Affiliation: University of California
- α-Synuclein and mitochondria: partners in crime?Ken Nakamura
Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
Neurotherapeutics 10:391-9. 2013..Understanding the functional consequences of synuclein's interactions with mitochondria is likely to provide important insights into disease pathophysiology, and may also reveal therapeutic strategies. ..
- Effects of unilateral subthalamic and pallidal deep brain stimulation on fine motor functions in Parkinson's diseaseKen Nakamura
Department of Neurology, University of California, San Francisco, CA, USA
Mov Disord 22:619-26. 2007..Our findings suggest that DBS of the STN or GPi results in a similar improvement in hand movements at short-term follow-up. Preoperative medication responsiveness predicts improvement in some but not other motor tasks...
- Direct membrane association drives mitochondrial fission by the Parkinson disease-associated protein alpha-synucleinKen Nakamura
Department of Neurology and Physiology, University of California, San Francisco, California 94158, USA
J Biol Chem 286:20710-26. 2011..Synuclein thus exerts a primary and direct effect on the morphology of an organelle long implicated in the pathogenesis of Parkinson disease...
- A neo-substrate that amplifies catalytic activity of parkinson's-disease-related kinase PINK1Nicholas T Hertz
Howard Hughes Medical Institute and Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA
Cell 154:737-47. 2013..Discovery of neo-substrates for kinases could provide a heretofore-unappreciated modality for regulating kinase activity...
- Increased expression of alpha-synuclein reduces neurotransmitter release by inhibiting synaptic vesicle reclustering after endocytosisVenu M Nemani
Departments of Neurology and Physiology, Graduate Program in Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA
Neuron 65:66-79. 2010..Increased levels of alpha-synuclein thus produce a specific, physiological defect in synaptic vesicle recycling that precedes detectable neuropathology...
- The behavior of alpha-synuclein in neuronsDoris L Fortin
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA
Mov Disord 25:S21-6. 2010..In addition to the presumed role of alpha-synuclein dynamics in synaptic function, changes in its physiological behavior may underlie the pathological changes associated with Parkinson's disease...
- Energy failure: does it contribute to neurodegeneration?Divya Pathak
Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, CA
Ann Neurol 74:506-16. 2013..Here we review the current evidence that energy failure occurs in and contributes to neurodegenerative disease, and consider new approaches that may allow us to better address this central issue...
- Optical reporters for the conformation of alpha-synuclein reveal a specific interaction with mitochondriaKen Nakamura
Graduate Program in Neuroscience, Department of Neurology, University of California at San Francisco, San Francisco, California 94143, USA
J Neurosci 28:12305-17. 2008..We find that the conformation of alpha-synuclein responds selectively to mitochondria, indicating a direct link between alpha-synuclein and an organelle strongly implicated in the pathogenesis of PD...
- Physiology versus pathology in Parkinson's diseaseKen Nakamura
Departments of Neurology and Physiology, University of California School of Medicine, 600 16th Street, GH N272B, San Francisco, CA 94158 2517, USA
Proc Natl Acad Sci U S A 104:11867-8. 2007
- The ubiquitin ligase parkin mediates resistance to intracellular pathogensPaolo S Manzanillo
Department of Microbiology and Immunology Program in Microbial Pathogenesis and Host Defense, University of California, San Francisco, San Francisco, California 94158, USA
Nature 501:512-6. 2013..Moreover, our work reveals an unexpected functional link between mitophagy and infectious disease. ..
- Mutant LRRK2 Toxicity in Neurons Depends on LRRK2 Levels and Synuclein But Not Kinase Activity or Inclusion BodiesGaia Skibinski
Gladstone Institute of Neurological Disease, the Taube Koret Center for Neurodegenerative Disease Research, and the Hellman Family Foundation Program in Alzheimer s Disease Research, San Francisco, California 94158, Departments of Neurology, Physiology, and Graduate Programs in Neuroscience and Biomedical Sciences, University of California, San Francisco, California 94158, and Laboratory of Neurogenetics, National Institutes of Health, Bethesda, Maryland 20892
J Neurosci 34:418-33. 2014..These findings suggest that LRRK2 levels are more important than kinase activity per se in predicting toxicity and implicate synuclein as a major mediator of LRRK2-induced neurodegeneration. ..