Virginia M Y Lee

Summary

Affiliation: University of Pennsylvania
Country: USA

Publications

  1. pmc Degradative organelles containing mislocalized alpha-and beta-synuclein proliferate in presenilin-1 null neurons
    Christina A Wilson
    Center for Neurodegenerative Disease Research, University of Pennsylvania, Philadelphia, PA 19104, USA
    J Cell Biol 165:335-46. 2004
  2. pmc BACE overexpression alters the subcellular processing of APP and inhibits Abeta deposition in vivo
    Edward B Lee
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine
    J Cell Biol 168:291-302. 2005
  3. ncbi request reprint Amyloid binding ligands as Alzheimer's disease therapies
    Virginia M Y Lee
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, HUP, Maloney Bldg, 3rd Floor, University of Pennsylvania School of Medicine, 36th and Spruce Streets, Philadelphia 19104, USA
    Neurobiol Aging 23:1039-42. 2002
  4. ncbi request reprint Assessment of pathological tau proteins in frontotemporal dementias: qualitative and quantitative approaches
    Victoria Zhukareva
    Center for Neurodegenerative Disease Research, Department of Paathology and Laboratory Medicine, University of Pennsylvania School of Medicine, PA 19104 4283, USA
    Am J Geriatr Psychiatry 12:136-45. 2004
  5. ncbi request reprint More than just two peas in a pod: common amyloidogenic properties of tau and alpha-synuclein in neurodegenerative diseases
    Virginia M Y Lee
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, and Institute on Aging, The University of Pennsylvania, Philadelphia, PA 19104 4283, USA
    Trends Neurosci 27:129-34. 2004
  6. ncbi request reprint Research on the brain
    Virginia M Y Lee
    Center for Neurodegenerative Disease Research, Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Sci Aging Knowledge Environ 2003:pe29. 2003
  7. ncbi request reprint Neurodegenerative tauopathies: human disease and transgenic mouse models
    V M Lee
    Department of Pathology and Laboratory Medicine, The University of Pennsylvania School of Medicine, Philadelphia 19104, USA
    Neuron 24:507-10. 1999
  8. ncbi request reprint Mechanisms of Parkinson's disease linked to pathological alpha-synuclein: new targets for drug discovery
    Virginia M Y Lee
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Institute on Aging, Maloney Building, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    Neuron 52:33-8. 2006
  9. ncbi request reprint Progress from Alzheimer's tangles to pathological tau points towards more effective therapies now
    Virginia M Y Lee
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, and Institute on Aging, The University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    J Alzheimers Dis 9:257-62. 2006
  10. pmc Enrichment of C-terminal fragments in TAR DNA-binding protein-43 cytoplasmic inclusions in brain but not in spinal cord of frontotemporal lobar degeneration and amyotrophic lateral sclerosis
    Lionel M Igaz
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 3600 Spruce St, 3rd Floor, Maloney Bldg, Philadelphia, PA 19104, USA
    Am J Pathol 173:182-94. 2008

Research Grants

  1. TRAINING IN AGE-RELATED NEURODEGENERATIVE DISEASES
    Virginia Lee; Fiscal Year: 2007
  2. BIOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENTS
    Virginia Lee; Fiscal Year: 2001
  3. BIOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENTS
    Virginia Lee; Fiscal Year: 2000
  4. BIOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENTS
    Virginia Lee; Fiscal Year: 1999
  5. BIOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENTS
    Virginia Lee; Fiscal Year: 1993
  6. BIOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENTS
    Virginia Lee; Fiscal Year: 1992

Collaborators

Detail Information

Publications137 found, 100 shown here

  1. pmc Degradative organelles containing mislocalized alpha-and beta-synuclein proliferate in presenilin-1 null neurons
    Christina A Wilson
    Center for Neurodegenerative Disease Research, University of Pennsylvania, Philadelphia, PA 19104, USA
    J Cell Biol 165:335-46. 2004
    ....
  2. pmc BACE overexpression alters the subcellular processing of APP and inhibits Abeta deposition in vivo
    Edward B Lee
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine
    J Cell Biol 168:291-302. 2005
    ....
  3. ncbi request reprint Amyloid binding ligands as Alzheimer's disease therapies
    Virginia M Y Lee
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, HUP, Maloney Bldg, 3rd Floor, University of Pennsylvania School of Medicine, 36th and Spruce Streets, Philadelphia 19104, USA
    Neurobiol Aging 23:1039-42. 2002
    ..Significantly both IMSB and TDZM inhibit Abeta fibrillization in test tubes and in cultured cells. Thus, small amyloid binding molecules such as IMSB and TDZM which cross the BBB are potential therapeutic agents for the treatment of AD...
  4. ncbi request reprint Assessment of pathological tau proteins in frontotemporal dementias: qualitative and quantitative approaches
    Victoria Zhukareva
    Center for Neurodegenerative Disease Research, Department of Paathology and Laboratory Medicine, University of Pennsylvania School of Medicine, PA 19104 4283, USA
    Am J Geriatr Psychiatry 12:136-45. 2004
    ....
