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Genomes and Genes | Jorge J PalopSummaryAffiliation: University of California Country: USA Publications
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Publications
Epilepsy and cognitive impairments in Alzheimer diseaseJorge 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...
Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's diseaseJorge 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...- 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.... - Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networksJorge 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... - Amyloid-β/Fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of Alzheimer's diseaseErik 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... - Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse modelErik 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... - Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's diseaseWilliam 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... - Transsynaptic progression of amyloid-β-induced neuronal dysfunction within the entorhinal-hippocampal networkJulie 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... - Reelin depletion in the entorhinal cortex of human amyloid precursor protein transgenic mice and humans with Alzheimer's diseaseJeannie 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... - Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer modelLaure 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... - Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's diseaseJeannie 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... - Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's diseaseRene 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... - Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer's disease modelPascal 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... - Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse modelsIrene 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... - Fyn kinase modulates synaptotoxicity, but not aberrant sprouting, in human amyloid precursor protein transgenic miceJeannie 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... - Arc regulates spine morphology and maintains network stability in vivoCarol 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... - Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer's DiseaseBinggui 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... - Distinct roles of GABAergic interneurons in the regulation of striatal output pathwaysAryn 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... - Aggressive amyloidosis in mice expressing human amyloid peptides with the Arctic mutationIrene 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... - Vulnerability of dentate granule cells to disruption of arc expression in human amyloid precursor protein transgenic miceJorge 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... - Altered navigational strategy use and visuospatial deficits in hAPP transgenic miceAmy 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... - Cellular source of apolipoprotein E4 determines neuronal susceptibility to excitotoxic injury in transgenic miceManuel 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... 
Quantifying biomarkers of cognitive dysfunction and neuronal network hyperexcitability in mouse models of Alzheimer's disease: depletion of calcium-dependent proteins and inhibitory hippocampal remodelingJorge 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...- A network dysfunction perspective on neurodegenerative diseasesJorge 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... - Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficitsJorge 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.... - Step-by-step in situ hybridization method for localizing gene expression changes in the brainJorge 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...