Steven Finkbeiner

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Disease-modifying pathways in neurodegeneration
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease and Department of Physiology, University of California, San Francisco, San Francisco, California 94158, USA
    J Neurosci 26:10349-57. 2006
  2. ncbi request reprint Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease
    Jorge J Palop
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Neuron 55:697-711. 2007
  3. pmc Tau reduction prevents Abeta-induced defects in axonal transport
    Keith A Vossel
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Science 330:198. 2010
  4. doi request reprint Bridging the Valley of Death of therapeutics for neurodegeneration
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease, Taube Koret Center for Huntington s Disease Research, Consortium for Fronto temporal Dementia Research, and Department of Neurology, University of California, San Francisco, California, USA
    Nat Med 16:1227-32. 2010
  5. ncbi request reprint An evaluation of specificity in activity-dependent gene expression in neurons
    John Bradley
    Departments of Neurology and Physiology, Gladstone Institute of Neurological Disease, University of California, San Francisco, CA 94103, USA
    Prog Neurobiol 67:469-77. 2002
  6. ncbi request reprint Splice variants of the NR1 subunit differentially induce NMDA receptor-dependent gene expression
    John Bradley
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141, USA
    J Neurosci 26:1065-76. 2006
  7. ncbi request reprint AMPA receptors regulate transcription of the plasticity-related immediate-early gene Arc
    Vikram R Rao
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    Nat Neurosci 9:887-95. 2006
  8. ncbi request reprint NMDA and AMPA receptors: old channels, new tricks
    Vikram R Rao
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Trends Neurosci 30:284-91. 2007
  9. pmc Arc regulates spine morphology and maintains network stability in vivo
    Carol L Peebles
    Gladstone Institute of Neurological Disease and the Keck Program in Striatal Physiology, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 107:18173-8. 2010
  10. pmc The serum response factor and a putative novel transcription factor regulate expression of the immediate-early gene Arc/Arg3.1 in neurons
    Sean A Pintchovski
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 29:1525-37. 2009