  5. ncbi request reprint More than just two peas in a pod: common amyloidogenic properties of tau and alpha-synuclein in neurodegenerative diseases
    Virginia M Y Lee
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, and Institute on Aging, The University of Pennsylvania, Philadelphia, PA 19104 4283, USA
    Trends Neurosci 27:129-34. 2004
    ..Thus, the ability of tau and alpha-synuclein to affect each other directly or indirectly might contribute to the overlap in the clinical and pathological features of tauopathies and synucleinopathies...
  6. ncbi request reprint Research on the brain
    Virginia M Y Lee
    Center for Neurodegenerative Disease Research, Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Sci Aging Knowledge Environ 2003:pe29. 2003
    ..This meeting report summarizes findings presented at this meeting. The presentations focused on clinicopathological correlations, therapy, genetics, and basic science research...
  7. ncbi request reprint Neurodegenerative tauopathies: human disease and transgenic mouse models
    V M Lee
    Department of Pathology and Laboratory Medicine, The University of Pennsylvania School of Medicine, Philadelphia 19104, USA
    Neuron 24:507-10. 1999
  8. ncbi request reprint Mechanisms of Parkinson's disease linked to pathological alpha-synuclein: new targets for drug discovery
    Virginia M Y Lee
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Institute on Aging, Maloney Building, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    Neuron 52:33-8. 2006
    ....
  9. ncbi request reprint Progress from Alzheimer's tangles to pathological tau points towards more effective therapies now
    Virginia M Y Lee
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, and Institute on Aging, The University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    J Alzheimers Dis 9:257-62. 2006
    ....
  10. pmc Enrichment of C-terminal fragments in TAR DNA-binding protein-43 cytoplasmic inclusions in brain but not in spinal cord of frontotemporal lobar degeneration and amyotrophic lateral sclerosis
    Lionel M Igaz
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 3600 Spruce St, 3rd Floor, Maloney Bldg, Philadelphia, PA 19104, USA
    Am J Pathol 173:182-94. 2008
    ..Therefore, regionally different pathogenic processes may underlie the development of abnormal TDP-43 proteinopathies...
  11. ncbi request reprint Neurodegenerative tauopathies
    V M Lee
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    Annu Rev Neurosci 24:1121-59. 2001
    ....
  12. ncbi request reprint Transgenic animal models of tauopathies
    Virginia M Y Lee
    University of Pennsylvania School of Medicine, Pathology, 3600 Spruce Street, HUP, 3rd Floor Maloney Building 1914104 4283, Philadelphia, PA, USA
    Biochim Biophys Acta 1739:251-9. 2005
    ..elegan to Drosophila melanogaster and mammalian transgenic mouse models of tauopathies have been generated and reported. This review summarizes the salient features of many of the known models of tauopathies...
  13. ncbi request reprint Retarded axonal transport of R406W mutant tau in transgenic mice with a neurodegenerative tauopathy
    Bin Zhang
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, and Institute on Aging, The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 4283, USA
    J Neurosci 24:4657-67. 2004
    ....
  14. ncbi request reprint Initiation and synergistic fibrillization of tau and alpha-synuclein
    Benoit I Giasson
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine
    Science 300:636-40. 2003
    ..This suggests that interactions between alpha-syn and tau can promote their fibrillization and drive the formation of pathological inclusions in human neurodegenerative diseases...
  15. ncbi request reprint Transgenic mouse model of tauopathies with glial pathology and nervous system degeneration
    Makoto Higuchi
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Neuron 35:433-46. 2002
    ..Thus, tau-positive glial lesions similar to human FTDs occur in these Tg mice, and these pathologies are linked to glial and axonal degeneration...
  16. ncbi request reprint Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury
    Valeria Conte
    Head Injury Center, University of Pennsylvania, Philadelphia, Pennsylvania, USA
    J Neurochem 90:758-64. 2004
    ..This study suggests that the exacerbation of brain oxidative stress following RCBI plays a mechanistic role in accelerating Alphabeta accumulation and behavioral impairments in the Tg2576 mice...
  17. ncbi request reprint Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein
    Benoit I Giasson
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, 3600 Spruce Street, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
    Neuron 34:521-33. 2002
    ..These mice demonstrate that A53T alpha-synuclein leads to the formation of toxic filamentous alpha-synuclein neuronal inclusions that cause neurodegeneration...
  18. ncbi request reprint Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis
    Manuela Neumann
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Science 314:130-3. 2006
    ..TDP-43 represents the common pathologic substrate linking these neurodegenerative disorders...
  19. ncbi request reprint Repetitive mild brain trauma accelerates Abeta deposition, lipid peroxidation, and cognitive impairment in a transgenic mouse model of Alzheimer amyloidosis
    Kunihiro Uryu
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 4283, USA
    J Neurosci 22:446-54. 2002
    ....
