Tony Wyss-Coray

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Chronic overproduction of transforming growth factor-beta1 by astrocytes promotes Alzheimer's disease-like microvascular degeneration in transgenic mice
    T Wyss-Coray
    Gladstone Institute of Neurological Disease, San Francisco, California 94141 9100, USA
    Am J Pathol 156:139-50. 2000
  2. ncbi request reprint Tgf-Beta pathway as a potential target in neurodegeneration and Alzheimer's
    Tony Wyss-Coray
    GRECC, VA Palo Alto Health Care System, Palo Alto, CA 94304, USA
    Curr Alzheimer Res 3:191-5. 2006
  3. ncbi request reprint Alzheimer's disease-like cerebrovascular pathology in transforming growth factor-beta 1 transgenic mice and functional metabolic correlates
    T Wyss-Coray
    Gladstone Institute of Neurological Disease, University of California, San Francisco 94141, USA
    Ann N Y Acad Sci 903:317-23. 2000
  4. ncbi request reprint TGF-beta1 promotes microglial amyloid-beta clearance and reduces plaque burden in transgenic mice
    T Wyss-Coray
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California, USA
    Nat Med 7:612-8. 2001
  5. pmc Prominent neurodegeneration and increased plaque formation in complement-inhibited Alzheimer's mice
    Tony Wyss-Coray
    Gladstone Institute of Neurological Disease, University of California, San Francisco, CA 94141, USA
    Proc Natl Acad Sci U S A 99:10837-42. 2002
  6. ncbi request reprint Inflammation in neurodegenerative disease--a double-edged sword
    Tony Wyss-Coray
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California San Francisco, San Francisco, CA 94141, USA
    Neuron 35:419-32. 2002
  7. ncbi request reprint Astroglial regulation of apolipoprotein E expression in neuronal cells. Implications for Alzheimer's disease
    Faith M Harris
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 279:3862-8. 2004
  8. pmc Beclin 1 gene transfer activates autophagy and ameliorates the neurodegenerative pathology in alpha-synuclein models of Parkinson's and Lewy body diseases
    Brian Spencer
    Department of Neurosciences, University of California, San Diego, La Jolla, California 92093 0624, USA
    J Neurosci 29:13578-88. 2009
  9. pmc Carboxyl-terminal-truncated apolipoprotein E4 causes Alzheimer's disease-like neurodegeneration and behavioral deficits in transgenic mice
    Faith M Harris
    Gladstone Institute of Neurological Disease, San Francisco, CA 94141 9100, USA
    Proc Natl Acad Sci U S A 100:10966-71. 2003
  10. ncbi request reprint Neuron-specific apolipoprotein e4 proteolysis is associated with increased tau phosphorylation in brains of transgenic mice
    Walter J Brecht
    Gladstone Institute of Neurological Disease, San Francisco, California 94141 9100, USA
    J Neurosci 24:2527-34. 2004

Detail Information

Publications47

  1. pmc Chronic overproduction of transforming growth factor-beta1 by astrocytes promotes Alzheimer's disease-like microvascular degeneration in transgenic mice
    T Wyss-Coray
    Gladstone Institute of Neurological Disease, San Francisco, California 94141 9100, USA
    Am J Pathol 156:139-50. 2000
    ..Closely related processes may induce cerebrovascular pathology in AD...
  2. ncbi request reprint Tgf-Beta pathway as a potential target in neurodegeneration and Alzheimer's
    Tony Wyss-Coray
    GRECC, VA Palo Alto Health Care System, Palo Alto, CA 94304, USA
    Curr Alzheimer Res 3:191-5. 2006
    ..Here I explore this evidence and discuss the pathway as a potential target for the treatment of neurodegeneration and AD...
  3. ncbi request reprint Alzheimer's disease-like cerebrovascular pathology in transforming growth factor-beta 1 transgenic mice and functional metabolic correlates
    T Wyss-Coray
    Gladstone Institute of Neurological Disease, University of California, San Francisco 94141, USA
    Ann N Y Acad Sci 903:317-23. 2000
    ..Similar mechanisms may be involved in AD pathogenesis...
