G William Rebeck

Summary

Affiliation: Georgetown University
Country: USA

Publications

  1. ncbi request reprint Cholesterol efflux as a critical component of Alzheimer's disease pathogenesis
    G William Rebeck
    Georgetown University School of Medicine, Washington, DC 20007, USA
    J Mol Neurosci 23:219-24. 2004
  2. ncbi request reprint Human APOE4 increases microglia reactivity at Aβ plaques in a mouse model of Aβ deposition
    Gustavo A Rodriguez
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road, NW Washington, DC 20057, USA
    J Neuroinflammation 11:111. 2014
  3. ncbi request reprint Extracellular proteolysis of apolipoprotein E (apoE) by secreted serine neuronal protease
    Irfan Y Tamboli
    Department of Neuroscience, Georgetown University, Washington DC, United States of America
    PLoS ONE 9:e93120. 2014
  4. pmc Parkinson-related parkin reduces α-Synuclein phosphorylation in a gene transfer model
    Preeti J Khandelwal
    Department of Neuroscience, Georgetown University Medical Center, Washington D, C, U, S, A, 20007
    Mol Neurodegener 5:47. 2010
  5. doi request reprint Nontraditional signaling mechanisms of lipoprotein receptors
    G William Rebeck
    Department of Neuroscience, Georgetown University, Washington, DC 20007, USA
    Sci Signal 2:pe28. 2009
  6. pmc Similarities and differences in structure, expression, and functions of VLDLR and ApoER2
    Sunil S Reddy
    Department of Neuroscience Georgetown University Medical Center, 3970 Reservoir Rd, NW, Washington, DC, 20007, USA
    Mol Neurodegener 6:30. 2011
  7. pmc The cytoplasmic adaptor protein X11alpha and extracellular matrix protein Reelin regulate ApoE receptor 2 trafficking and cell movement
    S Sakura Minami
    Department of Neurology, Georgetown University, 4000 Reservoir Road NW, Washington, DC 20057, USA
    FASEB J 24:58-69. 2010
  8. pmc ApoE receptor 2 regulates synapse and dendritic spine formation
    Sonya B Dumanis
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC, United States of America
    PLoS ONE 6:e17203. 2011
  9. pmc Interaction of reelin with amyloid precursor protein promotes neurite outgrowth
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057 1464, USA
    J Neurosci 29:7459-73. 2009
  10. pmc The effects of amyloid precursor protein on postsynaptic composition and activity
    HYANG SOOK HOE
    Departments of Neuroscience, Physiology and Biophysics, Pharmacology, and Neurology, Georgetown University Medical Center, Washington, D C 20057 1464, USA
    J Biol Chem 284:8495-506. 2009

Collaborators

Detail Information

Publications60

  1. ncbi request reprint Cholesterol efflux as a critical component of Alzheimer's disease pathogenesis
    G William Rebeck
    Georgetown University School of Medicine, Washington, DC 20007, USA
    J Mol Neurosci 23:219-24. 2004
    ..We suggest that the risk of amyloid deposition associated with high cholesterol may be through induction of the LXR system...
  2. ncbi request reprint Human APOE4 increases microglia reactivity at Aβ plaques in a mouse model of Aβ deposition
    Gustavo A Rodriguez
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road, NW Washington, DC 20057, USA
    J Neuroinflammation 11:111. 2014
    ..Whether APOE genotype affects Aβ-plaque-associated neuroinflammation remains unclear. In the current study, we address the role of APOE genotype on Aβ-associated microglial reactivity in the EFAD transgenic mouse model...
  3. ncbi request reprint Extracellular proteolysis of apolipoprotein E (apoE) by secreted serine neuronal protease
    Irfan Y Tamboli
    Department of Neuroscience, Georgetown University, Washington DC, United States of America
    PLoS ONE 9:e93120. 2014
    ..Primary glial cultures released an inhibitor of this proteolytic activity. Together, these studies reveal novel mechanism by which apoE can be regulated and therefore could be useful in designing apoE directed AD therapeutic approaches...
