W Xia

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc Dissembled DJ-1 high molecular weight complex in cortex mitochondria from Parkinson's disease patients
    Hikmet Nural
    Haldeman Laboratory of Molecular and Cellular Neurobiology, Sun Health Research Institute, Sun City, Arizona, USA
    Mol Neurodegener 4:23. 2009
  2. pmc Disassembled DJ-1 high molecular weight complex in cortex mitochondria from Parkinson's disease patients
    Zhenyu Zhong
    Haldeman Laboratory of Molecular and Cellular Neurobiology, Sun Health Research Institute, Sun City, AZ USA
    Mol Neurodegener 4:30. 2009
  3. pmc Phenotypic analysis of images of zebrafish treated with Alzheimer's gamma-secretase inhibitors
    Dilyara Arslanova
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Harvard University, Boston, MA, USA
    BMC Biotechnol 10:24. 2010
  4. pmc A specific enzyme-linked immunosorbent assay for measuring beta-amyloid protein oligomers in human plasma and brain tissue of patients with Alzheimer disease
    Weiming Xia
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, HIM 616, 77 Ave Louis Pasteur, Boston, MA 02115, USA
    Arch Neurol 66:190-9. 2009
  5. pmc Increased DJ-1 expression under oxidative stress and in Alzheimer's disease brains
    Stephanie Baulac
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Harvard University, Boston, MA 02115, USA
    Mol Neurodegener 4:12. 2009
  6. pmc Bioluminescence imaging reveals inhibition of tumor cell proliferation by Alzheimer's amyloid beta protein
    Hong Zhao
    Center for Neurologic Disease, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Cell Int 9:15. 2009
  7. ncbi request reprint Amyloid metabolism and secretases in Alzheimer's disease
    W Xia
    Center for Neurologic Diseases, Brigham and Women s Hospital, 77 Avenue Louis Pasteur, HIM 616, Boston, MA 02115, USA
    Curr Neurol Neurosci Rep 1:422-7. 2001
  8. doi request reprint Exploring Alzheimer's disease in zebrafish
    Weiming Xia
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
    J Alzheimers Dis 20:981-90. 2010
  9. ncbi request reprint Amyloid inhibitors and Alzheimer's disease
    Weiming Xia
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, 77 Ave Louis Pasteur, Boston, MA 02115, USA
    Curr Opin Investig Drugs 4:55-9. 2003
  10. ncbi request reprint Relationship between presenilinase and gamma-secretase
    Weiming Xia
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Harvard Institutes for Medicine, Boston, Massachusetts 02115, USA
    Drug News Perspect 16:69-74. 2003

Research Grants

Collaborators

Detail Information

Publications54

  1. pmc Dissembled DJ-1 high molecular weight complex in cortex mitochondria from Parkinson's disease patients
    Hikmet Nural
    Haldeman Laboratory of Molecular and Cellular Neurobiology, Sun Health Research Institute, Sun City, Arizona, USA
    Mol Neurodegener 4:23. 2009
    ..Moreover, in the PD cortex mitochondria fraction, the HMW DJ-1 complex is significantly lower than in the NPC. These results suggest abnormal DJ-1 expression levels and DJ-1 complex changes may contribute to PD pathogenesis...
  2. pmc Disassembled DJ-1 high molecular weight complex in cortex mitochondria from Parkinson's disease patients
    Zhenyu Zhong
    Haldeman Laboratory of Molecular and Cellular Neurobiology, Sun Health Research Institute, Sun City, AZ USA
    Mol Neurodegener 4:30. 2009
    ..ABSTRACT: Correction to Nural H, He P, Beach T, Sue L, Xia W, Shen Y. Disassembled DJ-1 high molecular weight complex in cortex mitochondria from Parkinson's disease patients Molecular Neurodegeneration 2009, 4:23...
  3. pmc Phenotypic analysis of images of zebrafish treated with Alzheimer's gamma-secretase inhibitors
    Dilyara Arslanova
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Harvard University, Boston, MA, USA
    BMC Biotechnol 10:24. 2010
    ..The gamma-secretase also cleaves Notch to generate Notch Intracellular domain (NICD), the signaling molecule that is implicated in tumorigenesis...