  20. pmc Neuropathologic substrates of Parkinson disease dementia
    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, Philadelphia, PA, USA
    Ann Neurol 72:587-98. 2012
    ..A study was undertaken to examine the neuropathological substrates of cognitive dysfunction and dementia in Parkinson disease (PD)...
  21. ncbi request reprint The transmembrane domain region of nicastrin mediates direct interactions with APH-1 and the gamma-secretase complex
    Vanessa A Morais
    Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Biol Chem 278:43284-91. 2003
    ....
  22. doi request reprint Evidence of multisystem disorder in whole-brain map of pathological TDP-43 in amyotrophic lateral sclerosis
    Felix Geser
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Alzheimer s Disease Core Center, Institute on Aging, Philadelphia, USA
    Arch Neurol 65:636-41. 2008
    ....
  23. ncbi request reprint Cerebrospinal fluid profile in frontotemporal dementia and Alzheimer's disease
    Murray Grossman
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    Ann Neurol 57:721-9. 2005
    ..We conclude that CSF tau levels are significantly reduced in many patients with FTD...
  24. 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...
  25. ncbi request reprint Impaired glutamate transport in a mouse model of tau pathology in astrocytes
    Deepa V Dabir
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Children s Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 26:644-54. 2006
    ..Thus, these Tg mice recapitulate features of astrocytic pathology observed in tauopathies and implicate a role for altered astrocyte function in the pathogenesis of these disorders...
  26. pmc Stages of pTDP-43 pathology in amyotrophic lateral sclerosis
    Johannes Brettschneider
    Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA Clinical Neuroanatomy Section, Department of Neurology, Center for Biomedical Research, University of Ulm, Ulm, Germany
    Ann Neurol 74:20-38. 2013
    ..To see whether the distribution patterns of phosphorylated 43kDa TAR DNA-binding protein (pTDP-43) intraneuronal inclusions in amyotrophic lateral sclerosis (ALS) permit recognition of neuropathological stages...
  27. pmc Frontotemporal dementia: clinicopathological correlations
    Mark S Forman
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    Ann Neurol 59:952-62. 2006
    ..This study assessed whether specific clinical features predict the underlying pathology...
  28. ncbi request reprint Amyotrophic lateral sclerosis/parkinsonism dementia complex: transgenic mice provide insights into mechanisms underlying a common tauopathy in an ethnic minority on Guam
    John Q Trojanowski
    The Center for Neurodegenerative Disease Research, The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    Exp Neurol 176:1-11. 2002
    ..Thus, tau Tg mice recapitulate key phenotypic features of ALS/PDC neuropathology in an ethnic minority on Guam, and these animal models provide new opportunities to discover novel therapies for this and related tauopathies...
  29. ncbi request reprint Detection of amyloid plaques by radioligands for Abeta40 and Abeta42: potential imaging agents in Alzheimer's patients
    Mei Ping Kung
    Department of Radiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    J Mol Neurosci 20:15-24. 2003
    ..Further structural modifications of TZDM to lower the background labeling will be needed to optimize the plaque-labeling property...
  30. ncbi request reprint Enhanced neurofibrillary tangle formation, cerebral atrophy, and cognitive deficits induced by repetitive mild brain injury in a transgenic tauopathy mouse model
    Yasumasa Yoshiyama
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    J Neurotrauma 22:1134-41. 2005
    ..The reasons for the augmentation of tau pathologies in only one T44 tau Tg mouse subjected to mrTBI remain to be elucidated...
  31. pmc Nitration of tau protein is linked to neurodegeneration in tauopathies
    Takashi Horiguchi
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    Am J Pathol 163:1021-31. 2003
    ..Taken together, these findings imply that nitrative injury is directly linked to the formation of filamentous tau inclusions...
  32. ncbi request reprint Transgenic mouse model of tau pathology in astrocytes leading to nervous system degeneration
    Mark S Forman
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 25:3539-50. 2005
    ..Thus, these Tg mice recapitulate key features of astrocytic pathology observed in human tauopathies and demonstrate functional consequences of this pathology including neuron degeneration in the absence of neuronal tau inclusions...
  33. pmc The microtubule-stabilizing agent, epothilone D, reduces axonal dysfunction, neurotoxicity, cognitive deficits, and Alzheimer-like pathology in an interventional study with aged tau transgenic mice
    Bin Zhang
    Center for Neurodegenerative Disease Research, Institute on Aging and Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 32:3601-11. 2012
    ..These data reveal that brain-penetrant MT-stabilizing drugs hold promise for the treatment of AD and related tauopathies, and that EpoD could be a candidate for clinical testing...
  34. pmc Therapeutic modulation of eIF2α phosphorylation rescues TDP-43 toxicity in amyotrophic lateral sclerosis disease models
    Hyung Jun Kim
    1 Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania, USA 2
    Nat Genet 46:152-60. 2014
    ..These findings indicate that the dysfunction induced by prolonged stress granule formation might contribute directly to ALS and that compounds that mitigate this process may represent a novel therapeutic approach. ..