  4. pmc Parkinson-related parkin reduces α-Synuclein phosphorylation in a gene transfer model
    Preeti J Khandelwal
    Department of Neuroscience, Georgetown University Medical Center, Washington D, C, U, S, A, 20007
    Mol Neurodegener 5:47. 2010
    ..Parkin mutations result in loss of parkin E3-ubiquitin ligase activity and cause autosomal recessive early onset parkinsonism...
  5. doi request reprint Nontraditional signaling mechanisms of lipoprotein receptors
    G William Rebeck
    Department of Neuroscience, Georgetown University, Washington, DC 20007, USA
    Sci Signal 2:pe28. 2009
    ..New evidence ties these receptors to the transactivation of Trk receptors. Thus, this single receptor family demonstrates several distinct mechanisms for transducing information across the plasma membrane...
  6. pmc Similarities and differences in structure, expression, and functions of VLDLR and ApoER2
    Sunil S Reddy
    Department of Neuroscience Georgetown University Medical Center, 3970 Reservoir Rd, NW, Washington, DC, 20007, USA
    Mol Neurodegener 6:30. 2011
    ..This review aims to summarize important aspects of VLDLR and ApoER2 that may account for interesting recent findings that highlight the unique functions of each receptor...
  7. pmc The cytoplasmic adaptor protein X11alpha and extracellular matrix protein Reelin regulate ApoE receptor 2 trafficking and cell movement
    S Sakura Minami
    Department of Neurology, Georgetown University, 4000 Reservoir Road NW, Washington, DC 20057, USA
    FASEB J 24:58-69. 2010
    ..05, n=4). In the present study, we are the first to demonstrate that ApoEr2 regulates cell movement, and both X11alpha and Reelin enhance this effect...
  8. pmc ApoE receptor 2 regulates synapse and dendritic spine formation
    Sonya B Dumanis
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC, United States of America
    PLoS ONE 6:e17203. 2011
    ..We examined the biological effects of ApoEr2 on synapse and dendritic spine formation-processes critical for learning and memory...
  9. pmc Interaction of reelin with amyloid precursor protein promotes neurite outgrowth
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057 1464, USA
    J Neurosci 29:7459-73. 2009
    ..Addition of an alpha3beta1 integrin antibody prevented APP and Reelin-induced neurite outgrowth. These findings demonstrate that Reelin interacts with APP, potentially having important effects on neurite development...
  10. pmc The effects of amyloid precursor protein on postsynaptic composition and activity
    HYANG SOOK HOE
    Departments of Neuroscience, Physiology and Biophysics, Pharmacology, and Neurology, Georgetown University Medical Center, Washington, D C 20057 1464, USA
    J Biol Chem 284:8495-506. 2009
    ..These results demonstrate a novel physiological role of postsynaptic APP in enhancing NMDAR function...
  11. doi request reprint Levels of soluble and insoluble tau reflect overall status of tau phosphorylation in vivo
    Chiho Hirata-Fukae
    Department of Neurology, Georgetown University Medical Center, Washington, DC 20057, USA
    Neurosci Lett 450:51-5. 2009
    ..Taken together, these findings suggest that levels of soluble and insoluble tau are indicative of overall levels of tau phosphorylation, and may be useful markers to evaluate the effects of anti-tau therapeutic strategies in vivo...
  12. pmc ApoE4 decreases spine density and dendritic complexity in cortical neurons in vivo
    Sonya B Dumanis
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057, USA
    J Neurosci 29:15317-22. 2009
    ....
  13. pmc FE65 as a link between VLDLR and APP to regulate their trafficking and processing
    Sonya B Dumanis
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057 1464, USA
    Mol Neurodegener 7:9. 2012
    ..In the present study, we tested whether FE65 can interact with another ApoE receptor, VLDLR, thereby altering its trafficking and processing, and whether FE65 can serve as a linker between APP and VLDLR...
  14. ncbi request reprint Fyn modulation of Dab1 effects on amyloid precursor protein and ApoE receptor 2 processing
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057, USA
    J Biol Chem 283:6288-99. 2008
    ..These data demonstrate that Fyn, due in part to its effects on Dab1, regulates the phosphorylation, trafficking, and processing of APP and apoEr2...