  4. ncbi request reprint TGF-beta1 promotes microglial amyloid-beta clearance and reduces plaque burden in transgenic mice
    T Wyss-Coray
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California, USA
    Nat Med 7:612-8. 2001
    ..These results demonstrate that TGF-beta1 is an important modifier of amyloid deposition in vivo and indicate that TGF-beta1 might promote microglial processes that inhibit the accumulation of Abeta in the brain parenchyma...
  5. pmc Prominent neurodegeneration and increased plaque formation in complement-inhibited Alzheimer's mice
    Tony Wyss-Coray
    Gladstone Institute of Neurological Disease, University of California, San Francisco, CA 94141, USA
    Proc Natl Acad Sci U S A 99:10837-42. 2002
    ....
  6. ncbi request reprint Inflammation in neurodegenerative disease--a double-edged sword
    Tony Wyss-Coray
    Gladstone Institute of Neurological Disease and Department of Neurology, University of California San Francisco, San Francisco, CA 94141, USA
    Neuron 35:419-32. 2002
    ..Since many inflammatory responses are beneficial, directing and instructing the inflammatory machinery may be a better therapeutic objective than suppressing it...
  7. ncbi request reprint Astroglial regulation of apolipoprotein E expression in neuronal cells. Implications for Alzheimer's disease
    Faith M Harris
    Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141 9100, USA
    J Biol Chem 279:3862-8. 2004
    ..Thus, neuronal expression of apoE is regulated by a diffusible factor or factors released from astrocytes, and this regulation depends on the activity of the Erk kinase pathway in neurons...
  8. pmc Beclin 1 gene transfer activates autophagy and ameliorates the neurodegenerative pathology in alpha-synuclein models of Parkinson's and Lewy body diseases
    Brian Spencer
    Department of Neurosciences, University of California, San Diego, La Jolla, California 92093 0624, USA
    J Neurosci 29:13578-88. 2009
    ..Thus, beclin 1 plays an important role in the intracellular degradation of alpha-syn either directly or indirectly through the autophagy pathway and may present a novel therapeutic target for LBD/PD...
  9. pmc Carboxyl-terminal-truncated apolipoprotein E4 causes Alzheimer's disease-like neurodegeneration and behavioral deficits in transgenic mice
    Faith M Harris
    Gladstone Institute of Neurological Disease, San Francisco, CA 94141 9100, USA
    Proc Natl Acad Sci U S A 100:10966-71. 2003
    ..Inhibiting their formation might inhibit apoE4-associated neuronal deficits...
  10. ncbi request reprint Neuron-specific apolipoprotein e4 proteolysis is associated with increased tau phosphorylation in brains of transgenic mice
    Walter J Brecht
    Gladstone Institute of Neurological Disease, San Francisco, California 94141 9100, USA
    J Neurosci 24:2527-34. 2004
    ..Neuron-specific proteolytic cleavage of apoE4 is associated with increased phosphorylation of tau and may play a key role in the development of AD-related neuronal deficits...
  11. pmc Cellular source of apolipoprotein E4 determines neuronal susceptibility to excitotoxic injury in transgenic mice
    Manuel Buttini
    Gladstone Institute of Neurological Disease, San Francisco, CA 94158 2261, USA
    Am J Pathol 177:563-9. 2010
    ..Thus, an imbalance between astrocytic (excitoprotective) and neuronal (neurotoxic) apoE4 expression may increase susceptibility to diverse neurological diseases involving excitotoxic mechanisms...
  12. pmc Collagen VI protects neurons against Abeta toxicity
    Jason S Cheng
    Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, California 94158, USA
    Nat Neurosci 12:119-21. 2009
    ..These results identify collagen VI as an important component of the neuronal injury response and demonstrate its neuroprotective potential...
  13. pmc The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice
    Fiona Pickford
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA
    J Clin Invest 118:2190-9. 2008
    ..We conclude that beclin 1 deficiency disrupts neuronal autophagy, modulates APP metabolism, and promotes neurodegeneration in mice and that increasing beclin 1 levels may have therapeutic potential in AD...