  35. ncbi request reprint Early vitamin E supplementation in young but not aged mice reduces Abeta levels and amyloid deposition in a transgenic model of Alzheimer's disease
    Syuan Sung
    Center for Experimental Therapeutics, Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    FASEB J 18:323-5. 2004
    ..These results support the hypothesis that oxidative stress is an important early event in AD pathogenesis, and antioxidant therapy may be beneficial only if given at this stage of the disease process...
  36. ncbi request reprint Mouse model of multiple system atrophy alpha-synuclein expression in oligodendrocytes causes glial and neuronal degeneration
    Ikuru Yazawa
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    Neuron 45:847-59. 2005
    ....
  37. ncbi request reprint Axonal degeneration induced by targeted expression of mutant human tau in oligodendrocytes of transgenic mice that model glial tauopathies
    Makoto Higuchi
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania, Philadelphia, Pennsylvania 19104
    J Neurosci 25:9434-43. 2005
    ..We suggest that similar defects may also occur in sporadic and hereditary human tauopathies with OLG tau pathologies...
  38. pmc CSF biomarkers cutoffs: the importance of coincident neuropathological diseases
    Jon B Toledo
    Department of Pathology and Laboratory Medicine, Institute on Aging, 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 124:23-35. 2012
    ....
  39. pmc Acetylated tau, a novel pathological signature in Alzheimer's disease and other tauopathies
    David J Irwin
    Centre for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Alzheimer s Disease Core Centre, Institute on Ageing, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 6021, USA
    Brain 135:807-18. 2012
    ..Thus, inhibiting tau acetylation could be a disease-modifying target for drug discovery target in tauopathies...
  40. 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...
  41. pmc Update on the biomarker core of the Alzheimer's Disease Neuroimaging Initiative subjects
    John Q Trojanowski
    Department of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
    Alzheimers Dement 6:230-8. 2010
    ..Further studies in ADNI will refine this model and render the biomarkers studied in ADNI more applicable to routine diagnosis and to clinical trials of disease modifying therapies...
  42. pmc Brain progranulin expression in GRN-associated frontotemporal lobar degeneration
    Alice S Chen-Plotkin
    Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Acta Neuropathol 119:111-22. 2010
    ....
  43. ncbi request reprint Clinical, genetic, and pathologic characteristics of patients with frontotemporal dementia and progranulin mutations
    Vivianna M Van Deerlin
    Department of Pathology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    Arch Neurol 64:1148-53. 2007
    ..Patients with frontotemporal dementia due to mutation of progranulin may have a distinct phenotype...
  44. pmc Risk genotypes at TMEM106B are associated with cognitive impairment in amyotrophic lateral sclerosis
    Ryan Vass
    Department of Neurology, University of Pennsylvania School of Medicine, 3400 Spruce Street, Philadelphia, PA 19104, USA
    Acta Neuropathol 121:373-80. 2011
    ..These findings implicate the FTLD-TDP risk gene TMEM106B in the development of cognitive impairment in ALS...
  45. ncbi request reprint IMPY: an improved thioflavin-T derivative for in vivo labeling of beta-amyloid plaques
    Mei Ping Kung
    Department of Radiology, University of Pennsylvania, 3700 Market Street, Room 305, Philadelphia, PA 19104, USA
    Brain Res 956:202-10. 2002
    ....
  46. ncbi request reprint Membrane topology and nicastrin-enhanced endoproteolysis of APH-1, a component of the gamma-secretase complex
    Ryan R Fortna
    Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Biol Chem 279:3685-93. 2004
    ..Furthermore, we found that APH-1 can be processed by several endoproteolytic events. One of these cleavages is strongly up-regulated by co-expression of nicastrin and generates a stable C-terminal fragment that associates with nicastrin...
  47. ncbi request reprint Membrane topology of gamma-secretase component PEN-2
    Adam S Crystal
    Department of Microbiology, The Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia 19104, USA
    J Biol Chem 278:20117-23. 2003
    ..A protease protection assay also demonstrated that the loop domain of PEN-2 is cytosolic. Thus, PEN-2 spans the membrane twice, with the N and C termini facing the lumen of the endoplasmic reticulum...
  48. ncbi request reprint 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...
  49. ncbi request reprint Reduction of detyrosinated microtubules and Golgi fragmentation are linked to tau-induced degeneration in astrocytes
    Yasumasa Yoshiyama
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 23:10662-71. 2003
    ..These results suggest that reduced stable Glu-MTs is a primary consequence of tau accumulation that initiates mechanisms underlying astrocyte dysfunction and death in human neurodegenerative glial tauopathies...
  50. ncbi request reprint Presenilin modulates Pen-2 levels posttranslationally by protecting it from proteasomal degradation
    Adam S Crystal
    Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    Biochemistry 43:3555-63. 2004
    ....