  4. pmc A specific enzyme-linked immunosorbent assay for measuring beta-amyloid protein oligomers in human plasma and brain tissue of patients with Alzheimer disease
    Weiming Xia
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, HIM 616, 77 Ave Louis Pasteur, Boston, MA 02115, USA
    Arch Neurol 66:190-9. 2009
    ....
  5. pmc Increased DJ-1 expression under oxidative stress and in Alzheimer's disease brains
    Stephanie Baulac
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Harvard University, Boston, MA 02115, USA
    Mol Neurodegener 4:12. 2009
    ..Therefore, our results strongly suggest that DJ-1 expression is not necessary during zebrafish development but can be induced in zebrafish exposed to oxidative stress and is present in human AD brains...
  6. pmc Bioluminescence imaging reveals inhibition of tumor cell proliferation by Alzheimer's amyloid beta protein
    Hong Zhao
    Center for Neurologic Disease, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Cell Int 9:15. 2009
    ..CONCLUSION: Our results suggest that Abeta plays an inhibitory role in tumor cell proliferation; this effect could depend on the type of tumor cells and amount of Abeta...
  7. ncbi request reprint Amyloid metabolism and secretases in Alzheimer's disease
    W Xia
    Center for Neurologic Diseases, Brigham and Women s Hospital, 77 Avenue Louis Pasteur, HIM 616, Boston, MA 02115, USA
    Curr Neurol Neurosci Rep 1:422-7. 2001
    ..These results provide the molecular basis for therapeutic interventions that reduce A beta accumulation in AD patients by inhibiting beta- or gamma-secretase...
  8. doi request reprint Exploring Alzheimer's disease in zebrafish
    Weiming Xia
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
    J Alzheimers Dis 20:981-90. 2010
    ..A transgenic zebrafish expressing mutant tau has been created, and the transgenic animals exhibit a neurodegeneration phenotype. The use of zebrafish as a model system for AD research has expanded our knowledge of Abeta and tau...
  9. ncbi request reprint Amyloid inhibitors and Alzheimer's disease
    Weiming Xia
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, 77 Ave Louis Pasteur, Boston, MA 02115, USA
    Curr Opin Investig Drugs 4:55-9. 2003
    ..This knowledge will allow us to fully understand the A beta-related pathways in AD pathogenesis and explore novel therapeutic interventions...
  10. ncbi request reprint Relationship between presenilinase and gamma-secretase
    Weiming Xia
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Harvard Institutes for Medicine, Boston, Massachusetts 02115, USA
    Drug News Perspect 16:69-74. 2003
    ..Lack of presenilinase inhibition by several potent gamma-secretase inhibitors suggests that these two protease activities are pharmacologically distinct...
  11. ncbi request reprint FAD mutations in presenilin-1 or amyloid precursor protein decrease the efficacy of a gamma-secretase inhibitor: evidence for direct involvement of PS1 in the gamma-secretase cleavage complex
    W Xia
    Department of Neurology, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Neurobiol Dis 7:673-81. 2000
    ..Taken together, these findings suggest that PS1 participates physically in a complex with APP during the gamma-secretase cleavage event...
  12. ncbi request reprint Intramembrane proteolysis by presenilin and presenilin-like proteases
    Weiming Xia
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Cell Sci 116:2839-44. 2003
    ..SPP cuts type II membrane proteins, illustrating that PS-like proteases play a key role in intramembrane proteolysis of single-pass membrane proteins oriented in either direction...
  13. ncbi request reprint From presenilinase to gamma-secretase, cleave to capacitate
    Weiming Xia
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Curr Alzheimer Res 5:172-8. 2008
    ....
  14. pmc Quantification of gamma-secretase modulation differentiates inhibitor compound selectivity between two substrates Notch and amyloid precursor protein
    Ting Yang
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard University, Boston, MA, USA
    Mol Brain 1:15. 2008
    ..In addition to APP, γ-secretase also cleaves other type I integral membrane proteins, including the Notch receptor, a key molecule involved in embryonic development...
