Edward B Lee

Summary

Affiliation: University of Pennsylvania
Country: USA

Publications

  1. doi Expansion of the classification of FTLD-TDP: distinct pathology associated with rapidly progressive frontotemporal degeneration
    Edward B Lee
    Translational Neuropathology Research Laboratory, Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, 613A Stellar Chance Laboratories, 422 Curie Blvd, Philadelphia, PA, 19104, USA
    Acta Neuropathol . 2017
  2. pmc Topography of FUS pathology distinguishes late-onset BIBD from aFTLD-U
    Edward B Lee
    Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA Translational Neuropathology Research Laboratory, 605B Stellar Chance Laboratories, 422 Curie Blvd, Philadelphia, PA 19104, USA Department of Pathology and Laboratory Medicine, Philadelphia, PA, USA
    Acta Neuropathol Commun 1:1-11. 2013
  3. pmc The neuropathology of obesity: insights from human disease
    Edward B Lee
    Translational Neuropathology Research Laboratory, Division of Neuropathology, Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, 605B Stellar Chance Laboratories, 422 Curie Blvd, Philadelphia, PA, 19104, USA
    Acta Neuropathol 127:3-28. 2014
  4. pmc Alteration of hypothalamic cellular dynamics in obesity
    Edward 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
  5. pmc Obesity, leptin, and Alzheimer's disease
    Edward 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
  6. doi 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
  7. pmc Development and validation of pedigree classification criteria for frontotemporal lobar degeneration
    Elisabeth M Wood
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Perelman School of Medicine at the University of Pennsylvania, Philadelphia
    JAMA Neurol 70:1411-7. 2013
  8. pmc Cerebrovascular atherosclerosis correlates with Alzheimer pathology in neurodegenerative dementias
    Mark Yarchoan
    3615 Chestnut Street, Philadelphia, PA 19104, USA
    Brain 135:3749-56. 2012
  9. pmc Deep clinical and neuropathological phenotyping of Pick disease
    David J Irwin
    University of Pennsylvania Frontotemporal Degeneration Center, Department of Neurology, University of Pennsylvania, Philadelphia, PA
    Ann Neurol 79:272-87. 2016
  10. pmc Pathological α-synuclein distribution in subjects with coincident Alzheimer's and Lewy body pathology
    Jon B Toledo
    Department of Pathology and Laboratory Medicine, University of Pennsylvania Medical Center, Philadelphia, PA, USA
    Acta Neuropathol 131:393-409. 2016