  51. ncbi request reprint Distinct cleavage patterns of normal and pathologic forms of alpha-synuclein by calpain I in vitro
    Amanda J Mishizen-Eberz
    Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA
    J Neurochem 86:836-47. 2003
    ..Elucidating the role of calpain I in the proteolytic processing of alpha-syn in normal and diseased brains may clarify mechanisms of neurodegenerative alpha-synucleinopathies...
  52. pmc Pathological α-synuclein transmission initiates Parkinson-like neurodegeneration in nontransgenic mice
    Kelvin C Luk
    Department of Pathology and Laboratory Medicine, Institute on Aging and Center for Neurodegenerative Disease Research, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104 4283, USA
    Science 338:949-53. 2012
    ..This recapitulation of a neurodegenerative cascade thus establishes a mechanistic link between transmission of pathologic α-Syn and the cardinal features of Parkinson's disease...
  53. pmc TMEM106B, the risk gene for frontotemporal dementia, is regulated by the microRNA-132/212 cluster and affects progranulin pathways
    Alice S Chen-Plotkin
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 32:11213-27. 2012
    ..Evidence for this pathogenic cascade includes the striking convergence of two independent, genomic-scale screens on a microRNA:mRNA regulatory pair. Our findings open novel directions for elucidating miR-based therapies in FTLD-TDP...
  54. pmc Plasma multianalyte profiling in mild cognitive impairment and Alzheimer disease
    William T Hu
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
    Neurology 79:897-905. 2012
    ..Here we aim to determine plasma biomarkers associated with AD in 2 independent cohorts and validate the findings in the multicenter Alzheimer's Disease Neuroimaging Initiative (ADNI)...
  55. ncbi request reprint Characterization of tau pathologies in gray and white matter of Guam parkinsonism-dementia complex
    Matthew J Winton
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    Acta Neuropathol 111:401-12. 2006
    ....
  56. pmc Epothilone D improves microtubule density, axonal integrity, and cognition in a transgenic mouse model of tauopathy
    Kurt R Brunden
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 30:13861-6. 2010
    ..These results suggest that certain brain-penetrant MT-stabilizing agents might provide a viable therapeutic strategy for the treatment of AD and FTDs...
  57. pmc Ubiquitination of alpha-synuclein is not required for formation of pathological inclusions in alpha-synucleinopathies
    Deepak M Sampathu
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    Am J Pathol 163:91-100. 2003
    ..These results suggest that ubiquitination of alpha-synuclein is not required for inclusion formation and follows the fibrillization of alpha-synuclein...
  58. pmc alpha-internexin is present in the pathological inclusions of neuronal intermediate filament inclusion disease
    Nigel J Cairns
    Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 4283, USA
    Am J Pathol 164:2153-61. 2004
    ..The discovery of alpha-internexin in the cytoplasmic inclusions implicates novel mechanisms of pathogenesis in NIFID and other neurological diseases with pathological accumulations of IFs...
  59. pmc Novel CSF biomarkers for Alzheimer's disease and mild cognitive impairment
    William T Hu
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    Acta Neuropathol 119:669-78. 2010
    ..In summary, our targeted proteomic screen revealed novel CSF biomarkers that can improve the distinction between AD and non-AD cases by established biomarkers alone...
  60. pmc Pathological heterogeneity of frontotemporal lobar degeneration with ubiquitin-positive inclusions delineated by ubiquitin immunohistochemistry and novel monoclonal antibodies
    Deepak M Sampathu
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 3600 Spruce St, 3rd Floor Maloney Bldg, Philadelphia, PA 19104, USA
    Am J Pathol 169:1343-52. 2006
    ..Identification of the disease proteins recognized by these mAbs will further advance understanding of molecular substrates of FTLD-U neurodegenerative pathways...
  61. pmc PolyQ repeat expansions in ATXN2 associated with ALS are CAA interrupted repeats
    Zhenming Yu
    Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America
    PLoS ONE 6:e17951. 2011
    ....
  62. ncbi request reprint Cleavage of alpha-synuclein by calpain: potential role in degradation of fibrillized and nitrated species of alpha-synuclein
    Amanda J Mishizen-Eberz
    Department of Neurology, University of Pennsylvania and The Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA
    Biochemistry 44:7818-29. 2005
    ..These results provide insight into possible disease mechanisms underlying synucleinopathies since the formation of alpha-syn fibrils could be causally linked to the onset/progression of these disorders...
  63. ncbi request reprint Reversible inhibition of alpha-synuclein fibrillization by dopaminochrome-mediated conformational alterations
    Erin H Norris
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Biol Chem 280:21212-9. 2005
    ..Thus, decreased dopamine levels in substantia nigra neurons might promote alpha-syn aggregation in Parkinson's disease...
  64. 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
    ....
  65. ncbi request reprint Effects of oxidative and nitrative challenges on alpha-synuclein fibrillogenesis involve distinct mechanisms of protein modifications
    Erin H Norris
    Center for Neurodegenerative Disease Research and the Department of Pathology and Laboratory Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104, USA
    J Biol Chem 278:27230-40. 2003
    ..These findings demonstrate that nitrative and/or oxidative stress results in distinct mechanisms of alpha-synuclein protein modifications that can influence the formation of stable alpha-synuclein fibrils...