  15. ncbi request reprint Presenilin 1 regulates the processing of beta-amyloid precursor protein C-terminal fragments and the generation of amyloid beta-protein in endoplasmic reticulum and Golgi
    W Xia
    Department of Neurology, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Biochemistry 37:16465-71. 1998
    ..Our results indicate PS1 and APP can interact in the ER and Golgi, where PS1 is required for proper gamma-secretase processing of APP CTFs, and that PS1 mutations augment Abeta42 levels principally in Golgi-like vesicles...
  16. ncbi request reprint Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and gamma-secretase activity
    M S Wolfe
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Nature 398:513-7. 1999
    ....
  17. pmc Presenilin complexes with the C-terminal fragments of amyloid precursor protein at the sites of amyloid beta-protein generation
    W Xia
    Department of Neurology and Program in Neuroscience, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 97:9299-304. 2000
    ..Thus, PSs are complexed with the gamma-secretase substrates C83 and C99 in the subcellular locations where Abeta is generated, indicating that PSs are directly involved in the pathogenically critical intramembranous proteolysis of APP...
  18. ncbi request reprint Aspartate mutations in presenilin and gamma-secretase inhibitors both impair notch1 proteolysis and nuclear translocation with relative preservation of notch1 signaling
    O Berezovska
    Alzheimer s Disease Research Laboratory, Department of Neurology, Harvard Medical School and Massachusetts General Hospital, Charlestown, California, USA
    J Neurochem 75:583-93. 2000
    ..The latter is an important finding from the perspective of therapeutic treatment of Alzheimer's disease by targeting gamma-secretase processing of APP to reduce Abeta production...
  19. ncbi request reprint The transmembrane aspartates in presenilin 1 and 2 are obligatory for gamma-secretase activity and amyloid beta-protein generation
    W T Kimberly
    Department of Neurology, Harvard Medical School and Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Biol Chem 275:3173-8. 2000
    ..We conclude that presenilins, and their TM aspartates in particular, are attractive targets for lowering Abeta therapeutically to prevent Alzheimer's disease...
  20. pmc Interaction between amyloid precursor protein and presenilins in mammalian cells: implications for the pathogenesis of Alzheimer disease
    W Xia
    Department of Neurology, Harvard Medical School, Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 94:8208-13. 1997
    ....
  21. ncbi request reprint Subcellular localization of presenilin 2 endoproteolytic C-terminal fragments
    T L Tekirian
    Genetics and Aging Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Brain Res Mol Brain Res 96:14-20. 2001
    ..In summary, these data suggest that the two presenilin 2 CTFs have different patterns of subcellular localization and that the N141I PS2 mutation alters the localization pattern of the PS2 caspase fragment...
  22. ncbi request reprint Enhancer function and novel DNA binding protein activity in the near upstream betaAPP gene promoter
    H W Querfurth
    Division of Neurology, St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA
    Gene 232:125-41. 1999
    ..An interaction model involving both domains and looping of interjacent DNA is proposed. We conclude that this newly described binding protein-enhancer complex is required for full betaAPP promoter activation...
  23. ncbi request reprint Presenilin proteins undergo heterogeneous endoproteolysis between Thr291 and Ala299 and occur as stable N- and C-terminal fragments in normal and Alzheimer brain tissue
    M B Podlisny
    Center for Neurologic Diseases, Harvard Medical School, Boston, Massachusetts, 02115, USA
    Neurobiol Dis 3:325-37. 1997
    ..Our results indicate that presenilins are rapidly processed to N- and C-terminal fragments in both neural and nonneural cells and that interference with this processing is not an obligatory feature of FAD-causing mutations...
  24. ncbi request reprint Presenilin endoproteolysis mediated by an aspartyl protease activity pharmacologically distinct from gamma-secretase
    William A Campbell
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurochem 85:1563-74. 2003
    ..Therefore, presenilinase has characteristics of an aspartyl protease, but this activity is distinct from gamma-secretase...
