Ken Nakamura, MD, PhD

Assistant Investigator

Phone: (415) 734-2550
Fax: (415) 355-0824
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Other Professional Titles

Assistant Professor, Neurology, University of California, San Francisco
Parkinson’s Disease and Movement Disorders clinic, for all clinical questions contact (415) 353-2273.

Administrative Assistant

Erica Nguyen
(415) 734-2516

More about Dr. Nakamura

Dr. Nakamura’s research focuses on the normal functioning of mitochondria—the “power centers” of cells, which convert nutrients into energy. He further studies how the disruption of mitochondria contributes to the development of neurodegenerative diseases—especially Parkinson’s and Alzheimer’s diseases. 

Dr. Nakamura has won numerous awards, including the Burroughs Wellcome Fund Career Award for Medical Scientists, the Larry L. Hillblom Foundation Fellowship and the University of Chicago’s Steven Lukes Memorial Prize for excellence in the fields of internal medicine and neurology.

A board-certified neurologist, Dr. Nakamura maintains a clinical practice treating patients with Parkinson’s disease and other movement disorders. He is a member of the American Academy of Neurology, the Movement Disorder Society and the Society for Neuroscience. 

Dr. Nakamura earned a bachelor’s degree in chemistry and biological sciences from Cornell University, and an MD and PhD in neurobiology from the University of Chicago. He completed his residency and chief residency at UCSF and a subspecialty training in movement disorders at UCSF and the San Francisco Veterans Administration Medical Center. He also completed a UCSF research fellowship investigating the role of a small protein (alpha-synuclein) in the development of Parkinson’s disease.



More scientific details, please

Other Professional Titles

Assistant Professor, Neurology, University of California, San Francisco
Parkinson’s Disease and Movement Disorders clinic, for all clinical questions contact (415) 353-2273.

Administrative Assistant

Erica Nguyen
(415) 734-2516

Areas of Investigation

Our laboratory has two broad objectives. The first is to gain insight into the normal physiology of mitochondria in the brain, with a particular emphasis on understanding the biologic functions of mitochondrial dynamics and turnover, and the role of mitochondria in synaptic transmission. The second is to understand how disruption of these mitochondrial functions contributes to the pathogenesis of neurodegenerative diseases, especially Parkinson's disease and Alzheimer's disease.

Mitochondria are dynamic organelles that undergo constant fusion and fission, play important roles in multiple cellular functions including energy production, and are ultimately degraded. However, many aspects of mitochondrial behavior and function are not understood, especially in the brain and at the synapse. Changes in mitochondria also play central and sometimes initiating roles in neurodegeneration, although the underlying mechanisms, or even the nature of the changes themselves, are poorly characterized. Advancing our understanding of the normal behavior and functions of mitochondria is thus a critical step in unraveling how mitochondrial biology is disrupted in disease, and in ultimately designing new mitochondria-based therapies.

We use an array of sophisticated microscopy approaches to study mitochondrial biology in the brain. Mitochondria are visualized live using targeted fluorescent probes, and mitochondrial movement, functions and turnover are imaged in mammalian cells including primary neurons. Transgenic mouse models and genetically modified viral vectors are also used to study mitochondria in vivo, and to determine how human mutations causing Parkinson's disease and Alzheimer's disease disrupt mitochondrial function and produce degeneration. To establish mechanism, we also use in vitro model systems with recombinant proteins and purified mitochondria or artificial membranes.

Current Lab Focus

  • What are the normal functions of mitochondrial fusion and fission in neurons?
  • How and why are mitochondria turned over?
  • How do mitochondria contribute to synaptic transmission?
  • How do Parkinson's disease proteins disrupt mitochondrial function and produce neurodegeneration?
  • How does mitochondrial dysfunction contribute to the pathogenesis of Alzheimer's disease?

Joined Gladstone


Why Gladstone?

I came to Gladstone because of the opportunity to work with innovative and talented scientists and staff, fully committed to advancing our understanding and treatment of neurodegenerative disease.  I greatly value the cohesive, stimulating and driven atmosphere, where cutting-edge basic science is applied to the development of new therapies.

Key Achievements

  • Found that synuclein preferentially binds to mitochondria versus other organelles because of its high affinity for the acidic phospholipid cardiolipin, which is enriched in mitochondria.
  • Discovered that the expression of synuclein produces a dramatic increase in mitochondrial fragmentation in a range of cell types, including dopamine neurons in transgenic models of Parkinson's disease. These findings reveal a new function of synuclein in regulating mitochondrial morphology, and establish a potential mechanism by which synuclein may produce degeneration in Parkinson's disease.


Cornell University (BA), Chemistry and Biological Sciences (1993)
University of Chicago (PhD), Neurobiology (1999)
University of Chicago (MD) (2001)


  • Steven Lukes Memorial Prize, University of Chicago (2001)
  • Burroughs Wellcome Fund Career Award for Medical Scientists (2008)
Syndicate publications

Featured Publications

Ken Nakamura, MD, PhDBerthet A, Margolis EB, Zhang J, Hsieh I, Zhang J, Hnasko T, Ahmad J, Edwards RH, Sesaki H, Huang EJ, Nakamura K. (2014) Loss of mitochondrial fission depletes axonal mitochondria in midbrain dopamine neurons. J Neuroscience. 34(43):14304-14317 View in: PubMed
Ken Nakamura, MD, PhDNakamura K, Nemani VM, Azarbal F, Skibinski G, Levy JM, Egami K, Munishkina L, Zhang J, Gardner B, Wakabayashi J, Sesaki H, Cheng Y, Finkbeiner S, Nussbaum RL, Masliah E, Edwards RH. Direct membrane association drives mitochondrial fission by the Parkinson disease-associated protein alpha-synuclein. J Biol Chem. 2011 Jun 10; 286(23):20710-26. View in: PubMed