Collaborators

Detail Information

Publications47

  1. doi Expansion of the classification of FTLD-TDP: distinct pathology associated with rapidly progressive frontotemporal degeneration
    Edward B Lee
    Translational Neuropathology Research Laboratory, Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, 613A Stellar Chance Laboratories, 422 Curie Blvd, Philadelphia, PA, 19104, USA
    Acta Neuropathol . 2017
    ....
  2. pmc Topography of FUS pathology distinguishes late-onset BIBD from aFTLD-U
    Edward B Lee
    Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA Translational Neuropathology Research Laboratory, 605B Stellar Chance Laboratories, 422 Curie Blvd, Philadelphia, PA 19104, USA Department of Pathology and Laboratory Medicine, Philadelphia, PA, USA
    Acta Neuropathol Commun 1:1-11. 2013
    ..In this study, we report the clinical and pathologic features of three cases of aFTLD-U and two cases of late-onset BIBD with an emphasis on the anatomic distribution of FUS inclusions...
  3. pmc The neuropathology of obesity: insights from human disease
    Edward B Lee
    Translational Neuropathology Research Laboratory, Division of Neuropathology, Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, 605B Stellar Chance Laboratories, 422 Curie Blvd, Philadelphia, PA, 19104, USA
    Acta Neuropathol 127:3-28. 2014
    ....
  4. pmc Alteration of hypothalamic cellular dynamics in obesity
    Edward 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...
  5. pmc Obesity, leptin, and Alzheimer's disease
    Edward 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...
  6. doi 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...
  7. pmc Development and validation of pedigree classification criteria for frontotemporal lobar degeneration
    Elisabeth M Wood
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Perelman School of Medicine at the University of Pennsylvania, Philadelphia
    JAMA Neurol 70:1411-7. 2013
    ..There is also great need to develop clinical tools and approaches that will assist clinicians in the identification and counseling of patients with FTLD and their families regarding the likelihood of an identifiable genetic cause...
  8. pmc Cerebrovascular atherosclerosis correlates with Alzheimer pathology in neurodegenerative dementias
    Mark Yarchoan
    3615 Chestnut Street, Philadelphia, PA 19104, USA
    Brain 135:3749-56. 2012
    ....
  9. pmc Deep clinical and neuropathological phenotyping of Pick disease
    David J Irwin
    University of Pennsylvania Frontotemporal Degeneration Center, Department of Neurology, University of Pennsylvania, Philadelphia, PA
    Ann Neurol 79:272-87. 2016
    ..To characterize sequential patterns of regional neuropathology and clinical symptoms in a well-characterized cohort of 21 patients with autopsy-confirmed Pick disease...
  10. pmc Pathological α-synuclein distribution in subjects with coincident Alzheimer's and Lewy body pathology
    Jon B Toledo
    Department of Pathology and Laboratory Medicine, University of Pennsylvania Medical Center, Philadelphia, PA, USA
    Acta Neuropathol 131:393-409. 2016
    ....
  11. ncbi 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 mice
    Edward 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...
  12. pmc Semi-automated quantification of C9orf72 expansion size reveals inverse correlation between hexanucleotide repeat number and disease duration in frontotemporal degeneration
    Eunran Suh
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Perelman School of Medicine at the University of Pennsylvania, 3600 Spruce Street, Philadelphia, PA, 19104 4283, USA
    Acta Neuropathol 130:363-72. 2015
    ..Our finding suggests that C9orf72 repeat size may be a molecular disease modifier in FTD linked to hexanucleotide repeat expansion...
  13. pmc Intraneuronal APP, not free Aβ peptides in 3xTg-AD mice: implications for tau versus Aβ-mediated Alzheimer neurodegeneration
    Matthew 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...
  14. pmc α-Syn suppression reverses synaptic and memory defects in a mouse model of dementia with Lewy bodies
    Youngshin 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...
  15. pmc Dysregulation of the ALS-associated gene TDP-43 leads to neuronal death and degeneration in mice
    Lionel 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...
  16. doi Tauopathy with hippocampal 4-repeat tau immunoreactive spherical inclusions: a report of three cases
    Gabor G Kovacs
    Center for Neurodegenerative Disease Research, Institute on Aging and Department of Pathology and Laboratory Medicine, USA
    Brain Pathol . 2016
    ..The precise definition of the clinicopathological relevance of these unusual tau pathologies merits further study. This article is protected by copyright. All rights reserved...
  17. pmc 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 disease
    Syaun Sung
    Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104, USA
    Am J Pathol 165:2197-206. 2004
    ....
  18. pmc Semi-Automated Digital Image Analysis of Pick's Disease and TDP-43 Proteinopathy
    David J Irwin
