Steve Finkbeiner, MD, PhD

Associate Director and Senior Investigator

Phone: (415) 734-2508
Fax: (415) 355-0824
Fewer scientific details, please
Download a Printable PDF

Other Professional Titles

Director, Taube-Koret Center for Neurodegenerative Disease Research at Gladstone

Investigator, Roddenberry Center for Stem Cell Biology and Medicine at Gladstone

Professor, Neurology and Physiology, University of California, San Francisco

Administrative Assistant

Kelley Nelson
(415) 734-2509
knelson@gladstone.ucsf.edu

More about Dr. Finkbeiner

Dr. Finkbeiner studies the molecular mechanisms that are responsible for learning, memory and neurodegeneration. A better understanding of the mechanisms that control memory formation in neurons will yield crucial insights into the development and progression of neurodegenerative diseases—and the memory disorders that often characterize them.

As one of the first investigators to join the Gladstone Institute of Neurological Disease in 1999, Dr. Finkbeiner is best known for his pioneering work on neurodegenerative diseases. He invented robotic microscopy, a new form of imaging that has helped unravel cause-and-effect relationships in amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease), Huntington’s, Alzheimer’s and other neurodegenerative diseases. Dr. Finkbeiner used his robotic microscope to resolve a long-standing puzzle in Huntington’s disease. A study based on results from the microscope became the most-cited paper in the field of neuroscience in the last decade.

With the help of Bay Area philanthropists, Dr. Finkbeiner established the Taube-Koret Center in 2009 to accelerate the development of drug therapies for patients suffering from conditions such as Huntington’s disease. Also at Gladstone, he directs the Hellman Family Foundation Alzheimer’s Disease Research Program.

Dr. Finkbeiner is Associate Editor of Autophagy and serves on the editorial board of the Journal of Huntington’s Disease and BioMed Central. He has received numerous awards for his work, including the Lieberman Award, the Taube-Koret Prize and the Award for Outstanding Research Achievement from Nature Biotechnology. He is a member of several scientific and professional societies, including the American Neurological Association, the Society for Neuroscience, the Society for Cell Biology and the Biophysical Society. He is active in graduate training and is a member of the Neuroscience, Biomedical Sciences and Medical Scientist Training Programs at UCSF.

In 1986, Dr. Finkbeiner earned a bachelor’s degree from Wheaton College. He earned both an MD and a PhD in neuroscience from Yale University in 1991. He completed an internship in internal medicine and chief residency in neurology at UCSF, followed by a research fellowship at Harvard Medical School.

More scientific details, please

Other Professional Titles

Director, Taube-Koret Center for Neurodegenerative Disease Research at Gladstone

Investigator, Roddenberry Center for Stem Cell Biology and Medicine at Gladstone

Professor, Neurology and Physiology, University of California, San Francisco

Administrative Assistant

Kelley Nelson
(415) 734-2509
knelson@gladstone.ucsf.edu

Areas of Investigation

Research in our laboratory focuses on molecular mechanisms of plasticity and neurodegeneration. A long-term goal of our research is to understand how neuronal activity elicits changes in gene expression that are important for learning and memory. Memory disturbances occur in several neurodegenerative diseases, and we have developed models of several of them including Huntington’s disease (HD), Parkinson’s Disease (PD), amyotrophic lateral sclerosis (ALS) and Alzheimer’s disease.  A better understanding of the mechanisms that control memory formation and neurodegeneration will yield crucial insights into the pathogenesis of neurodegenerative diseases and the memory disorders that often characterize them. 

Current Lab Focus

  • Which genes are critical for forming memories and how do they do so?
  • How do genetic mutations in selected genes lead to elective degeneration in certain types of neurons in HD, PD and ALS?
  • What are the critical coping mechanisms that brain cells generate to mitigate the effects of genetic mutations that cause neurodegeneration?
  • With our unique robotic microscope technology, can we identify the major determinants of cell fate during normal development of stem cells and in neurodegenerative disease?
  • How can we effectively advance the discoveries we make in the laboratory into medicines to help patients?

Joined Gladstone

1999

Why Gladstone?

I joined Gladstone to study neurological diseases, with an emphasis on HD. Working at Gladstone lets me do cutting-edge research in a stimulating and productive environment, with the potential for breakthrough discoveries.

Key Achievements

  • Found that proteins bound to the cytoplasmic portion of one subtype of glutamate receptor, the N-methyl-D-aspartate receptor, play a critical role coupling local Ca2+ influx through the channel to elicit adaptive gene transcription in neurons. This may be a general mechanism by which diverse Ca2+ channels achieve specific and distinct neuronal responses.
  • Developed primary culture models of activity-dependent gene transcription and of HD. These models faithfully recapitulate critical features of these processes and allow us to test hypotheses about their underlying mechanisms.
  • Shown that the nucleus is a critical subcellular site in which mutant huntingtin induces neurodegeneration. However, mutant huntingtin need not aggregate into inclusions to induce neurodegeneration.
  • Developed an automated imaging system that we call a “robotic microscope.” This instrument enables us to track living neurons over long time periods to quantify quickly the adaptive or maladaptive responses of thousands of neurons. Along with special statistical methods, we now have the ability to determine whether and to what extent a variable that is observed on one day can predict the fate of that neuron on another day. This ability will enable us to unravel confounding cause-and-effect mechanisms.

Education

Wheaton College (BS), Chemistry (1986)
Yale University (PhD), Neuroscience (1991)
Yale University (MD), Cum Laude (1991)

Affiliations

Director, Hellman Family Foundation Alzheimer’s Disease Research Program
American Neurological Association
Society for Neuroscience
Society for Cell Biology
Biophyical Society
Vertex Pharmaceutical, Scientific Advisory Board
LINK Medicine, Scientific Advisory Board
FivePrime, Inc., Consultant

Awards

  • Charles E. Culpepper Medical Scholar Award (1999)
  • W.M. Keck Research Excellence Award (2001)
  • Klingenstein Award in Neuroscience (2001)
  • Therapeutics Initiative Award, Huntington’s Disease Society of America (2005)
  • Taube Prize for Outstanding Work in Huntington’s Disease (2005)
  • Lieberman Award for Outstanding Work on Huntington’s Disease (2005)
  • UCSF Annual Outstanding Faculty Mentorship Award, Graduate Student Association, University of California, San Francisco (2008)
  • Distinguished Leadership Award, Huntington’s Disease Society of America, (2008)
  • Award for Outstanding Research Achievement, Nature Biotechnology (2011)
Syndicate publications

Featured Publications

Steve Finkbeiner, MD, PhDMiller J, Arrasate M, Brooks E, Libeu CP, Legleiter J, Hatters D, Curtis J, Cheung K, Krishnan P, Mitra S, Widjaja K, Shaby BA, Lotz GP, Newhouse Y, Mitchell EJ, Osmand A, Gray M, Thulasiramin V, Saudou F, Segal M, Yang XW, Masliah E, Thompson LM, Muchowski PJ, Weisgraber KH, Finkbeiner S. Identifying polyglutamine protein species in situ that best predict neurodegeneration. Nat Chem Biol. 2012; 8(3):318. View in: PubMed
Steve Finkbeiner, MD, PhDBarmada SJ, Skibinski G, Korb E, Rao EJ, Wu JY, Finkbeiner S. Cytoplasmic mislocalization of TDP-43 is toxic to neurons and enhanced by a mutation associated with familial amyotrophic lateral sclerosis. J Neurosci. 2010 Jan 13; 30(2):639-49. View in: PubMed