Erik D Roberson

Summary

Affiliation: University of Alabama at Birmingham
Country: USA

Publications

  1. pmc Challenges and opportunities for characterizing cognitive aging across species
    Erik D Roberson
    Departments of Neurology and Neurobiology, Evelyn F McKnight Brain Institute, University of Alabama at Birmingham Birmingham, AL, USA
    Front Aging Neurosci 4:6. 2012
  2. pmc Mouse models of frontotemporal dementia
    Erik D Roberson
    Departments of Neurology and Neurobiology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama, Birmingham, AL 35294, USA
    Ann Neurol 72:837-49. 2012
  3. pmc Amyloid-β/Fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of Alzheimer's disease
    Erik D Roberson
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 31:700-11. 2011
  4. pmc Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's disease
    William J Meilandt
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 28:5007-17. 2008
  5. 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
  6. ncbi request reprint Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model
    Erik D Roberson
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Science 316:750-4. 2007
  7. doi request reprint Quantifying biomarkers of cognitive dysfunction and neuronal network hyperexcitability in mouse models of Alzheimer's disease: depletion of calcium-dependent proteins and inhibitory hippocampal remodeling
    Jorge J Palop
    Department of Neurology, Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, CA, USA
    Methods Mol Biol 670:245-62. 2011
  8. doi request reprint Geriatric epilepsy: research and clinical directions for the future
    Erik D Roberson
    Department of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Epilepsy Behav 22:103-11. 2011
  9. pmc Seizure resistance without parkinsonism in aged mice after tau reduction
    Zhiyong Li
    Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL, USA
    Neurobiol Aging 35:2617-24. 2014
  10. pmc The Alzheimer's disease risk factor CD2AP maintains blood-brain barrier integrity
    J Nicholas Cochran
    Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Hum Mol Genet 24:6667-74. 2015