  66. ncbi request reprint Sporadic Pick's disease: a tauopathy characterized by a spectrum of pathological tau isoforms in gray and white matter
    Victoria Zhukareva
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania, 3600 Spruce Street, Philadelphia, PA 19104 4283, USA
    Ann Neurol 51:730-9. 2002
    ....
  67. pmc Cognitive decline and reduced survival in C9orf72 expansion frontotemporal degeneration and amyotrophic lateral sclerosis
    David J Irwin
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Alzheimer s Disease Core Center, Institute on Aging, Philadelphia, Pennsylvania, USA
    J Neurol Neurosurg Psychiatry 84:163-9. 2013
    ..To clarify this issue, we compared a large C9P cohort with carefully matched non-expansion (C9N) cases with a known or highly-suspected underlying TAR DNA-binding protein 43 (TDP-43) proteinopathy...
  68. pmc Cerebrovascular atherosclerosis correlates with Alzheimer pathology in neurodegenerative dementias
    Mark Yarchoan
    3615 Chestnut Street, Philadelphia, PA 19104, USA
    Brain 135:3749-56. 2012
    ....
  69. pmc Comparison of cerebrospinal fluid levels of tau and Aβ 1-42 in Alzheimer disease and frontotemporal degeneration using 2 analytical platforms
    David J Irwin
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Institute on Aging, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA
    Arch Neurol 69:1018-25. 2012
    ..To use values of cerebrospinal fluid tau and β-amyloid obtained from 2 different analytical immunoassays to differentiate Alzheimer disease (AD) from frontotemporal lobar degeneration (FTLD)...
  70. 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...
  71. pmc Clinical and pathological continuum of multisystem TDP-43 proteinopathies
    Felix Geser
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    Arch Neurol 66:180-9. 2009
    ....
  72. ncbi request reprint Aluminum modulates brain amyloidosis through oxidative stress in APP transgenic mice
    Domenico Pratico
    Center for Experimental Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    FASEB J 16:1138-40. 2002
    ..These results indicate that dietary Al can modulate in vivo AD-like amyloidosis in Tg2576 by increasing brain oxidative stress...
  73. pmc Plasma epidermal growth factor levels predict cognitive decline in Parkinson disease
    Alice S Chen-Plotkin
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
    Ann Neurol 69:655-63. 2011
    ..Most people with Parkinson disease (PD) eventually develop cognitive impairment (CI). However, neither the timing of onset nor the severity of cognitive symptoms can be accurately predicted. We sought plasma-based biomarkers for CI in PD...
  74. pmc The acetylation of tau inhibits its function and promotes pathological tau aggregation
    Todd J Cohen
    Department of Pathology and Laboratory Medicine, Institute on Aging, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    Nat Commun 2:252. 2011
    ..This study suggests that tau K280 acetylation is a potential target for drug discovery and biomarker development for AD and related tauopathies...
  75. pmc Microglial activation and TDP-43 pathology correlate with executive dysfunction in amyotrophic lateral sclerosis
    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 123:395-407. 2012
    ..In contrast, AD pathology in ALS is primarily related to increasing age and associated with a poorer performance on the MMSE...
  76. ncbi request reprint TDP-43 pathologic lesions and clinical phenotype in frontotemporal lobar degeneration with ubiquitin-positive inclusions
    Murray Grossman
    Department of Neurology, University of Pennsylvania School of Medicine, 2 Gibson, 3400 Spruce St, Philadelphia, PA 19104 4283, USA
    Arch Neurol 64:1449-54. 2007
    ..TDP-43 is a major ubiquitinated disease protein in the pathologic condition of frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U)...
  77. ncbi request reprint Pathological TDP-43 in parkinsonism-dementia complex and amyotrophic lateral sclerosis of Guam
    Felix Geser
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, Alzheimer s Disease Core Center, Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, PA, 19104 4283, USA
    Acta Neuropathol 115:133-45. 2008
    ..Finally, we conclude that the spectrum of TDP-43 proteinopathies should be expanded to include neurodegenerative cognitive and motor diseases, affecting the Chamorro population of Guam...
  78. ncbi request reprint Fibrillization of alpha-synuclein and tau in familial Parkinson's disease caused by the A53T alpha-synuclein mutation
    Paul T Kotzbauer
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Exp Neurol 187:279-88. 2004
    ..Our data implicate fibrillization of alpha-syn and tau in the pathogenesis of PD, and suggest that distinct amyloidogenic proteins may cross-seed each other in neurodegenerative diseases...
  79. pmc Concomitant TAR-DNA-binding protein 43 pathology is present in Alzheimer disease and corticobasal degeneration but not in other tauopathies
    Kunihiro Uryu
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
    J Neuropathol Exp Neurol 67:555-64. 2008
    ..These findings provide further insight into the burden and clinical significance of TDP-43 pathology in disorders other than FTLD-U and amyotrophic lateral sclerosis...