  15. ncbi request reprint Apolipoprotein E receptor 2 interactions with the N-methyl-D-aspartate receptor
    HYANG SOOK HOE
    Department of Neuroscience and Physiology, Georgetown University Medical Center, Washington, DC 20057 1464, USA
    J Biol Chem 281:3425-31. 2006
    ..These studies suggest that ApoEr2 can form a multiprotein complex with NMDA receptor subunits and PSD95...
  16. ncbi request reprint The metalloprotease inhibitor TIMP-3 regulates amyloid precursor protein and apolipoprotein E receptor proteolysis
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057 1464, USA
    J Neurosci 27:10895-905. 2007
    ..TIMP-3 protein levels were increased in human Alzheimer's disease (AD) brain and in APP transgenic mice, suggesting that increased levels of TIMP-3 in AD may contribute to higher levels of Abeta...
  17. pmc Beta-amyloid1-42 gene transfer model exhibits intraneuronal amyloid, gliosis, tau phosphorylation, and neuronal loss
    G William Rebeck
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA
    J Biol Chem 285:7440-6. 2010
    ..Targeted delivery of Abeta will allow speedy delineation of pathological mechanisms associated with specific neurodegenerative lesions...
  18. pmc Fyn kinase regulates the association between amyloid precursor protein and Dab1 by promoting their localization to detergent-resistant membranes
    S Sakura Minami
    Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia 20057 1464, USA
    J Neurochem 118:879-90. 2011
    ..These findings suggest that Reelin treatment promotes the localization of APP and Dab1 to DRMs, and affects their phosphorylation by Fyn, thus regulating their interaction...
  19. pmc Wild type and P301L mutant Tau promote neuro-inflammation and α-Synuclein accumulation in lentiviral gene delivery models
    Preeti J Khandelwal
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA
    Mol Cell Neurosci 49:44-53. 2012
    ..This change of α-Synuclein in Tau gene transfer models suggests that Tau pathology may lead to α-Synuclein modification in neurodegenerative diseases...
  20. pmc Decreased dendritic spine density and abnormal spine morphology in Fyn knockout mice
    Lenard W Babus
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057 1464, USA
    Brain Res 1415:96-102. 2011
    ..These findings suggest that Fyn regulates dendritic spine number and morphology over time and provide further support for Fyn's role in maintaining proper synaptic function in vivo...
  21. pmc Cortical injury increases cholesterol 24S hydroxylase (Cyp46) levels in the rat brain
    CASANDRA M CARTAGENA
    Department of Neuroscience, Georgetown University Medical Center, Washington, D C 20057, USA
    J Neurotrauma 25:1087-98. 2008
    ....
  22. ncbi request reprint FE65 interaction with the ApoE receptor ApoEr2
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, Washington, D C 20057 1464, USA
    J Biol Chem 281:24521-30. 2006
    ..In addition, full-length FE65 decreased Abeta to a significantly greater extent than individual FE65 domains. These data suggest that FE65 can bind APP and ApoEr2 at the same time and affect the processing of each...
  23. ncbi request reprint Effects of apoE on neuronal signaling and APP processing in rodent brain
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University, 3970 Reservoir Road NW, Washington, DC 20057 1464, USA
    Brain Res 1112:70-9. 2006
    ..The increase in ERK activation is consistent with a role for apoE in a neuronal response to stress, and the decrease in JNK activation suggests that apoE may have anti-apoptotic effects, over several days...
  24. ncbi request reprint DAB1 and Reelin effects on amyloid precursor protein and ApoE receptor 2 trafficking and processing
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057 1464, USA
    J Biol Chem 281:35176-85. 2006
    ..Together, these data suggest that Dab1 alters trafficking and processing of APP and apoEr2, and this effect is influenced by extracellular ligands...