    Penn Frontotemporal Degeneration Center, Department of Neurology DJI, MDB, CTM, FC, MG, University of Pennsylvania Perelman School of Medicine, University of Pennsylvania, Philadelphia, PennsylvaniaCenter for Neurodegenerative Disease Research, DJI, MDB, FC, SEA, EBL, VMVD, VML, JQT, Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, University of Pennsylvania, Philadelphia, PennsylvaniaTranslational Neuropathology Research Lab EBL, Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, University of Pennsylvania, Philadelphia, PennsylvaniaUniversity of Pennsylvania Memory Center, Department of Psychiatry SEA, University of Pennsylvania Perelman School of Medicine, University of Pennsylvania, Philadelphia, PennsylvaniaDepartment of Biostatistics and Epidemiology SXX, University of Pennsylvania Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
    J Histochem Cytochem 64:54-66. 2016
    ....
  19. pmc Common neuropathological features underlie distinct clinical presentations in three siblings with hereditary diffuse leukoencephalopathy with spheroids caused by CSF1R p.Arg782His
    John L Robinson
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Perelman School of Medicine at the University of Pennsylvania, 3600 Spruce Street, 19104, Philadelphia, PA, USA
    Acta Neuropathol Commun 3:42. 2015
    ..Our findings underscore the critical importance of genetic testing for establishing a clinical and pathological diagnosis of HDLS. ..
  20. pmc Hypermethylation of repeat expanded C9orf72 is a clinical and molecular disease modifier
    Jenny Russ
    Translational Neuropathology Research Laboratory, Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, 605B Stellar Chance Laboratories, 422 Curie Blvd, Philadelphia, PA, 19104, USA
    Acta Neuropathol 129:39-52. 2015
    ..These results support the hypothesis that expression of the hexanucleotide repeat expansion is associated with a toxic gain of function...
  21. pmc Sequential distribution of pTDP-43 pathology in behavioral variant frontotemporal dementia (bvFTD)
    Johannes Brettschneider
    Center for Neurodegenerative Disease Research CNDR, Perelman School of Medicine at the University of Pennsylvania, 3rd Floor Maloney Building, 3600 Spruce Street, Philadelphia, PA, 19104, USA
    Acta Neuropathol 127:423-39. 2014
    ..We interpret the four neuropathological patterns in bvFTD to be consistent with the hypothesis that pTDP-43 pathology can spread sequentially and may propagate along axonal pathways...
  22. pmc Frontotemporal lobar degeneration: defining phenotypic diversity through personalized medicine
    David J Irwin
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Institute on Ageing, University of Pennsylvania School of Medicine, HUP Maloney 3rd Floor, 36th and Spruce Streets, Philadelphia, PA, 19104 4283, USA
    Acta Neuropathol 129:469-91. 2015
    ....
  23. pmc Comparative survey of the topographical distribution of signature molecular lesions in major neurodegenerative diseases
    Steven E Arnold
    Penn Memory Center, Departments of Psychiatry and Neurology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, 19104
    J Comp Neurol 521:4339-55. 2013
    ....
  24. pmc A platform for discovery: The University of Pennsylvania Integrated Neurodegenerative Disease Biobank
    Jon B Toledo
    Department of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, Philadelphia, Pennsylvania, USA
    Alzheimers Dement 10:477-84.e1. 2014
    ..We describe a biobanking system that is a platform for discovery research at the Center for Neurodegenerative Disease Research at the University of Pennsylvania...
  25. pmc Phosphorylated tau/amyloid beta 1-42 ratio in ventricular cerebrospinal fluid reflects outcome in idiopathic normal pressure hydrocephalus
    Sunil Patel
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Fluids Barriers CNS 9:7. 2012
    ..The aim of this study was to investigate the relationship between the phosphorylated tau/amyloid beta 1-42 (ptau/Aβ1-42) ratio in ventricular CSF and shunt outcome in patients with iNPH...
  26. pmc TDP-43 pathology and neuronal loss in amyotrophic lateral sclerosis spinal cord
    Johannes 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 128:423-37. 2014
    ....
  27. pmc Abnormal serine phosphorylation of insulin receptor substrate 1 is associated with tau pathology in Alzheimer's disease and tauopathies
    Mark Yarchoan
    Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA
    Acta Neuropathol 128:679-89. 2014
    ....
  28. pmc Olfactory epithelium amyloid-beta and paired helical filament-tau pathology in Alzheimer disease
    Steven 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...
  29. pmc Pattern of ubiquilin pathology in ALS and FTLD indicates presence of C9ORF72 hexanucleotide expansion
    Johannes 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...
  30. pmc Cognitive reserve in frontotemporal degeneration: Neuroanatomic and neuropsychological evidence
    Katerina Placek
    From the Department of Neurology, Penn Frontotemporal Degeneration Center K P, L M, C O, K T, K F, D I, M G, C T M, and Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research V V D, E B L, J Q T, V M Y L, D I, University of Pennsylvania, Philadelphia
    Neurology 87:1813-1819. 2016
    ....