  80. pmc Expression of TDP-43 C-terminal Fragments in Vitro Recapitulates Pathological Features of TDP-43 Proteinopathies
    Lionel M Igaz
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, USA
    J Biol Chem 284:8516-24. 2009
    ..Thus, our results show that TDP-43 CTF expression recapitulates key biochemical features of pathological TDP-43 and support the hypothesis that the generation of TDP-43 CTFs is an important step in the pathogenesis of FTLD-U and ALS...
  81. pmc Biomarker discovery for Alzheimer's disease, frontotemporal lobar degeneration, and Parkinson's disease
    William T Hu
    Department of Neurology, University of Pennsylvania, Philadelphia, PA, USA
    Acta Neuropathol 120:385-99. 2010
    ....
  82. pmc TDP-43 mediates degeneration in a novel Drosophila model of disease caused by mutations in VCP/p97
    Gillian P Ritson
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 30:7729-39. 2010
    ..We suggest that these findings are likely relevant to the pathogenic mechanism of a broad array of TDP-43 proteinopathies, including frontotemporal lobar degeneration and amyotrophic lateral sclerosis...
  83. pmc Forebrain overexpression of alpha-synuclein leads to early postnatal hippocampal neuron loss and synaptic disruption
    Youngshin Lim
    Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Exp Neurol 221:86-97. 2010
    ..These data imply that developing neurons are more vulnerable to degenerate than mature neurons as a consequence of forebrain WT and mutant alpha-syn overexpression...
  84. ncbi request reprint TDP-43-positive white matter pathology in frontotemporal lobar degeneration with ubiquitin-positive inclusions
    Manuela Neumann
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
    J Neuropathol Exp Neurol 66:177-83. 2007
    ..Taken together, these results expand the spectrum of TDP-43 pathology in FTLD-U, suggesting that white matter pathology might contribute to the neurodegenerative process and clinical symptoms in FTLD-U...
  85. ncbi request reprint Novel monoclonal antibodies demonstrate biochemical variation of brain parkin with age
    Aaron C Pawlyk
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Biol Chem 278:48120-8. 2003
    ....
  86. ncbi request reprint Biochemical and pathological characterization of frontotemporal dementia due to a Leu266Val mutation in microtubule-associated protein tau in an African American individual
    Vivianna M Van Deerlin
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research and Institute on Aging, University of Pennsylvania, 3600 Spruce St, 3 Maloney Bldg, Philadelphia, PA, 19104, USA
    Acta Neuropathol 113:471-9. 2007
    ..This is also the first reported case of any MAPT mutation in an individual of African American ethnicity...
  87. pmc Paclitaxel C-10 carbamates: potential candidates for the treatment of neurodegenerative tauopathies
    Carlo Ballatore
    Department of Chemistry, University of Pennsylvania, 231 South 34th St, Philadelphia, PA 19104 6323, USA
    Bioorg Med Chem Lett 17:3642-6. 2007
    ....
  88. ncbi request reprint Chaperone suppression of alpha-synuclein toxicity in a Drosophila model for Parkinson's disease
    Pavan K Auluck
    Department of Neuroscience, University of Pennsylvania and University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Science 295:865-8. 2002
    ..Furthermore, Lewy bodies in human postmortem tissue immunostained for molecular chaperones, also suggesting that chaperones may play a role in Parkinson's disease progression...
  89. ncbi request reprint Synapse loss and microglial activation precede tangles in a P301S tauopathy mouse model
    Yasumasa Yoshiyama
    The Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Neuron 53:337-51. 2007
    ..Thus, hippocampal synaptic pathology and microgliosis may be the earliest manifestations of neurodegenerative tauopathies, and abrogation of tau-induced microglial activation could retard progression of these disorders...
  90. pmc Common variants at 7p21 are associated with frontotemporal lobar degeneration with TDP-43 inclusions
    Vivianna M Van Deerlin
    1 Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA 2 These authors contributed equally to this work
    Nat Genet 42:234-9. 2010
    ..TMEM106B variants also contribute to genetic risk for FTLD-TDP in individuals with mutations in GRN. Our data implicate variants in TMEM106B as a strong risk factor for FTLD-TDP, suggesting an underlying pathogenic mechanism...
  91. ncbi request reprint Thromboxane receptor activation mediates isoprostane-induced increases in amyloid pathology in Tg2576 mice
    Diana W Shineman
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 28:4785-94. 2008
    ..S18886 treatment reduced amyloid plaques, insoluble Abeta, and APP levels, thereby implicating TP receptor signaling as a novel target for AD therapy...
  92. pmc Exogenous alpha-synuclein fibrils seed the formation of Lewy body-like intracellular inclusions in cultured cells
    Kelvin C Luk
    Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Center for Neurodegenerative Disease Research, Institute on Aging, Philadelphia, PA 19104 4283, USA
    Proc Natl Acad Sci U S A 106:20051-6. 2009
    ....