Collaborators

Detail Information

Publications18

  1. pmc Challenges and opportunities for characterizing cognitive aging across species
    Erik D Roberson
    Departments of Neurology and Neurobiology, Evelyn F McKnight Brain Institute, University of Alabama at Birmingham Birmingham, AL, USA
    Front Aging Neurosci 4:6. 2012
    ..Finally, we highlight some of the challenges of studying cognitive aging in human subjects...
  2. pmc Mouse models of frontotemporal dementia
    Erik D Roberson
    Departments of Neurology and Neurobiology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama, Birmingham, AL 35294, USA
    Ann Neurol 72:837-49. 2012
    ..There are also opportunities for capitalizing on conservation of the salience network, which is selectively vulnerable in FTD, and the availability of FTD-related behavioral paradigms to analyze mouse models of the disease...
  3. pmc Amyloid-β/Fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of Alzheimer's disease
    Erik D Roberson
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 31:700-11. 2011
    ..Our results indicate that Aβ, tau, and Fyn jointly impair synaptic and network function and suggest that disrupting the copathogenic relationship between these factors could be of therapeutic benefit...
  4. pmc Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's disease
    William J Meilandt
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Neurosci 28:5007-17. 2008
    ..We conclude that enkephalin elevations may contribute to cognitive impairments in hAPP mice and possibly in humans with AD. The therapeutic potential of reducing enkephalin production or signaling merits further exploration...
  5. 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...
  6. ncbi request reprint Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model
    Erik D Roberson
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Science 316:750-4. 2007
    ..Thus, tau reduction can block Abeta- and excitotoxin-induced neuronal dysfunction and may represent an effective strategy for treating Alzheimer's disease and related conditions...
  7. doi request reprint Quantifying biomarkers of cognitive dysfunction and neuronal network hyperexcitability in mouse models of Alzheimer's disease: depletion of calcium-dependent proteins and inhibitory hippocampal remodeling
    Jorge J Palop
    Department of Neurology, Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, CA, USA
    Methods Mol Biol 670:245-62. 2011
    ..In addition, since we have found that the severity of these changes relates to the degree of Aβ-dependent cognitive impairments, the protocols are useful for quantifying biomarkers of cognitive impairment in mouse models of AD...
  8. doi request reprint Geriatric epilepsy: research and clinical directions for the future
    Erik D Roberson
    Department of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Epilepsy Behav 22:103-11. 2011
    ..Dr. Hope will outline key issues, as well as her work, relating to defining and measuring quality care in geriatric epilepsy...
  9. pmc Seizure resistance without parkinsonism in aged mice after tau reduction
    Zhiyong Li
    Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL, USA
    Neurobiol Aging 35:2617-24. 2014
    ....
  10. pmc The Alzheimer's disease risk factor CD2AP maintains blood-brain barrier integrity
    J Nicholas Cochran
    Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Hum Mol Genet 24:6667-74. 2015
    ..Taken together, our results support a role of CD2AP in mediating blood-brain barrier integrity and suggest that cerebrovascular roles of CD2AP could contribute to its effects on Alzheimer's disease risk. ..
  11. pmc Early retinal neurodegeneration and impaired Ran-mediated nuclear import of TDP-43 in progranulin-deficient FTLD
    Michael E Ward
    Gladstone Institute of Neurological Diseases, Department of Neurology, Department of Medicine, Gladstone Institute of Cardiovascular Disease, University of California, San Franciso, San Francisco, CA 94158 Gladstone Institute of Neurological Diseases, Department of Neurology, Department of Medicine, Gladstone Institute of Cardiovascular Disease, University of California, San Franciso, San Francisco, CA 94158
    J Exp Med 211:1937-45. 2014
    ..Our findings establish retinal neurodegeneration as a new phenotype in progranulin-deficient FTLD, and suggest a pathological loop involving reciprocal loss of Ran and nuclear TDP-43 as an underlying mechanism. ..
  12. pmc AlphaScreen HTS and live-cell bioluminescence resonance energy transfer (BRET) assays for identification of Tau-Fyn SH3 interaction inhibitors for Alzheimer disease
    J Nicholas Cochran
    Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL, USA
    J Biomol Screen 19:1338-49. 2014
    ..This screen has identified a variety of chemically tractable hits, suggesting that the Tau-Fyn interaction may represent a good drug target for AD. ..
  13. pmc Tau-mediated NMDA receptor impairment underlies dysfunction of a selectively vulnerable network in a mouse model of frontotemporal dementia
    Brian A Warmus
    Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, Medical Scientist Training Program, University of Alabama at Birmingham, Birmingham, Alabama 35294, and
    J Neurosci 34:16482-95. 2014
    ....
  14. pmc The dendritic hypothesis for Alzheimer's disease pathophysiology
    J Nicholas Cochran
    Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, United States
    Brain Res Bull 103:18-28. 2014
    ..These dendritic mechanisms serve as a framework for therapeutic target identification and for efforts to develop disease-modifying therapeutics for Alzheimer's disease...
  15. pmc Dissociation of frontotemporal dementia-related deficits and neuroinflammation in progranulin haploinsufficient mice
    Anthony J Filiano
    Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    J Neurosci 33:5352-61. 2013
    ....
  16. doi request reprint Contemporary approaches to Alzheimer's disease and frontotemporal dementia
    Erik D Roberson
    Department of Neurology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL, USA
    Methods Mol Biol 670:1-9. 2011
    ..We then review molecules involved in their pathogenesis and protocols for working with these species and conclude with a discussion of experimental systems and outcome measures for studying these disorders...
  17. pmc Mouse models of Alzheimer's disease
    Alicia M Hall
    Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Brain Res Bull 88:3-12. 2012
    ..The discussion highlights key features and important differences between these mouse models. We conclude with a discussion about the role of AD mouse models in the translational pipeline...
  18. doi request reprint Step-by-step in situ hybridization method for localizing gene expression changes in the brain
    Jorge J Palop
    Department of Neurology, Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, CA, USA
    Methods Mol Biol 670:207-30. 2011
    ..With virtually all genomic coding sequences cloned or being cloned into cDNA plasmids, this technique has become highly accessible to explore gene expression profiles at the cellular and brain region level...