  14. ncbi request reprint Molecular and functional dissection of TGF-beta1-induced cerebrovascular abnormalities in transgenic mice
    Marion Buckwalter
    Department of Neurology, Gladstone Institute of Neurological Disease, University of California, San Francisco, CA 94141, USA
    Ann N Y Acad Sci 977:87-95. 2002
    ..Thus, chronic overproduction of TGF-beta1 in the brain results in structural and functional impairments reminiscent of those in AD cases with amyloid angiopathy...
  15. ncbi request reprint ALK5-dependent TGF-β signaling is a major determinant of late-stage adult neurogenesis
    Yingbo He
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA
    Nat Neurosci 17:943-52. 2014
    ..Our findings describe an unexpected role for ALK5-dependent TGF-β signaling as a regulator of the late stages of adult hippocampal neurogenesis, which may have implications for changes in neurogenesis during aging and disease. ..
  16. pmc Neural progenitor cells regulate microglia functions and activity
    Kira I Mosher
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA
    Nat Neurosci 15:1485-7. 2012
    ..Thus, neural precursor cells may not only be shaped by microglia, but also regulate microglia functions and activity...
  17. pmc Genes contributing to prion pathogenesis
    GULTEKIN TAMGUNEY
    Institute for Neurodegenerative Diseases, University of California, San Francisco, CA, USA
    J Gen Virol 89:1777-88. 2008
    ....
  18. ncbi request reprint Adult mouse astrocytes degrade amyloid-beta in vitro and in situ
    Tony Wyss-Coray
    Geriatric Research, Education and Clinical Center, VA Palo Alto Health Care System, Palo Alto, California, USA
    Nat Med 9:453-7. 2003
    ..Treatments that increase removal of Abeta by astrocytes may therefore be a critical mechanism to reduce the neurodegeneration associated with AD...
  19. pmc Angiotensin II sustains brain inflammation in mice via TGF-beta
    Tobias V Lanz
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA
    J Clin Invest 120:2782-94. 2010
    ..These data suggest that AT1R antagonists, frequently prescribed as antihypertensives, may be useful to interrupt this proinflammatory, CNS-specific pathway in individuals with MS...
  20. ncbi request reprint Young blood reverses age-related impairments in cognitive function and synaptic plasticity in mice
    Saul A Villeda
    1 Department of Anatomy, University of California San Francisco, San Francisco, California, USA 2 The Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research, San Francisco, California, USA 3 Neuroscience Graduate Program, University of California San Francisco, San Francisco, California, USA 4 Biomedical Sciences Graduate Program, University of California San Francisco, San Francisco, California, USA 5 Developmental and Stem Cell Biology Graduate Program, University of California San Francisco, San Francisco, California, USA 6 Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA
    Nat Med 20:659-63. 2014
    ..Our data indicate that exposure of aged mice to young blood late in life is capable of rejuvenating synaptic plasticity and improving cognitive function. ..
  21. pmc TDP-43 frontotemporal lobar degeneration and autoimmune disease
    Zachary A Miller
    UCSF Memory and Aging Center, University of California San Francisco, San Francisco, California 94143 1207, USA
    J Neurol Neurosurg Psychiatry 84:956-62. 2013
    ..Given the association between systemic inflammation and other neurodegenerative processes, links between autoimmunity and FTD need to be explored...
  22. pmc Mild cognitive impairment: baseline and longitudinal structural MR imaging measures improve predictive prognosis
    Linda K McEvoy
    Department of Radiology, University of California, San Diego, 9500 Gilman Dr, La Jolla, CA 92093, USA
    Radiology 259:834-43. 2011
    ..To assess whether single-time-point and longitudinal volumetric magnetic resonance (MR) imaging measures provide predictive prognostic information in patients with amnestic mild cognitive impairment (MCI)...
  23. pmc Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis
    Jian Luo
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305 5235, USA
    J Clin Invest 117:3306-15. 2007
    ..Importantly, inhibition of TGF-beta signaling may have benefits in the treatment of the acute phase of autoimmune CNS inflammation...
