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Cellular Neurology Section - Division of Intramural Research


Craig Blackstone Image

Craig Blackstone, M.D., Ph.D., Senior Investigator

Dr. Blackstone received B.S. and M.S. degrees in 1987 from the University of Chicago and M.D. and Ph.D. degrees in 1994 from Johns Hopkins University. His graduate studies, in the laboratory of Richard Huganir, were on the structure and regulation of glutamate receptors, for which he received the David Israel Macht Award. After a neurology residency at the Harvard-Longwood Neurology Program, Dr. Blackstone completed a fellowship in clinical movement disorders at the Massachusetts General Hospital. During this time he also conducted postdoctoral research with Morgan Sheng at Harvard Medical School, investigating the functions of proteins implicated in hereditary dystonias. Dr. Blackstone joined the NINDS as an investigator in 2001. His laboratory investigates the cellular and molecular mechanisms underlying hereditary movement disorders.

Laboratory Staff

Caroline Anderson, M.S., Graduate Student
Jaerak Chang, Ph.D., Postdoctoral Fellow
Do Jin Kim, Ph.D., Postdoctoral Fellow
Seongju Lee, Ph.D., Postdoctoral Fellow
Brianna Malone, B.S., Postbaccalaureate IRTA
Benoit Renvoise, Ph.D., Research Fellow
Ricardo Roda, M.D., Ph.D., Clinical Fellow
Julia Stadler, B.A., Research Assistant
Guohua Zhao, M.D., Visiting Fellow
Peng-Peng Zhu, M.D., Staff Scientist
Craig Blackstone Staff Image

Research Interests

Our research group investigates cellular mechanisms underlying inherited neurological disorders, with an emphasis on neuromuscular and movement disorders. In particular, the pathogenesis of hereditary spastic paraplegias, which affect corticospinal motor axons in a length-dependent manner, is an area of very active interest. These disorders comprise well over 50 distinct genetic loci, with over 30 genes identified whose proteins segregate into a few common cellular themes. In addition to an active clinical program assessing new patients with these disorders, we investigate the functions of the disease gene products at the cellular level and in animal models. We have identified that the most common forms of inherited spastic paraplegia are due to mutations in genes encoding proteins with hydrophobic hairpin domains that help shape the distinct morphology of the tubular endoplasmic reticulum network. A number of these proteins as well as other spastic paraplegia proteins implicated in endocytic processes also act as inhibitors of bone morphogenetic protein signaling, providing an exciting translational line of investigation. Our current studies investigate both the disease pathogenic mechanisms as well as the more fundamental aspects of how organelles are shaped in cells, and why this is particularly important for neurons. The common pathogenic themes that are emerging will likely represent novel targets for therapeutic intervention.


Selected Recent Publications

  • Chang J, Lee S, Blackstone C
    Protrudin binds atlastins and endoplasmic reticulum-shaping proteins and regulates network formation, Proc Natl Acad Sci USA, 2013, vol. 110, pp. 14954-14959. Full Text/Abstract
  • Renvoise B, Stadler J, Singh R, Bakowska JC, Blackstone C
    Spg20-/- mice reveal multimodal functions for Troyer syndrome protein spartin in lipid droplet maintenance, cytokinesis, and BMP signaling, Hum Mol Genet, 2012, vol. 21, pp. 3604-3618. Full Text/Abstract
  • Blackstone C
    Cellular pathways of hereditary spastic paraplegia, Annu Rev Neurosci, 2012, vol. 35, pp. 25-47. Full Text/Abstract
  • Blackstone C, O'Kane CJ, Reid E
    Hereditary spastic paraplegias: membrane traffic and the motor pathway, Nat Rev Neurosci, 2011, vol. 12, pp. 31-42. Full Text/Abstract
  • Park SH, Zhu P-P, Parker RL, Blackstone C
    Spastic paraplegia proteins REEP1, spastin, and atlastin-1 coordinate microtubule interactions with the tubular ER network, J Clin Invest, 2010, vol. 120, pp. 1097-1110. Full Text/Abstract
  • Hu J, Shibata Y, Zhu P-P, Voss C, Rismanchi N, Prinz WA, Rapoport TA, Blackstone C
    A class of dynamin-like GTPases involved in the generation of the tubular ER network, Cell, 2009, vol. 138, pp. 549-561. Full Text/Abstract
  • Yang D, Rismanchi N, Renvoise B, Lippincott-Schwartz J, Blackstone C, Hurley JH
    Structural basis for midbody targeting of spastin by the ESCRT-III protein CHMP1B, Nat Struct Mol Biol, 2008, vol. 15, pp. 1278-1286. Full Text/Abstract
  • Blackstone C, Murphy TH, Moss SJ, Baraban JM, Huganir RL
    Cyclic AMP and synaptic activity-dependent phosphorylation of AMPA-preferring glutamate receptors, J Neurosci, 1994, vol. 14, pp. 7585-7593.

Selected Earlier Publications


Contact Information

Cellular Neurology Section, NINDS
Porter Neuroscience Research Center
Building 35, Room 2C-913
35 Convent Drive, MSC 3704
Bethesda, MD 20892-3704

Telephone: 301-451-9680 (office), 301-480-4888 (fax)
Email: blackstc@ninds.nih.gov