Jorge J Palop

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Epilepsy and cognitive impairments in Alzheimer disease
    Jorge J Palop
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, CA 94158, USA
    Arch Neurol 66:435-40. 2009
  2. pmc Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks
    Jorge J Palop
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, California, USA
    Nat Neurosci 13:812-8. 2010
  3. pmc Synaptic depression and aberrant excitatory network activity in Alzheimer's disease: two faces of the same coin?
    Jorge J Palop
    Gladstone Institute of Neurological Disease and University of California, San Francisco, California, USA
    Neuromolecular Med 12:48-55. 2010
  4. 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
  5. 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
  6. 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
  7. 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
  8. pmc Transsynaptic progression of amyloid-β-induced neuronal dysfunction within the entorhinal-hippocampal network
    Julie A Harris
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Neuron 68:428-41. 2010
  9. ncbi request reprint Reelin depletion in the entorhinal cortex of human amyloid precursor protein transgenic mice and humans with Alzheimer's disease
    Jeannie Chin
    Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, California 94158, USA
    J Neurosci 27:2727-33. 2007
  10. pmc Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model
    Laure Verret
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Cell 149:708-21. 2012

Collaborators

Detail Information

Publications27

  1. pmc Epilepsy and cognitive impairments in Alzheimer disease
    Jorge J Palop
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, CA 94158, USA
    Arch Neurol 66:435-40. 2009
    ..We conclude that beta-amyloid peptides may contribute to cognitive decline in AD by eliciting similar aberrant neuronal activity in humans and discuss potential clinical and therapeutic implications of this hypothesis...
  2. pmc Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks
    Jorge J Palop
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, California, USA
    Nat Neurosci 13:812-8. 2010
    ..Strategies that block these Abeta effects may prevent cognitive decline in Alzheimer's disease. Potential obstacles and next steps toward this goal are discussed...
  3. pmc Synaptic depression and aberrant excitatory network activity in Alzheimer's disease: two faces of the same coin?
    Jorge J Palop
    Gladstone Institute of Neurological Disease and University of California, San Francisco, California, USA
    Neuromolecular Med 12:48-55. 2010
    ....
  4. 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...
  5. 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...
  6. 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...
  7. 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...
  8. pmc Transsynaptic progression of amyloid-β-induced neuronal dysfunction within the entorhinal-hippocampal network
    Julie A Harris
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Neuron 68:428-41. 2010
    ..Thus, APP/Aβ expression in EC neurons causes transsynaptic deficits that could initiate the cortical-hippocampal network dysfunction in mouse models and human patients with AD...
  9. ncbi request reprint Reelin depletion in the entorhinal cortex of human amyloid precursor protein transgenic mice and humans with Alzheimer's disease
    Jeannie Chin
    Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, California 94158, USA
    J Neurosci 27:2727-33. 2007
    ..We conclude that alterations in Reelin processing or signaling may be involved in AD-related neuronal dysfunction...
  10. pmc Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model
    Laure Verret
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Cell 149:708-21. 2012
    ..We conclude that reduced Nav1.1 levels and PV cell dysfunction critically contribute to abnormalities in oscillatory rhythms, network synchrony, and memory in hAPP mice and possibly in AD...
  11. ncbi request reprint Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease
    Jeannie Chin
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    J Neurosci 25:9694-703. 2005
    ..Thus, increased Fyn expression is sufficient to trigger prominent neuronal deficits in the context of even relatively moderate Abeta levels, and inhibition of Fyn activity may help counteract Abeta-induced impairments...
  12. pmc Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's disease
    Rene O Sanchez-Mejia
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    Nat Neurosci 11:1311-8. 2008
    ..Inhibition of GIVA-PLA(2) may be beneficial in the treatment and prevention of Alzheimer's disease...
  13. pmc Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer's disease model
    Pascal E Sanchez
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA
    Proc Natl Acad Sci U S A 109:E2895-903. 2012