  93. ncbi request reprint Lewy bodies in the amygdala: increase of alpha-synuclein aggregates in neurodegenerative diseases with tau-based inclusions
    Anca Popescu
    Department of Neurology, Drexel University College of Medicine, 3300 Henry Avenue, Philadelphia, PA 19129, USA
    Arch Neurol 61:1915-9. 2004
    ..However, the spectrum of disorders in which secondary inclusions are likely to occur has not been defined. Amygdala neurons commonly develop large numbers of secondary LBs, making it a practical region for studying this phenomenon...
  94. pmc Neuroinflammation and oxidation/nitration of alpha-synuclein linked to dopaminergic neurodegeneration
    Hui Ming Gao
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 28:7687-98. 2008
    ..This study advances understanding of the role of neuroinflammation and abnormal SYN in the pathogenesis of PD and opens new avenues for the discovery of more effective therapies for PD...
  95. pmc Convergence of heat shock protein 90 with ubiquitin in filamentous alpha-synuclein inclusions of alpha-synucleinopathies
    Kunihiro Uryu
    The Center for Neurodegenerative Disease Research, University of Pennsylvania, Philadelphia, Pennsylvania 19104 4283, USA
    Am J Pathol 168:947-61. 2006
    ..These data implicate predominantly Hsp90 in the formation of alpha-syn inclusions in PD and related alpha-synucleinopathies...
  96. pmc Burden of neurodegenerative diseases in a cohort of medical examiner subjects
    Kunihiro Uryu
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104 4283, USA
    J Forensic Sci 55:642-5. 2010
    ..Our study suggests that decedents >65 years of age in an ME practice are afflicted by common causes of dementia such as AD and FTLD which could contribute wholly or in part to their causes of death...
  97. pmc Effects of TNFalpha-converting enzyme inhibition on amyloid beta production and APP processing in vitro and in vivo
    Minkyu L Kim
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 28:12052-61. 2008
    ..Accordingly, it is possible that TACE inhibitors could reduce TNFalpha levels without increasing Abeta levels within the AD brain...
  98. ncbi request reprint Co-morbidity of TDP-43 proteinopathy in Lewy body related diseases
    Hanae Nakashima-Yasuda
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, HUP Maloney 3rd Floor, Philadelphia, PA 19104 4283, USA
    Acta Neuropathol 114:221-9. 2007
    ..This study expands the concept of TDP-43 proteinopathies by implicating TDP-43 lesions in mechanisms of neurodegeneration in LB disorders...
  99. pmc A90V TDP-43 variant results in the aberrant localization of TDP-43 in vitro
    Matthew J Winton
    Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    FEBS Lett 582:2252-6. 2008
    ..Thus, A90V may be a genetic risk factor for FTLD/ALS because it predisposes nuclear TDP-43 to redistribute to the cytoplasm and form pathological aggregates...
  100. pmc Inhibition of tau fibrillization by oleocanthal via reaction with the amino groups of tau
    Wenkai Li
    Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 94305, USA
    J Neurochem 110:1339-51. 2009
    ..These findings provide a potential scheme for the development of novel therapies for neurodegenerative tauopathies...
  101. ncbi request reprint GSK-3alpha regulates production of Alzheimer's disease amyloid-beta peptides
    Christopher J Phiel
    Department of Medicine, Division of Hematology Oncology and Howard Hughes Medical Institute, University of Pennsylvania School of Medicine, Philadelphia, Philadelphia 19104 6148, USA
    Nature 423:435-9. 2003
    ....

Research Grants14

  1. TRAINING IN AGE-RELATED NEURODEGENERATIVE DISEASES
    Virginia Lee; Fiscal Year: 2007
    ..Physician trainees also can acquire training in patient oriented research from trainers and consulting faculty with expertise in this increasing important facet of aging research. ..
  2. BIOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENTS
    Virginia Lee; Fiscal Year: 2001
    ..Successful completion of the proposed studies could lead to an understanding of the sequence of events that lead to the hyperphosphorylation of tau, the formation of PHFs and the destabilization of the neuronal cytoskeleton in AD. ..
  3. BIOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENTS
    Virginia Lee; Fiscal Year: 2000
    ..Successful completion of the proposed studies could lead to an understanding of the sequence of events that lead to the hyperphosphorylation of tau, the formation of PHFs and the destabilization of the neuronal cytoskeleton in AD. ..
  4. BIOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENTS
    Virginia Lee; Fiscal Year: 1999
    ..Successful completion of the proposed studies could lead to an understanding of the sequence of events that lead to the hyperphosphorylation of tau, the formation of PHFs and the destabilization of the neuronal cytoskeleton in AD. ..
  5. BIOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENTS
    Virginia Lee; Fiscal Year: 1993
    ....
  6. BIOLOGY OF ALZHEIMER PAIRED HELICAL FILAMENTS
    Virginia Lee; Fiscal Year: 1992
    ....