  25. ncbi request reprint Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice
    M Citron
    Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts, USA
    Nat Med 3:67-72. 1997
    ..Our data demonstrate that the presenilin mutations cause a dominant gain of function and may induce AD by enhancing A beta 42 production, thus promoting cerebral beta-amyloidosis...
  26. ncbi request reprint Role of presenilin in gamma-secretase cleavage of amyloid precursor protein
    W Xia
    Department of Neurology, Harvard Medical School, School and Center for Neurologic Diseases, Brigham and Women s Hospital, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    Exp Gerontol 35:453-60. 2000
    ..Furthermore, studies on the gamma-secretase-like proteolytic processing of Notch and Ire1 suggest a common mechanism for the involvement of PS1 in intramembrane proteolysis of membrane proteins...
  27. ncbi request reprint L-3-n-butylphthalide improves cognitive impairment and reduces amyloid-beta in a transgenic model of Alzheimer's disease
    Ying Peng
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 30:8180-9. 2010
    ..L-NBP shows promising preclinical potential as a multitarget drug for the prevention and/or treatment of Alzheimer's disease...
  28. pmc The acyl-coenzyme A: cholesterol acyltransferase inhibitor CI-1011 reverses diffuse brain amyloid pathology in aged amyloid precursor protein transgenic mice
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Genetics and Aging Research Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neuropathol Exp Neurol 69:777-88. 2010
    ..Collectively, these data suggest that CI-1011 treatment reduces amyloid burden in human APP mice by limiting generation and increasing clearance of diffusible Abeta...
  29. ncbi request reprint Zebrafish lacking Alzheimer presenilin enhancer 2 (Pen-2) demonstrate excessive p53-dependent apoptosis and neuronal loss
    William A Campbell
    Center for Neurologic Diseases, Department of Neurology, Harvard Medical School, Boston, Massachusetts, USA
    J Neurochem 96:1423-40. 2006
    ....
  30. ncbi request reprint The prolyl isomerase Pin1 regulates amyloid precursor protein processing and amyloid-beta production
    Lucia Pastorino
    Cancer Biology Program, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Nature 440:528-34. 2006
    ..These findings provide new insight into the pathogenesis and treatment of Alzheimer's disease...
  31. ncbi request reprint Rapid Notch1 nuclear translocation after ligand binding depends on presenilin-associated gamma-secretase activity
    O Berezovska
    Alzheimer s Disease Research Laboratory, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129, USA
    Ann N Y Acad Sci 920:223-6. 2000
    ....
  32. ncbi request reprint Are presenilins intramembrane-cleaving proteases? Implications for the molecular mechanism of Alzheimer's disease
    M S Wolfe
    Department of Pharmaceutical Sciences, University of Tennessee, Memphis 38163, USA
    Biochemistry 38:11223-30. 1999
    ..Thus, presenilins and S2P appear to be members of a new type of polytopic protease with an intramembranous active site...
  33. pmc Performance characteristics of plasma amyloid-beta 40 and 42 assays
    Olivia I Okereke
    Division of Aging, Department of Medicine, Brigham and Women s Hospital, and Harvard Medical School, Boston, MA 02115, USA
    J Alzheimers Dis 16:277-85. 2009
    ..While these preliminary findings suggest that measuring plasma Abeta(40) and Abeta(42) may be feasible in varied research settings, additional work in this area is necessary...
  34. ncbi request reprint The cytosolic loop of the gamma-secretase component presenilin enhancer 2 protects zebrafish embryos from apoptosis
    Henrik Zetterberg
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 281:11933-9. 2006
    ....
  35. pmc Ten-year change in plasma amyloid beta levels and late-life cognitive decline
    Olivia I Okereke
    Division of Aging and Channing Laboratory, Department of Medicine, Brigham and Women s Hospital and Harvard Medical School, 181 Longwood Ave, Third Floor, Boston, MA 02115, USA
    Arch Neurol 66:1247-53. 2009
    ..Plasma levels of amyloid beta peptide (Abeta) are potential biomarkers of early cognitive impairment and decline and of Alzheimer disease risk...
