development of Alzheimer’s disease. Focusing on cholesterol lowering therapies, such as statin drugs, we have found that production of the toxic proteins that are the hallmark of Alzheimer’s disease can be reduced by over 50%.


PUBLICATIONS:

  1. Hoe, H.S., Cooper, M., Burns, M.P., Lewis, P.A., van der Brug, M., Chakraborty, G., Cartegena, C., Pak, D.T.S., Cookson, M.R., Rebeck., G.W. The metalloprotease inhibitor TIMP-3 regulates APP and ApoE receptor proteolysis. J. Neurosci. In Press.
  2. Eckert, G.P., Vardanian, L., Rebeck G.W. and Burns, M.P. Regulation of central nervous system cholesterol homeostasis by the liver X receptor agonist  TO-901317. Neursci Lett. 423: 47-52.
  3. Czech, C., Burns, M.P. (joint first author), Vardanian, L., Augustine, A., Jacobsen, H., Baumann, K. and Rebeck G.W. Cholesterol independent effect of LXR agonist TO-901317 on gamma-secretase. J Neurochem. 101: 929-936.
  4. Burns, M., Vardanian, L., Pajoohesh-Ganji, A., Wang L., Cooper M., Harris, D.C., Duff, K. and Rebeck G.W. The effects of ABCA1 on cholesterol efflux and Ab levels in vitro and in vivo. J Neurochem. 98: 792-800.
  5. Burns, M., Igbavboa, U., Wang, L., Wood, G.W. and Duff, K. Cholesterol distribution, not total levels, correlate with altered amyloid precursor protein processing in statin treated mice, 2006. NeuroMolecular Medicine. 8: 319-328.
  6. Noble, W., Planel, E., Zehr, C., Olm, V., Meyerson, J., Suleman, F., Gaynor, K., Wang, L., LaFrancois, J., Feinstein, B., Burns, M., Krishnamurthy, P., Wen, Y., Bhat, R., Lewis, J., Dickson, D. and Duff, K. Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivo, 2005. Proc Natl Acad Sci USA. 102: 6990-6995.
  7. Burns, M. and Duff, K. Brains on steroids resists neurodegeneration, 2004. Nat Med 10: 675-676.
  8. Harkin, A, Connor, T.J., Burns M. and Kelly, J.P. Nitric oxide synthase inhibitors augment the effects of serotonin re-uptake inhibitors in the forced swim test, 2004. Eur. Neuropsychopharmacol. 14: 274-281.
  9. Burns, M., Gaynor, K., Olm, V., Mercken, M., LaFrancois, J., Wang, L., Mathews, P.M., Noble, W., Matsuoka, Y. and Duff, K. Presenilin redistribution associated with aberrant cholesterol transport enhances b-amyloid production in vivo, 2003. J Neurosci. 23: 5645-5649.
  10. Noble, W., Olm, V., Takata, K., Casey, E., O, M., Meyerson, J., Gaynor, K., LaFrancois, J., Wang, L., Kondo, T., Davies, P., Burns, M., Veeranna, Nixon, R., Dickson, D., Matsuoka, Y., Ahlijanian, M., Lau, LF., Duff, K., CDK5 is a key factor in tau aggregation and tangle formation in vivo, 2003. Neuron 38:555-565.
  11. Burns, M., Noble, W.J., Olm, V., Gaynor, K., Casey, L. and Duff, K.E. Co-localization of cholesterol, apolipoprotein E and fibrillar A-beta in amyloid plaques, 2003. Mol Brain Res. 110: 119-25.
  12. Burns, M. and Duff, K.E. Use of in vivo models to study the role of cholesterol in the etiology of Alzheimer’s disease, 2003. Neurochem Res. 28: 979-86.
  13. Burns, M. and Duff, K. Intracellular cholesterol homeostasis and Alzheimer’s disease, 2003. In: “Alzheimer's disease and related disorders: Research Advances” Iqbal, K. and Winblad, B. (eds)  Ana Aslan Intl. Acad. Aging, Bucharest, Romania. pp: 559-567.
  14. Burns, M. and Duff, K.E. Cholesterol in Alzheimer’s disease and tauopathy, 2002. Ann NY Acad Sci. 977: 367-376.