Collaborators

Detail Information

Publications20

  1. ncbi request reprint Disease-modifying pathways in neurodegeneration
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease and Department of Physiology, University of California, San Francisco, San Francisco, California 94158, USA
    J Neurosci 26:10349-57. 2006
  2. ncbi request reprint Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease
    Jorge J Palop
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Neuron 55:697-711. 2007
    ..Aberrant increases in network excitability and compensatory inhibitory mechanisms in the hippocampus may contribute to Abeta-induced neurological deficits in hAPP mice and, possibly, also in humans with AD...
  3. pmc Tau reduction prevents Abeta-induced defects in axonal transport
    Keith A Vossel
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Science 330:198. 2010
    ..Lowering tau levels prevented these defects without affecting baseline axonal transport. Thus, Aβ requires tau to impair axonal transport, and tau reduction protects against Aβ-induced axonal transport defects...
  4. doi request reprint Bridging the Valley of Death of therapeutics for neurodegeneration
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease, Taube Koret Center for Huntington s Disease Research, Consortium for Fronto temporal Dementia Research, and Department of Neurology, University of California, San Francisco, California, USA
    Nat Med 16:1227-32. 2010
    ..Here we consider the many obstacles to the development of therapeutics for neurodegenerative disease within academia, with a special focus on organizational issues...
  5. ncbi request reprint An evaluation of specificity in activity-dependent gene expression in neurons
    John Bradley
    Departments of Neurology and Physiology, Gladstone Institute of Neurological Disease, University of California, San Francisco, CA 94103, USA
    Prog Neurobiol 67:469-77. 2002
    ..In particular, we describe data which suggests that Ca2+ channels may function in signal complexes at the synapse to propagate signals that contribute to distinct nuclear responses...
  6. ncbi request reprint Splice variants of the NR1 subunit differentially induce NMDA receptor-dependent gene expression
    John Bradley
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141, USA
    J Neurosci 26:1065-76. 2006
    ..Thus, the NR1 C terminus couples to multiple downstream signaling pathways that can be modulated selectively by RNA splicing...
  7. ncbi request reprint AMPA receptors regulate transcription of the plasticity-related immediate-early gene Arc
    Vikram R Rao
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    Nat Neurosci 9:887-95. 2006
    ..These results provide insights into the activity-dependent mechanisms of Arc expression and suggest that, in addition to effecting short-term plasticity, AMPA receptors regulate genes involved in long-term plasticity...
  8. ncbi request reprint NMDA and AMPA receptors: old channels, new tricks
    Vikram R Rao
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Trends Neurosci 30:284-91. 2007
    ..We discuss evidence that signals from NMDA receptors and AMPA receptors are integrated to specify transcriptional responses for particular plasticity related genes...
  9. pmc Arc regulates spine morphology and maintains network stability in vivo
    Carol L Peebles
    Gladstone Institute of Neurological Disease and the Keck Program in Striatal Physiology, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 107:18173-8. 2010
    ..Supporting this, loss of Arc in vivo leads to a significant decrease in the proportion of thin spines and an epileptic-like network hyperexcitability...
  10. pmc The serum response factor and a putative novel transcription factor regulate expression of the immediate-early gene Arc/Arg3.1 in neurons
    Sean A Pintchovski
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 29:1525-37. 2009
    ..This element binds serum response factor, which is recruited by synaptic activity to regulate Arc. Thus, Arc is the first target of serum response factor that functions at synapses to mediate plasticity...
  11. pmc Quantitative relationships between huntingtin levels, polyglutamine length, inclusion body formation, and neuronal death provide novel insight into huntington's disease molecular pathogenesis
    Jason Miller
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    J Neurosci 30:10541-50. 2010
    ..Finally, the model that emerges from our quantitative measurements places critical limits on the potential mechanisms by which mutant htt might induce neurodegeneration, which should help direct future research...
  12. pmc A small-molecule scaffold induces autophagy in primary neurons and protects against toxicity in a Huntington disease model
    Andrey S Tsvetkov
    Gladstone Institute of Neurological Disease and Taube Koret Center for Huntington s Disease Research and Consortium for Fronto temporal Dementia Research, University of California, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 107:16982-7. 2010
    ..This pharmacophore should prove useful in studying autophagy in neurons and in developing therapies for neurodegenerative proteinopathies...
  13. pmc Cytoplasmic mislocalization of TDP-43 is toxic to neurons and enhanced by a mutation associated with familial amyotrophic lateral sclerosis
    Sami J Barmada
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 30:639-49. 2010
    ..These results suggest that mutant TDP-43 is mislocalized to the cytoplasm, where it exhibits a toxic gain-of-function and induces cell death...
  14. pmc Protein turnover and inclusion body formation
    Siddhartha Mitra
    Gladstone Institute of Neurological Disease, San Francisco, CA 945158, USA
    Autophagy 5:1037-8. 2009
    ..These findings suggest that IB formation is a protective cellular response mediated in part by increased degradation of intracellular protein...
  15. pmc Single neuron ubiquitin-proteasome dynamics accompanying inclusion body formation in huntington disease
    Siddhartha Mitra
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Biol Chem 284:4398-403. 2009
    ..After forming IBs, impairment is lower in neurons with IBs than in those without. These findings suggest IBs are a protective cellular response to mutant protein mediated in part by improving intracellular protein degradation...
  16. pmc The ubiquitin-proteasome pathway in Huntington's disease
    Steven Finkbeiner
    Gladstone Institute of Neurological Disease, 1650 Owens St, San Francisco, CA94158, USA
    ScientificWorldJournal 8:421-33. 2008
    ..A number of potential mechanisms that link compromised ubiquitin-proteasome pathway function and neurodegeneration have been proposed and may offer opportunities for therapeutic intervention...
  17. pmc Automated microscope system for determining factors that predict neuronal fate
    Montserrat Arrasate
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 102:3840-5. 2005
    ..The ability to monitor complex processes at single-cell resolution quickly, quantitatively, and over long intervals should have wide applications for biology...
  18. ncbi request reprint Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death
    Montserrat Arrasate
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141, USA
    Nature 431:805-10. 2004
    ..Surprisingly, inclusion body formation predicts improved survival and leads to decreased levels of mutant huntingtin elsewhere in a neuron. Thus, inclusion body formation can function as a coping response to toxic mutant huntingtin...
  19. ncbi request reprint RNA decay back in play
    Carol L Peebles
    Nat Neurosci 10:1083-4. 2007
  20. ncbi request reprint The IGF-1/Akt pathway is neuroprotective in Huntington's disease and involves Huntingtin phosphorylation by Akt
    Sandrine Humbert
    UMR 146 CNRS Institut Curie, Centre Universitaire, 91405 Orsay Cedex, France
    Dev Cell 2:831-7. 2002
    ..Finally, we show that Akt is altered in Huntington's disease patients. Taken together, these results support a potential role of the Akt pathway in Huntington's disease...