  25. pmc Fyn knock-down increases Aβ, decreases phospho-tau, and worsens spatial learning in 3×Tg-AD mice
    S Sakura Minami
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057 1464, USA
    Neurobiol Aging 33:825.e15-24. 2012
    ..Overall, these findings suggest that loss of Fyn at early stages of disease increases soluble Aβ accumulation and worsens spatial learning in the absence of changes in tau phosphorylation...
  26. pmc Parkin mediates beclin-dependent autophagic clearance of defective mitochondria and ubiquitinated Abeta in AD models
    Preeti J Khandelwal
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA
    Hum Mol Genet 20:2091-102. 2011
    ..Parkin-mediated clearance of ubiquitinated Aβ may act in parallel with autophagy to clear molecular debris and defective mitochondria and restore neurotransmitter balance...
  27. pmc Young APOE4 targeted replacement mice exhibit poor spatial learning and memory, with reduced dendritic spine density in the medial entorhinal cortex
    Gustavo A Rodriguez
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057, USA
    Learn Mem 20:256-66. 2013
    ..These findings suggest that human APOE-ε4 may affect cognitive function and neuronal morphology early in life...
  28. doi request reprint Regulated proteolysis of APP and ApoE receptors
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road, NW, Washington, DC 20057 1464, USA
    Mol Neurobiol 37:64-72. 2008
    ..Thus, the functions of apoE receptors and by analogy of APP will be modified by the various extracellular and intracellular interactions reviewed in this paper...
  29. pmc F-spondin interaction with the apolipoprotein E receptor ApoEr2 affects processing of amyloid precursor protein
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057 1464, USA
    Mol Cell Biol 25:9259-68. 2005
    ..These studies suggest that the extracellular matrix molecule F-spondin can cluster APP and ApoEr2 together on the cell surface and affect the processing of each, resulting in decreased production of Abeta...
  30. pmc Therapeutic versus neuroinflammatory effects of passive immunization is dependent on Aβ/amyloid burden in a transgenic mouse model of Alzheimer's disease
    S Sakura Minami
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057, USA
    J Neuroinflammation 7:57. 2010
    ..This therapeutic strategy is under intense scrutiny in clinical studies, but its application is limited by neuroinflammatory side effects (autoimmune encephalitis and vasogenic edema)...
  31. pmc Modulation of ABCA1 by an LXR agonist reduces β-amyloid levels and improves outcome after traumatic brain injury
    David J Loane
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA
    J Neurotrauma 28:225-36. 2011
    ..T0901317 also limited motor coordination deficits in injured mice and reduced brain lesion volume. These data indicate that activation of LXR can reduce Aβ accumulation after TBI, and is accompanied by improved functional recovery...
  32. pmc Low-density lipoprotein receptors regulate microglial inflammation through c-Jun N-terminal kinase
    Ana Pocivavsek
    Department of Neuroscience, Georgetown University, New Research Building, Washington, District of Columbia 20057 1464, USA
    Glia 57:444-53. 2009
    ..These data suggest that microglial LDL receptors regulate JNK activation, which is necessary for apoE modulation of the inflammatory response...
  33. pmc 24S-hydroxycholesterol effects on lipid metabolism genes are modeled in traumatic brain injury
    CASANDRA M CARTAGENA
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road, NW, Washington, DC 20057, USA
    Brain Res 1319:1-12. 2010
    ..Thus, changes to transcription of cholesterol synthesis genes after TBI were consistent with increases in Cyp46 activity, but changes to fatty acid synthesis genes must be regulated by other mechanisms...
  34. pmc Microglial low-density lipoprotein receptor-related protein 1 modulates c-Jun N-terminal kinase activation
    Ana Pocivavsek
    Department of Neuroscience, Georgetown University, Washington, DC 20057 1464, USA
    J Neuroimmunol 214:25-32. 2009
    ..Microglial LRP1 was also essential for EP to suppress JNK activation induced by lipopolysaccharide...
  35. pmc APOE genotype affects the pre-synaptic compartment of glutamatergic nerve terminals
    Sonya B Dumanis
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057, USA
    J Neurochem 124:4-14. 2013
    ..These factors may contribute to the increased risk of neurodegeneration associated with APOE-ε4, and also act as surrogate markers for Alzheimer's disease risk...