  36. pmc The common inhalational anesthetic sevoflurane induces apoptosis and increases beta-amyloid protein levels
    Yuanlin Dong
    Genetics and Aging Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA
    Arch Neurol 66:620-31. 2009
    ..Subjects Naive mice, H4 human neuroglioma cells, and H4 human neuroglioma cells stably transfected to express full-length amyloid precursor protein...
  37. ncbi request reprint RNA interference silencing of the adaptor molecules ShcC and Fe65 differentially affect amyloid precursor protein processing and Abeta generation
    Zhongcong Xie
    Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129 2060, USA
    J Biol Chem 282:4318-25. 2007
    ..These findings suggest that pharmacologically blocking interaction of APP with ShcC and Fe65 may provide novel therapeutic strategies against AD...
  38. ncbi request reprint Endoproteolysis of presenilin in vitro: inhibition by gamma-secretase inhibitors
    William A Campbell
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Biochemistry 41:3372-9. 2002
    ..Our studies provide a biochemical approach to characterize and identify this elusive presenilinase...
  39. pmc APP processing is regulated by cytoplasmic phosphorylation
    Ming Sum Lee
    Department of Pathology, Harvard Medical School and Howard Hughes Medical Institute, 200 Longwood Ave, Boston, MA 02115, USA
    J Cell Biol 163:83-95. 2003
    ..Together, these results suggest that T668 phosphorylation may facilitate the BACE1 cleavage of APP to increase Abeta generation...
  40. ncbi request reprint Functional gamma-secretase complex assembly in Golgi/trans-Golgi network: interactions among presenilin, nicastrin, Aph1, Pen-2, and gamma-secretase substrates
    Stephanie Baulac
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Neurobiol Dis 14:194-204. 2003
    ..Immunofluorescent staining of the individual gamma-secretase components supported our biochemical evidence that the gamma-secretase components assemble into the proteolytically active gamma-secretase complex in the Golgi/TGN compartment...
  41. ncbi request reprint Computerized image analysis for quantitative neuronal phenotyping in zebrafish
    Tianming Liu
    Center for Bioinformatics, Harvard Center for Neurodegeneration and Repair, Harvard Medical School, and Department of Radiology, Brigham and Women s Hospital, Boston, MA 02115, USA
    J Neurosci Methods 153:190-202. 2006
    ..Development of such an automated data analysis pipeline represents a significant step forward to achieve accurate and reproducible quantification of neuronal phenotypes in large scale or high-throughput zebrafish imaging studies...
  42. pmc A presenilin-1 mutation identified in familial Alzheimer disease with cotton wool plaques causes a nearly complete loss of gamma-secretase activity
    Elizabeth A Heilig
    Center for Human Genetic Research and Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    J Biol Chem 285:22350-9. 2010
    ..Rather, our findings provide support for the hypothesis that pathogenic mutations cause a general loss of presenilin function...
  43. ncbi request reprint HtrA2 regulates beta-amyloid precursor protein (APP) metabolism through endoplasmic reticulum-associated degradation
    Henri J Huttunen
    Neurobiology of Disease Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    J Biol Chem 282:28285-95. 2007
    ..Based on these results we suggest a novel function for HtrA2 as a regulator of APP metabolism through ER-associated degradation...
  44. pmc The inhalation anesthetic desflurane induces caspase activation and increases amyloid beta-protein levels under hypoxic conditions
    Bin Zhang
    Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129 2060, USA
    J Biol Chem 283:11866-75. 2008
    ..Pending in vivo confirmation, these data may have profound implications for anesthesia care in elderly patients, and especially those with AD...
  45. doi request reprint In vivo manifestation of Notch related phenotypes in zebrafish treated with Alzheimer's amyloid reducing gamma-secretase inhibitors
    Ting Yang
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurochem 113:1200-9. 2010
    ..In conclusion, phenotypic profile in whole animals offers important information on Notch related pathways and provides prediction of safe compounds during early development stages of therapeutic GSIs...