  31. pmc C9orf72 hypermethylation protects against repeat expansion-associated pathology in ALS/FTD
    Elaine Y Liu
    Translational Neuropathology Research Laboratory, Perelman School of Medicine at the University of Pennsylvania, 605B Stellar Chance Laboratories, 422 Curie Blvd, Philadelphia, PA, 19104, USA
    Acta Neuropathol 128:525-41. 2014
    ....
  32. ncbi Meningoencephalitis associated with passive immunization of a transgenic murine model of Alzheimer's amyloidosis
    Edward 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...
  33. pmc Lack of shunt response in suspected idiopathic normal pressure hydrocephalus with Alzheimer disease pathology
    Roy Hamilton
    Department of Neurology, University of Pennsylvania, Philadelphia, PA, USA
    Ann Neurol 68:535-40. 2010
    ....
  34. pmc Neuropathological and genetic correlates of survival and dementia onset in synucleinopathies: a retrospective analysis
    David J Irwin
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Morris K Udall Parkinson s Disease Center of Excellence, Institute on Aging, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA Department of Neurology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA Electronic address
    Lancet Neurol 16:55-65. 2017
    ..We aimed to identify genetic and pathological markers that have the strongest association with these features of clinical heterogeneity in synucleinopathies...
  35. pmc Transcriptomic Changes Due to Cytoplasmic TDP-43 Expression Reveal Dysregulation of Histone Transcripts and Nuclear Chromatin
    Alexandre Amlie-Wolf
    Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States of America
    PLoS ONE 10:e0141836. 2015
    ..These transcriptomic alterations correlate with observed histologic abnormalities in heterochromatin structure and nuclear size in transgenic mouse and human brains. ..
  36. pmc A comparison of Aβ amyloid pathology staging systems and correlation with clinical diagnosis
    Susana Boluda
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, PA, 19104, USA
    Acta Neuropathol 128:543-50. 2014
    ..Yet, further research is needed to define strategies to relate CERAD and TAP Aβ plaque scores to compare their utility and for determining the clinical associations of these different amyloid staging systems with aging and AD. ..
  37. doi Photo essay. MRI and positron emission tomography findings in Heidenhain variant Creutzfeldt-Jakob disease
    Sashank 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...
  38. ncbi Supranuclear vertical gaze abnormalities in sporadic Creutzfeldt-Jakob disease
    Sashank 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...
  39. doi Hemangiomas of the brachial plexus: a case series
    Nathan 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...
  40. pmc Multimodal imaging evidence of pathology-mediated disease distribution in corticobasal syndrome
    Corey T McMillan
    From the Department of Neurology C T M, C B, R G G, J W, K F, K R, D A W, D J I, M G and Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine J B T, L S, D J I, E B L, J Q T, Perelman School of Medicine, University of Pennsylvania, Philadelphia
    Neurology 87:1227-34. 2016
    ..To use multimodal neuroimaging to evaluate the influence of heterogeneous underlying pathology in corticobasal syndrome (CBS) on the neuroanatomical distribution of disease...
  41. ncbi Genetically modified NT2N human neuronal cells mediate long-term gene expression as CNS grafts in vivo and improve functional cognitive outcome following experimental traumatic brain injury
    Deborah J Watson
    Department of Pathobiology, Center for Comparative Medical Genetics, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, USA
    J Neuropathol Exp Neurol 62:368-80. 2003
    ..These results demonstrate that defined populations of genetically modified human NT2N neurons are a practical and effective platform for stable ex vivo gene delivery into the CNS...
  42. pmc Perforant path synaptic loss correlates with cognitive impairment and Alzheimer's disease in the oldest-old
    John L Robinson
    1 Centre for Neurodegenerative Disease Research, Institute on Aging and Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, USA
    Brain 137:2578-87. 2014
    ....
  43. pmc Gains or losses: molecular mechanisms of TDP43-mediated neurodegeneration
    Edward 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. 2011
    ..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...
  44. ncbi TDP-43 immunoreactivity in anoxic, ischemic and neoplastic lesions of the central nervous system
    Edward 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...
  45. pmc Metabolic dysfunction associated with adiponectin deficiency enhances kainic acid-induced seizure severity
    Edward 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...
  46. pmc Microtubule-binding drugs offset tau sequestration by stabilizing microtubules and reversing fast axonal transport deficits in a tauopathy model
    Bin 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...
  47. ncbi Secretion and intracellular generation of truncated Abeta in beta-site amyloid-beta precursor protein-cleaving enzyme expressing human neurons
    Edward 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...