  24. pmc Bioluminescence in vivo imaging of autoimmune encephalomyelitis predicts disease
    Jian Luo
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA
    J Neuroinflammation 5:6. 2008
    ..The disease is scored typically by observing signs of paralysis, which do not always correspond with pathological changes...
  25. ncbi request reprint Killing pain, killing neurons?
    Tony Wyss-Coray
    Nat Med 11:472-3. 2005
  26. ncbi request reprint Reduced brain tissue perfusion in TGF-beta 1 transgenic mice showing Alzheimer's disease-like cerebrovascular abnormalities
    Roger F Gaertner
    Laboratoire de Recherches Cerebrovasculaires, CNRS UPR 646, Universite Paris 7, Paris, France
    Neurobiol Dis 19:38-46. 2005
    ....
  27. ncbi request reprint Insights into the pathogenesis of hydrocephalus from transgenic and experimental animal models
    Leslie Crews
    Department of Neurosciences, University of California San Diego, La Jolla 92093 0624, USA
    Brain Pathol 14:312-6. 2004
    ..In this context, the main objective of this manuscript is to provide an overview on the cellular and molecular mechanisms of hydrocephalus based on studies derived from tg and experimental animal models...
  28. ncbi request reprint Transforming growth factor-beta signaling pathway as a therapeutic target in neurodegeneration
    Tony Wyss-Coray
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Mol Neurosci 24:149-53. 2004
    ..Directing the brain's natural mechanisms for clearing Abeta or increasing neuroprotection might therefore be reasonable approaches in interfering with AD pathogenesis...
  29. ncbi request reprint Loss of TGF-beta 1 leads to increased neuronal cell death and microgliosis in mouse brain
    Thomas C Brionne
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    Neuron 40:1133-45. 2003
    ..Because individual TGF-beta1 expression levels in the brain vary considerably between humans, this finding could have important implications for susceptibility to neurodegeneration...
  30. pmc Deficiency in neuronal TGF-beta signaling promotes neurodegeneration and Alzheimer's pathology
    Ina Tesseur
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA
    J Clin Invest 116:3060-9. 2006
    ..These results show that reduced neuronal TGF-beta signaling increases age-dependent neurodegeneration and AD-like disease in vivo. Increasing neuronal TGF-beta signaling may thus reduce neurodegeneration and be beneficial in AD...
  31. ncbi request reprint Small molecule tgf-beta mimetics as potential neuroprotective factors
    Hui Zhang
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    Curr Alzheimer Res 2:183-6. 2005
    ..If active in vivo, these mimetics could be developed into candidates for the treatment of neurodegeneration...
  32. pmc Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1
    Marion S Buckwalter
    Neurology and Neurological Sciences, Stanford University, Stanford, California 94305, USA
    J Neurosci 26:11437-41. 2006
    ..Likewise, levels of TGF-beta1 or other immune factors in brains of AD patients may influence the response to Abeta(1-42) immunization...
  33. ncbi request reprint Global analysis of Smad2/3-dependent TGF-beta signaling in living mice reveals prominent tissue-specific responses to injury
    Amy H Lin
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Immunol 175:547-54. 2005
    ....
  34. ncbi request reprint Neurodegeneration and neuroprotection in multiple sclerosis and other neurodegenerative diseases
    Suhayl Dhib-Jalbut
    UMDNJ Robert Wood Johnson Medical School, New Brunswick, NJ 08901, and The Cleveland Clinic, OH, USA
    J Neuroimmunol 176:198-215. 2006
    ..Elucidating the mechanisms that orchestrate neuronal diseases should facilitate development of neuroprotective and neurorestorative strategies...
  35. ncbi request reprint Inflammation in Alzheimer disease: driving force, bystander or beneficial response?
    Tony Wyss-Coray
    Geriatric Research, Education and Clinical Center, Veterans Administration Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, California 94304, USA
    Nat Med 12:1005-15. 2006
    ..Related factors, on the other hand, elicit beneficial responses and can reduce disease...
  36. ncbi request reprint A role for TGF-beta signaling in neurodegeneration: evidence from genetically engineered models
    Ina Tesseur
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    Curr Alzheimer Res 3:505-13. 2006
    ..Future studies will have to determine whether dysregulation of TGF-beta signaling in neurodegenerative diseases is significant and whether this signaling pathway may even be a target for treatment...