  36. ncbi request reprint Tarenflurbil protection from cytotoxicity is associated with an upregulation of neurotrophins
    Xu Zhao
    Department of Biochemistry, Molecular and Cellular Biology, Georgetown University Medical Center, Washington, DC 20007, USA
    J Alzheimers Dis 15:397-407. 2008
    ..These findings suggest that up-regulation of neurotrophins might represent an underlying mechanism contributing to the beneficial effects seen with tarenflurbil in AD...
  37. pmc Wild type TDP-43 induces neuro-inflammation and alters APP metabolism in lentiviral gene transfer models
    Alexander M Herman
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA
    Exp Neurol 235:297-305. 2012
    ..Here we show that TDP-43 up-regulates APP metabolism and suggest a mechanistic link between TDP-43 and BACE...
  38. pmc Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury
    David J Loane
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA
    Nat Med 15:377-9. 2009
    ..Thus, APP secretases are promising targets for treatment of TBI...
  39. pmc Intracellular cholesterol homeostasis and amyloid precursor protein processing
    Mark P Burns
    Georgetown University Medical Center, Department of Neuroscience, Washington, DC 20057, USA
    Biochim Biophys Acta 1801:853-9. 2010
    ....
  40. ncbi request reprint Females exhibit more extensive amyloid, but not tau, pathology in an Alzheimer transgenic model
    Chiho Hirata-Fukae
    Department of Neurology, Georgetown University Medical Center, Washington, DC 20057, USA
    Brain Res 1216:92-103. 2008
    ..These findings confirm progressive Abeta pathology in 3xTg-AD transgenic mice, and provide guidance for their use in therapeutic research...
  41. pmc ApoE mimetic peptide decreases Abeta production in vitro and in vivo
    S Sakura Minami
    Department of Neuroscience, Georgetown University, 3970 Reservoir Rd, NW, Washington, DC 20057, USA
    Mol Neurodegener 5:16. 2010
    ..Here, we further examined whether peptides containing tandem repeats of the apoE receptor-binding region (amino acids 141-149) affected APP trafficking, APP processing, and Abeta production...
  42. pmc Inhibition of c-Jun N-terminal kinase increases apoE expression in vitro and in vivo
    Ana Pocivavsek
    Department of Neuroscience, Georgetown University, 3970 Reservoir Road NW, Washington, DC 20057 1464, USA
    Biochem Biophys Res Commun 387:516-20. 2009
    ..Our work in primary glia and in vivo in mice injected with JNK inhibitor demonstrates that inhibition of JNK may be an effective way to increase apoE expression...
  43. pmc Age-related loss of noradrenergic neurons in the brains of triple transgenic mice
    Kebreten F Manaye
    Department of Physiology and Biophysics, College of Medicine, Howard University, 520 W St NW, Washington, DC 20059, USA
    Age (Dordr) 35:139-47. 2013
    ..Understanding the neurobiology of this apparent neuroprotection could lead to an improved understanding of age-related cognitive function in general, and the development of novel strategies for the therapeutic management of AD patients...
  44. pmc β-amyloid triggers ALS-associated TDP-43 pathology in AD models
    Alexander M Herman
    Department of Biochemistry Molecular and Cell Biology, Georgetown University Medical Center, Washington, DC 20007, USA
    Brain Res 1386:191-9. 2011
    ..These data indicate an overlap in TDP-43 pathology between AD and ALS-FTLD and suggest that Aβ triggers modifications of TDP-43...
  45. pmc Parkin promotes intracellular Abeta1-42 clearance
    Mark P Burns
    Department of Neuroscience, Georgetown University School of Medicine, Washington, DC 20057, USA
    Hum Mol Genet 18:3206-16. 2009
    ..These data indicate that parkin promotes ubiquitination and proteasomal degradation of intracellular Abeta(1-42) and demonstrate a protective effect in neurodegenerative diseases with Abeta deposits...
