Cellular Neurology Unit - Division of Intramural Research

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Craig  Blackstone Image

 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

Joanna Bakowska, Ph.D. Special Volunteer  301-451- 9682
Chuang-Rung Chang, Ph.D. Postdoctoral Fellow  301-451- 9684
Michael Hanna, Ph.D. Research Fellow  301-451- 9686
Henri Jupille, B.S. Post baccalaureate Fellow  301-451- 9683
Benoit Renvoise, Ph.D. Visiting Fellow  301-451- 9682
Neggy Rismanchi, Ph.D. Postdoctoral Fellow  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


Craig  
					Blackstone Staff Image

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

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

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

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

Soderblom C, Blackstone C
Traffic accidents: molecular genetic insights into the pathogenesis of the hereditary spastic paraplegias - Pharmacol Ther  109 42-56 2006

Zhu P-P, Soderblom C, Tao-Cheng J-H, Stadler J, Blackstone C
SPG3A protein atlastin-1 is enriched in growth cones and promotes axon elongation during neuronal development - Hum Mol Genet  15 1343-1353 2006

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