  37. ncbi request reprint Immune cells may fend off Alzheimer disease
    Markus Britschgi
    Nat Med 13:408-9. 2007
  38. ncbi request reprint Orally administered TGF-beta is biologically active in the intestinal mucosa and enhances oral tolerance
    Takashi Ando
    Department of Immunology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan
    J Allergy Clin Immunol 120:916-23. 2007
    ..However, it is unclear whether orally administered TGF-beta, such as TGF-beta in human milk, retains and exerts its activity in the intestinal mucosa and can affect immune response (tolerance) to dietary antigens...
  39. pmc Chronically increased transforming growth factor-beta1 strongly inhibits hippocampal neurogenesis in aged mice
    Marion S Buckwalter
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, SUMC Rm 343A, Stanford, CA 94305 5235, USA
    Am J Pathol 169:154-64. 2006
    ..Together, these data show that TGF-beta1 is a potent inhibitor of hippocampal neural progenitor cell proliferation in adult mice and suggest that it plays a key role in limiting injury and age-related neurogenesis...
  40. pmc Highly sensitive and specific bioassay for measuring bioactive TGF-beta
    Ina Tesseur
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    BMC Cell Biol 7:15. 2006
    ..To study the biological functions of TGF-beta, sensitive, specific, and convenient bioassays are necessary. Here we describe a new cell-based bioassay that fulfills these requirements...
  41. ncbi request reprint Systemic and acquired immune responses in Alzheimer's disease
    Markus Britschgi
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA
    Int Rev Neurobiol 82:205-33. 2007
    ..Here we will review evidence for systemic alterations in immune responses and a role for acquired immunity in AD and discuss their potential contribution to the disease...
  42. pmc Bioluminescence imaging of Smad signaling in living mice shows correlation with excitotoxic neurodegeneration
    Jian Luo
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 103:18326-31. 2006
    ..This and related mouse models may provide valuable tools to study mechanisms and treatments for neurodegeneration...
  43. doi request reprint Microglia--a wrench in the running wheel?
    Saul Villeda
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    Neuron 59:527-9. 2008
    ....
  44. ncbi request reprint Live imaging of Smad2/3 signaling in mouse skin wound healing
    Alphonsus K S Chong
    Division of Plastic and Reconstructive Surgery, Stanford University Medical Center, Stanford, California 94305, USA
    Wound Repair Regen 15:762-6. 2007
    ..Our findings suggest that signaling increases after wound healing, which contrasts with other studies that show raised TGF-beta signaling in the initial days following wounding...
  45. ncbi request reprint In vitro analysis of transforming growth factor-beta1 inhibition in novel transgenic SBE-luciferase mice
    Thomas S Satterwhite
    Section of Plastic Surgery, Department of Veterans Affairs and Division of Plastic Surgery, Stanford University Medical Center, Stanford, CA 94305, USA
    Ann Plast Surg 59:207-13. 2007
    ..A novel transgenic mouse model with a Smad2/3-responsive luciferase reporter construct (SBE-luc) has been developed. We hypothesized that bioluminescence in SBE-luc dermal fibroblasts could be measured to assess TGF-beta1 inhibition...
  46. ncbi request reprint Selective expansion of foxp3-positive regulatory T cells and immunosuppression by suppressors of cytokine signaling 3-deficient dendritic cells
    Yumiko Matsumura
    Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
    J Immunol 179:2170-9. 2007
    ..These results indicate an important role of SOCS3 in determining on immunity or tolerance by DCs...
  47. ncbi request reprint Classification and prediction of clinical Alzheimer's diagnosis based on plasma signaling proteins
    Sandip Ray
    Satoris, Inc, 2686 Middlefield Road, Suite E, Redwood City, California 94063, USA
    Nat Med 13:1359-62. 2007
    ..Biological analysis of the 18 proteins points to systemic dysregulation of hematopoiesis, immune responses, apoptosis and neuronal support in presymptomatic Alzheimer's disease...