    ..Our findings support the hypothesis that aberrant network activity contributes causally to synaptic and cognitive deficits in hAPP mice. LEV might also help ameliorate related abnormalities in people who have or are at risk for AD...
  14. ncbi request reprint Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models
    Irene H Cheng
    Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA
    J Biol Chem 282:23818-28. 2007
    ..Thus, Abeta*56 is a likelier determinant of functional deficits in hAPP mice than fibrillar Abeta deposits. Therapeutic interventions that reduce Abeta fibrils at the cost of augmenting nonfibrillar Abeta assemblies could be harmful...
  15. ncbi request reprint Fyn kinase modulates synaptotoxicity, but not aberrant sprouting, in human amyloid precursor protein transgenic mice
    Jeannie Chin
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, California 94141 9100, USA
    J Neurosci 24:4692-7. 2004
    ..We conclude that Fyn-dependent pathways are critical in AD-related synaptotoxicity and that the pathogenesis of hAPP/Abeta-induced neuronal alterations may be mechanistically heterogenous...
  16. 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...
  17. pmc Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer's Disease
    Binggui Sun
    Gladstone Institute of Neurological Disease, University of California, San Francisco, 94158, USA
    Cell Stem Cell 5:624-33. 2009
    ..Abeta-induced increases in GABAergic neurotransmission or an imbalance between GABAergic and glutamatergic neurotransmission may contribute to impaired neurogenesis in AD...
  18. pmc Distinct roles of GABAergic interneurons in the regulation of striatal output pathways
    Aryn H Gittis
    Gladstone Institute of Neurological Disease, Department of Physiology, and Department of Neurology, University of California, San Francisco, San Francisco, California 94158, USA
    J Neurosci 30:2223-34. 2010
    ..Surprisingly, we find that FS interneurons preferentially target direct-pathway MSNs over indirect-pathway MSNs, suggesting a potential mechanism for rapid pathway-specific regulation of striatal output pathways...
  19. ncbi request reprint Aggressive amyloidosis in mice expressing human amyloid peptides with the Arctic mutation
    Irene H Cheng
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    Nat Med 10:1190-2. 2004
    ..Amyloid plaques formed faster and were more extensive in Arctic mice than in hAPP mice expressing wild-type Abeta, even though Arctic mice had lower Abeta(1-42/1-40) ratios. Thus, the Arctic mutation is highly amyloidogenic in vivo...
  20. ncbi request reprint Vulnerability of dentate granule cells to disruption of arc expression in human amyloid precursor protein transgenic mice
    Jorge J Palop
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94158, USA
    J Neurosci 25:9686-93. 2005
    ..The brain region-specific depletion of factors that participate in activity-dependent modification of synapses may critically contribute to cognitive deficits in hAPP mice and possibly in humans with Alzheimer's disease...
  21. ncbi request reprint Altered navigational strategy use and visuospatial deficits in hAPP transgenic mice
    Amy R Deipolyi
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158, USA
    Neurobiol Aging 29:253-66. 2008
    ..Interventions promoting flexibility in selecting learning strategies might help circumvent otherwise debilitating navigational deficits caused by AD-related hippocampal dysfunction...
  22. pmc Cellular source of apolipoprotein E4 determines neuronal susceptibility to excitotoxic injury in transgenic mice
    Manuel Buttini
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158 2261, USA
    Am J Pathol 177:563-9. 2010
    ..Thus, an imbalance between astrocytic (excitoprotective) and neuronal (neurotoxic) apoE4 expression may increase susceptibility to diverse neurological diseases involving excitotoxic mechanisms...
  23. 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...
  24. pmc Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficits
    Jorge J Palop
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, CA 94141, USA
    Proc Natl Acad Sci U S A 100:9572-7. 2003
    ....
  25. ncbi request reprint A network dysfunction perspective on neurodegenerative diseases
    Jorge J Palop
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, California 94158, USA
    Nature 443:768-73. 2006
    ..These ideas have far-reaching therapeutic implications...
  26. pmc Lamin B1 mediates cell-autonomous neuropathology in a leukodystrophy mouse model
    Mary Y Heng
    Department of Neurology, UCSF, San Francisco, California 94158, USA
    J Clin Invest 123:2719-29. 2013
    ..These studies identify a mechanism by which lamin B1 overexpression mediates oligodendrocyte cell-autonomous neuropathology in ADLD and implicate lamin B1 as an important regulator of myelin formation and maintenance during aging...
  27. 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...