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Genomes and Genes | Edward B LeeSummaryAffiliation: University of Pennsylvania Country: USA Publications
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Publications
Alteration of hypothalamic cellular dynamics in obesityEdward B Lee
Department of Pathology and Laboratory Medicine, Perelman School of Medicine at University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
J Clin Invest 122:22-5. 2012..These findings support the notion that obesity is a disease that affects multiple organs, including the brain, and that disruption of normal brain function leads to abnormal regulation of peripheral metabolism...- Obesity, leptin, and Alzheimer's diseaseEdward B Lee
Translational Neuropathology Research Laboratory, Division of Neuropathology, Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
Ann N Y Acad Sci 1243:15-29. 2011..These studies will serve as a framework for understanding the role of adipokines in brain health... 
Thyroid transcription factor 1 expression in sellar tumors: a histogenetic marker?Edward B Lee
Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19106, USA
J Neuropathol Exp Neurol 68:482-8. 2009..Our observations may have implications for the classification of these rare sellar neoplasms, all the while acknowledging the morphological diversity of pituicyte-related neoplasms...- Cerebrovascular atherosclerosis correlates with Alzheimer pathology in neurodegenerative dementiasMark Yarchoan
3615 Chestnut Street, Philadelphia, PA 19104, USA
Brain 135:3749-56. 2012.... 
Targeting amyloid-beta peptide (Abeta) oligomers by passive immunization with a conformation-selective monoclonal antibody improves learning and memory in Abeta precursor protein (APP) transgenic miceEdward B Lee
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, 19104, USA
J Biol Chem 281:4292-9. 2006..These data implicated Abeta oligomers as a pathologic substrate for cognitive decline in Alzheimer disease...- Intraneuronal APP, not free Aβ peptides in 3xTg-AD mice: implications for tau versus Aβ-mediated Alzheimer neurodegenerationMatthew J Winton
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
J Neurosci 31:7691-9. 2011..Although we cannot corroborate the presence of intraneuronal Aβ peptide in 3xTg-AD mice, our findings warrant further study as to the role of aberrant APP accumulation in this unique model of AD... - α-Syn suppression reverses synaptic and memory defects in a mouse model of dementia with Lewy bodiesYoungshin Lim
Department of Pathology and Laboratory Medicine, Institute on Aging and Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
J Neurosci 31:10076-87. 2011..Furthermore, when α-syn expression was suppressed, we observed partial clearing of pre-existing α-syn pathology and reversal of structural synaptic defects, resulting in an improvement in memory function... - Phosphorylated tau/amyloid beta 1-42 ratio in ventricular cerebrospinal fluid reflects outcome in idiopathic normal pressure hydrocephalusSunil Patel
Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Fluids Barriers CNS 9:7. 2012..abstract:.. - Olfactory epithelium amyloid-beta and paired helical filament-tau pathology in Alzheimer diseaseSteven E Arnold
Alzheimer s Disease Core Center, University of Pennsylvania, Philadelphia, PA 19104, USA
Ann Neurol 67:462-9. 2010..However, their frequency, abundance, and disease specificity, and the relationships of OE pathology to brain pathology have not been established... - Lack of shunt response in suspected idiopathic normal pressure hydrocephalus with Alzheimer disease pathologyRoy Hamilton
Department of Neurology, University of Pennsylvania, Philadelphia, PA, USA
Ann Neurol 68:535-40. 2010.... - Meningoencephalitis associated with passive immunization of a transgenic murine model of Alzheimer's amyloidosisEdward B Lee
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, HUP, Philadelphia, 19104-4283, USA
FEBS Lett 579:2564-8. 2005..This report indicates that current passive immunization in humans should proceed with careful regard for autoimmune complications... - Photo essay. MRI and positron emission tomography findings in Heidenhain variant Creutzfeldt-Jakob diseaseSashank Prasad
Departments of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA
J Neuroophthalmol 30:260-2. 2010..Nuclear imaging provides a considerably more sensitive measure of neural dysfunction early in the course of this disease... - Hemangiomas of the brachial plexus: a case seriesNathan J Ranalli
Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
Neurosurgery 65:A181-8. 2009..We present 5 cases of extraneural hemangiomas causing brachial plexopathy, including pre-, intra-, and postoperative decision making, with an emphasis on diagnostic and management issues as well as outcomes... - Supranuclear vertical gaze abnormalities in sporadic Creutzfeldt-Jakob diseaseSashank Prasad
Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia 19104, United States
J Neurol Sci 253:69-72. 2007..Both patients were found to have sporadic CJD after genetic testing. Distinguishing familial from sporadic CJD in this setting has important genetic and epidemiological implications... - Pattern of ubiquilin pathology in ALS and FTLD indicates presence of C9ORF72 hexanucleotide expansionJohannes Brettschneider
Center for Neurodegenerative Disease Research CNDR, University of Pennsylvania School of Medicine, 3rd Floor Maloney Building, 3600 Spruce Street, Philadelphia, PA 19104, USA
Acta Neuropathol 123:825-39. 2012..Our study indicates that this pathology is associated with alterations in clinical phenotype, and suggests that the presence of C9ORF72 repeat expansions may indicate a worse prognosis in ALS... - Gains or losses: molecular mechanisms of TDP43-mediated neurodegenerationEdward B Lee
Translational Neuropathology Research Laboratory, Division of Neuropathology, Department of Pathology and Laboratory Medicine, University of Pennsylvania, 605B Stellar Chance Laboratories, 422 Curie Boulevard, Philadelphia, Pennsylvania 19104, USA
Nat Rev Neurosci 13:38-50. 2012..In addition, the distinct possibility of pleotropic or combined effects - in which gains of toxic properties and losses of normal TDP43 functions act together - needs to be considered... - Microtubule-binding drugs offset tau sequestration by stabilizing microtubules and reversing fast axonal transport deficits in a tauopathy modelBin Zhang
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 3600 Spruce Street, Philadelphia, PA 19104, USA
Proc Natl Acad Sci U S A 102:227-31. 2005..Thus, MT-stabilizing drugs could have therapeutic potential for treating neurodegenerative tauopathies by offsetting losses of tau function that result from the sequestration of this MT-stabilizing protein into filamentous inclusions... - Dysregulation of the ALS-associated gene TDP-43 leads to neuronal death and degeneration in miceLionel M Igaz
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, and Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
J Clin Invest 121:726-38. 2011..Our data suggest that perturbation of endogenous nuclear TDP-43 results in loss of normal TDP-43 function(s) and gene regulatory pathways, culminating in degeneration of selectively vulnerable affected neurons... - Metabolic dysfunction associated with adiponectin deficiency enhances kainic acid-induced seizure severityEdward B Lee
Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
J Neurosci 31:14361-6. 2011..These findings demonstrate that metabolic syndrome modulates the outcome of seizures and brain injury... - TDP-43 immunoreactivity in anoxic, ischemic and neoplastic lesions of the central nervous systemEdward B Lee
Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Acta Neuropathol 115:305-11. 2008..These findings expand our knowledge of the distribution and localization of TDP-43, and indicate that the TDP-43 inclusions seen in frontotemporal dementias and motor neuron diseases are specific to a neurodegenerative process... - Modulation of nuclear factor-kappa B activity by indomethacin influences A beta levels but not A beta precursor protein metabolism in a model of Alzheimer's diseaseSyaun Sung
Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104, USA
Am J Pathol 165:2197-206. 2004.... - Secretion and intracellular generation of truncated Abeta in beta-site amyloid-beta precursor protein-cleaving enzyme expressing human neuronsEdward B Lee
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
J Biol Chem 278:4458-66. 2003..Therefore, we conclude that Abeta11-40/42 is generated prior to deposition in senile plaques and that N-terminally truncated Abeta peptides may contribute to the downstream effects of amyloid accumulation in Alzheimer's disease...