Cellular Neurology Unit - Division of Intramural Research

 Craig   Blackstone  M.D., Ph.D., 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

Chuang-Rung Chang, Ph.D., Postdoctoral Fellow , 301-451- 9684
Michael Hanna, Ph.D., Special Volunteer , 301-451- 9686
Seong-hee Park, Ph.D., Postdoctoral Fellow
Benoit Renvoise, Ph.D., Postdoctoral Fellow , 301-451- 9682
Neggy Rismanchi, Ph.D., Special Volunteer , 301-496- 0284
Cynthia Soderblom, B.S., Predoctoral Fellow , 301-451- 9683
Julia Stadler, B.A., Research Assistant , 301-451- 9685
Peng-Peng Zhu, M.D., Staff Scientist , 301-451- 9687

Research Interests

Research in the Cellular Neurology Unit emphasizes two major disease-related aims. The first focuses on understanding the cellular pathogenesis of a group of disorders known as the hereditary spastic paraplegias (HSPs), whose cardinal feature is a length-dependent axonopathy of corticospinal motor neurons. A particular advantage in piecing together the molecular and cellular pathogenesis underlying the HSPs is that well over 30 genetic loci (SPG1-33) have been mapped, with 16 gene products already identified that segregate into a smaller number of functional groups. Many of these proteins are suspected to be involved in protein and membrane trafficking, and we are currently studying HSP disease proteins involved in both secretory and endocytic pathways.

Selected Recent Publications

Blackstone C
Infantile parkinsonism-dystonia: a dopamine 'transportopathy' - J Clin Invest  119 1455-1458 2009

Rismanchi N, Soderblom C, Stadler J, Zhu P-P, Blackstone C
Atlastin GTPases are required for Golgi apparatus and ER morphogenesis - Hum Molec Genet  17 1591-1604 2008

Bakowska JC, Wang H, Xin B, Sumner CJ, Blackstone C
Loss of spartin protein in Troyer syndrome: a loss-of-function disease mechanism? - Arch Neurol  65 520-524 2008

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  15 1278-1286 2008

Chang C-R, Blackstone C
Cyclic-AMP-dependent phosphorylation of Drp1 regulates its GTPase activity and mitochondrial morphology - J Biol Chem  282 21583-21587 2007

Bakowska J, Jupille H, Fatheddin P, Puertollano R, Blackstone C
Troyer syndrome protein spartin is mono-ubiquitinated and functions in EGF receptor trafficking - Mol Biol Cell  18 1683-1692 2007

Selected Earlier Publications

Contact Information

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

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