  46. ncbi request reprint Regulation of ApoE receptor proteolysis by ligand binding
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University, 3970 Reservoir Road NW, Washington, DC 20057 1464, USA
    Brain Res Mol Brain Res 137:31-9. 2005
    ..Similar promotion of receptor cleavage was seen with two other ligands, reelin and activated alpha2-macroglobulin. We suggest that signaling promoted by these receptors depends in part on these regulated proteolytic events...
  47. pmc No cross-sectional influence of APOE epsilon4 dose on clinical tests in Alzheimer's disease
    Rochelle E Tractenberg
    Department of Neurology, Georgetown University School of Medicine, Washington, DC, USA
    Neurobiol Aging 30:1327-8. 2009
    ..No significant influence of epsilon4 was detected. APOE's effect in AD may occur prior to clinical symptoms, or may simply be more subtle than these instruments can detect...
  48. ncbi request reprint The effects of ABCA1 on cholesterol efflux and Abeta levels in vitro and in vivo
    Mark P Burns
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20007, USA
    J Neurochem 98:792-800. 2006
    ..These data show that promoting cholesterol efflux is a viable target for Abeta reducing strategies; however, knockout of cholesterol transporters is not sufficient to alter Abeta in vitro or in vivo...
  49. ncbi request reprint Multiple pathways of apolipoprotein E signaling in primary neurons
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University, Washington, DC 20057 1464, USA
    J Neurochem 93:145-55. 2005
    ....
  50. ncbi request reprint Lack of association of the cholesterol 24-hydroxylase (CYP46) intron 2 polymorphism with Alzheimer's disease
    Martin Ingelsson
    Harvard Medical School, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA
    Neurosci Lett 367:228-31. 2004
    ..Despite growing evidence implicating cholesterol metabolism in AD risk and Abeta generation, our data does not support a robust genetic relationship between the CYP46 intron 2 polymorphism and AD risk or neuropathology...
  51. ncbi request reprint Lack of association of two lipoprotein lipase polymorphisms with Alzheimer's disease
    Matthew D Martin-Rehrmann
    Alzheimer Research Unit, 114 16th Street, Massachusetts General Hospital, Charlestown, MA 02129, USA
    Neurosci Lett 328:109-12. 2002
    ..Thus, our study does not support associations between AD and two common polymorphisms in LPL...
  52. ncbi request reprint Apolipoprotein E and Alzheimer's disease: the protective effects of ApoE2 and E3
    G William Rebeck
    Alzheimer Research Unit, Massachusetts General Hospital, Charlestown, MA 02129, USA
    J Alzheimers Dis 4:145-54. 2002
  53. ncbi request reprint LRP and senile plaques in Alzheimer's disease: colocalization with apolipoprotein E and with activated astrocytes
    Katrin Arelin
    Alzheimer Research Unit, Department of Neurology, Massachusetts General Hospital, 114 16th Street, Room 2009, Charlestown, MA 02129, USA
    Brain Res Mol Brain Res 104:38-46. 2002
    ..The upregulation of LRP would allow increased clearance of LRP ligands as well as clearance of Abeta/ApoE complexes...
  54. ncbi request reprint Induction of the cholesterol transporter ABCA1 in central nervous system cells by liver X receptor agonists increases secreted Abeta levels
    Hiroaki Fukumoto
    Alzheimer Research Unit, Massachusetts General Hospital, Charlestown 02129, USA
    J Biol Chem 277:48508-13. 2002
    ..The increase in secreted Abeta levels was reduced by RNAi blocking of ABCA1 expression. These data suggest that the cholesterol efflux molecule ABCA1 may also be involved in the secretion of the membrane-associated molecule, Abeta...
  55. ncbi request reprint Regulation of central nervous system cholesterol homeostasis by the liver X receptor agonist TO-901317
    Gunter P Eckert
    Department of Pharmacology, ZAFES, Biocenter Niederursel, University of Frankfurt, Frankfurt, Germany
    Neurosci Lett 423:47-52. 2007
    ..These data show that the LXR agonist TO-901317 is capable of reducing cholesterol in neurons of the CNS...