  46. ncbi request reprint Amyloid-lowering isocoumarins are not direct inhibitors of gamma-secretase
    William P Esler
    Nat Cell Biol 4:E110-1; author reply E111-2. 2002
  47. ncbi request reprint The search for gamma-secretase and development of inhibitors
    Jui Yi Tsai
    PPG Industrial, 440 College Park Drive, Monroeville, PA 15146, USA
    Curr Med Chem 9:1087-106. 2002
    ..In this article, we review the current knowledge of gamma-secretase biochemistry and cell biology and the development of inhibitors of this important therapeutic target...
  48. ncbi request reprint Characterization of presenilin-amyloid precursor interaction using bacterial expression and two-hybrid systems for human membrane proteins
    Mona Harnasch
    Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3US, UK
    Mol Membr Biol 21:373-83. 2004
    ..The implications of these findings for the function of gamma-secretase are discussed...
  49. ncbi request reprint Elevated beta-secretase expression and enzymatic activity detected in sporadic Alzheimer disease
    Li Bang Yang
    Nat Med 9:3-4. 2003
  50. ncbi request reprint Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration
    Ahmad Salehi
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, California 94305, USA
    Neuron 51:29-42. 2006
    ..Our study thus provides evidence for a pathogenic mechanism for DS in which increased expression of App, in the context of trisomy, causes abnormal transport of NGF and cholinergic neurodegeneration...
  51. ncbi request reprint Presenilin-1-mediated retention of APP derivatives in early biosynthetic compartments
    Marloes Réchards
    Cell Microscopy Center, Department of Cell Biology, University Medical Center and Institute for Biomembranes, 3584 CX Utrecht, The Netherlands
    Traffic 7:354-64. 2006
    ..Malfunctioning of PS-1 in this role may have important consequences for the progress of AD...
  52. ncbi request reprint The inhalation anesthetic isoflurane induces a vicious cycle of apoptosis and amyloid beta-protein accumulation
    Zhongcong Xie
    Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Charlestown, Massachusetts 02129 2060, USA
    J Neurosci 27:1247-54. 2007
    ..Accumulation of aggregated Abeta in the media can then promote apoptosis. The result is a vicious cycle of isoflurane-induced apoptosis, Abeta generation and aggregation, and additional rounds of apoptosis, leading to cell death...
  53. ncbi request reprint Presenilin-1 exists in both pre- and post-Golgi compartments and recycles via COPI-coated membranes
    Marloes Réchards
    Department of Cell Biology, University Medical Center and Institute for Biomembranes, Center for Biomedical Genetics, Utrecht University, 3584 CX Utrecht, The Netherlands
    Traffic 4:553-65. 2003
    ....
  54. ncbi request reprint Intracellular Abeta is increased by okadaic acid exposure in transfected neuronal and non-neuronal cell lines
    Xiaoyan Sun
    Laboratory for Alzheimer s Disease, Brain Science Institute of the RIKEN, 2 1 Hirosawa, Wako, 351 0198, Saitama, Japan
    Neurobiol Aging 23:195-203. 2002
    ..The increased full-length APP and decreased APPC99 were also observed. This is the first study to demonstrate that OA treatment significantly increases intracellular Abeta...

Research Grants4

  1. PRESENILIN ENDOPROTEASE & GAMMA-SECRETASE ACTIVITY
    Weiming Xia; Fiscal Year: 2000
    ..abstract_text> ..
  2. PRESENILIN ENDOPROTEASE & GAMMA-SECRETASE ACTIVITY
    Weiming Xia; Fiscal Year: 2001
    ..abstract_text> ..
  3. PRESENILIN ENDOPROTEASE & GAMMA-SECRETASE ACTIVITY
    Weiming Xia; Fiscal Year: 2002
    ..abstract_text> ..
  4. PRESENILIN ENDOPROTEASE & GAMMA-SECRETASE ACTIVITY
    Weiming Xia; Fiscal Year: 2003
    ..abstract_text> ..