  56. ncbi request reprint Kinetics of cerebral amyloid angiopathy progression in a transgenic mouse model of Alzheimer disease
    Elissa M Robbins
    MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neurosci 26:365-71. 2006
    ..35% of total available vessel area per day (95% confidence interval, 0.3-0.4%). The consistent rate of disease progression implies that this model is amenable to investigations of therapeutic interventions...
  57. ncbi request reprint APOE epsilon 3/ epsilon 4 heterozygotes have an elevated proportion of apolipoprotein E4 in cerebrospinal fluid relative to plasma, independent of Alzheimer's disease diagnosis
    Hiroaki Fukumoto
    Alzheimer Disease Research Unit, Massachusetts General Hospital East, B114 2010, 114 16th St, Charlestown, MA 02129, USA
    Exp Neurol 183:249-53. 2003
    ..However, the greater proportion of apoE4 in the cerebrospinal fluid suggests differential production or metabolism of the protein in the central nervous system (CNS), with the apoE4 isoform dominating...
  58. ncbi request reprint Progression of cerebral amyloid angiopathy in transgenic mouse models of Alzheimer disease
    Sarah B Domnitz
    Alzheimer Research Unit, Massachusetts General Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA
    J Neuropathol Exp Neurol 64:588-94. 2005
    ..This approach should lead to more informed analysis of the consequences of evolving therapeutic options for AD on this related form of vascular pathology...
  59. ncbi request reprint Cholesterol independent effect of LXR agonist TO-901317 on gamma-secretase
    Christian Czech
    F Hoffmann La Roche, Pharmaceuticals Division, Basel, Switzerland
    J Neurochem 101:929-36. 2007
    ..A cell-free gamma-secretase assay confirmed that TO-901317 can directly alter gamma-secretase activity. These data demonstrate that TO-901317 can directly modulate the site of cleavage of APP by gamma-secretase in vitro...

Research Grants13

  1. Functions of Lipoprotein Receptors in Alzheimer Disease
    G Rebeck; Fiscal Year: 2002
    ..C) We will test whether these molecules are involved in the phosphorylation of tau observed in neurofibrillary tangles of AD brains. ..
  2. Apolipoprotein E receptors and Alzheimers disease
    G William Rebeck; Fiscal Year: 2010
    ..abstract_text> ..
  3. Apolipoprotein E receptors and Alzheimers disease
    G Rebeck; Fiscal Year: 2009
    ..abstract_text> ..
  4. Apolipoprotein E receptors and Alzheimers disease
    G Rebeck; Fiscal Year: 2007
    ....
  5. Apolipoprotein E receptors and Alzheimers disease
    G Rebeck; Fiscal Year: 2006
    ....
  6. Functions of Lipoprotein Receptors in Alzheimer Disease
    G Rebeck; Fiscal Year: 2004
    ..C) We will test whether these molecules are involved in the phosphorylation of tau observed in neurofibrillary tangles of AD brains. ..
  7. Functions of Lipoprotein Receptors in Alzheimer Disease
    G Rebeck; Fiscal Year: 2005
    ..C) We will test whether these molecules are involved in the phosphorylation of tau observed in neurofibrillary tangles of AD brains. ..
  8. Functions of Lipoprotein Receptors in Alzheimer Disease
    G Rebeck; Fiscal Year: 2004
    ..C) We will test whether these molecules are involved in the phosphorylation of tau observed in neurofibrillary tangles of AD brains. ..
  9. Functions of Lipoprotein Receptors in Alzheimer Disease
    G Rebeck; Fiscal Year: 2004
    ..C) We will test whether these molecules are involved in the phosphorylation of tau observed in neurofibrillary tangles of AD brains. ..
  10. Functions of Lipoprotein Receptors in Alzheimer Disease
    G Rebeck; Fiscal Year: 2003
    ..C) We will test whether these molecules are involved in the phosphorylation of tau observed in neurofibrillary tangles of AD brains. ..
  11. ApOE effects on neuron signaling and function via ApoER2
    G William Rebeck; Fiscal Year: 2010
    ..This proposed research will address the actions of apoE in the brain, and identify ways that it could be affecting Alzheimer's disease. ..