Tony Wyss-Coray

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. pmc The ageing systemic milieu negatively regulates neurogenesis and cognitive function
    Saul A Villeda
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA
    Nature 477:90-4. 2011
  2. pmc Colony-stimulating factor 1 receptor (CSF1R) signaling in injured neurons facilitates protection and survival
    Jian Luo
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Exp Med 210:157-72. 2013
  3. 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
  4. 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
  5. 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
  6. 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
  7. pmc All-you-can-eat: autophagy in neurodegeneration and neuroprotection
    Philipp A Jaeger
    Geriatric Research Education and Clinical Center, VA Palo Alto Health Care System, 3801 Miranda Ave, Palo Alto, California, USA
    Mol Neurodegener 4:16. 2009
  8. pmc The p75 neurotrophin receptor promotes amyloid-beta(1-42)-induced neuritic dystrophy in vitro and in vivo
    JULIET K KNOWLES
    Department of Neurology and Neurological Science, Stanford University, Stanford, California 94305, USA
    J Neurosci 29:10627-37. 2009
  9. pmc Microglial beclin 1 regulates retromer trafficking and phagocytosis and is impaired in Alzheimer's disease
    Kurt M Lucin
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA Center for Tissue Regeneration, Repair and Restoration, Veterans Administration Palo Alto Health Care System, Palo Alto, CA 94304, USA
    Neuron 79:873-86. 2013
  10. 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

Research Grants

Collaborators

Detail Information

Publications63

  1. pmc The ageing systemic milieu negatively regulates neurogenesis and cognitive function
    Saul A Villeda
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA
    Nature 477:90-4. 2011
    ..Together our data indicate that the decline in neurogenesis and cognitive impairments observed during ageing can be in part attributed to changes in blood-borne factors...
  2. pmc Colony-stimulating factor 1 receptor (CSF1R) signaling in injured neurons facilitates protection and survival
    Jian Luo
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Exp Med 210:157-72. 2013
    ..We conclude that CSF1 and IL-34 provide powerful neuroprotective and survival signals in brain injury and neurodegeneration involving CSF1R expression on neurons...
  3. 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...
  4. 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...
  5. 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...
  6. 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...
  7. pmc All-you-can-eat: autophagy in neurodegeneration and neuroprotection
    Philipp A Jaeger
    Geriatric Research Education and Clinical Center, VA Palo Alto Health Care System, 3801 Miranda Ave, Palo Alto, California, USA
    Mol Neurodegener 4:16. 2009
    ..We will review here the current knowledge of autophagy in the central nervous system and provide an overview of the various models that have been used to study acute and chronic neurodegeneration...
  8. pmc The p75 neurotrophin receptor promotes amyloid-beta(1-42)-induced neuritic dystrophy in vitro and in vivo
    JULIET K KNOWLES
    Department of Neurology and Neurological Science, Stanford University, Stanford, California 94305, USA
    J Neurosci 29:10627-37. 2009
    ....
  9. pmc Microglial beclin 1 regulates retromer trafficking and phagocytosis and is impaired in Alzheimer's disease
    Kurt M Lucin
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA Center for Tissue Regeneration, Repair and Restoration, Veterans Administration Palo Alto Health Care System, Palo Alto, CA 94304, USA
    Neuron 79:873-86. 2013
    ..These findings position beclin 1 as a link between autophagy, retromer trafficking, and receptor-mediated phagocytosis and provide insight into mechanisms by which phagocytosis is regulated and how it may become impaired in AD. ..
  10. 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...
  11. 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...
  12. 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...
  13. pmc Complement receptor 2 is expressed in neural progenitor cells and regulates adult hippocampal neurogenesis
    Maiko Moriyama
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Palo Alto, California 94305, USA
    J Neurosci 31:3981-9. 2011
    ..We conclude that Cr2 regulates hippocampal neurogenesis and propose that increased C3d and IFN-α production associated with brain injury or viral infections may inhibit neurogenesis...
  14. 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
    ....
  15. pmc Deficiency of terminal complement pathway inhibitor promotes neuronal tau pathology and degeneration in mice
    Markus Britschgi
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, 1201 Welch Road MSLS Bldg, Rm P208, Stanford, CA 94305 5489, USA
    J Neuroinflammation 9:220. 2012
    ..Because tauopathies are accompanied by neuroinflammation and the complement cascade forms a key innate immune pathway, we asked whether the complement system has a role in the development of tau pathology...
  16. pmc Antiviral drug ganciclovir is a potent inhibitor of microglial proliferation and neuroinflammation
    Zhaoqing Ding
    Stanford, Department of Radiology Stanford University School of Medicine, Stanford, CA 94305
    J Exp Med 211:189-98. 2014
    ..Our experiments suggest GCV may have beneficial effects in the CNS beyond its antiviral properties. ..
  17. 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...
  18. pmc The immunology of neurodegeneration
    Eva Czirr
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305 5489, USA
    J Clin Invest 122:1156-63. 2012
    ....
  19. pmc Regulation of amyloid precursor protein processing by the Beclin 1 complex
    Philipp A Jaeger
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 5:e11102. 2010
    ..Together, our findings suggest that autophagy and the BECN1-PIK3C3 complex regulate APP processing and play an important role in AD pathology...
  20. 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...
  21. 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...
  22. 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...
  23. 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...
  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. 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
    ....
  26. ncbi request reprint Small molecule p75NTR ligand prevents cognitive deficits and neurite degeneration in an Alzheimer's mouse model
    JULIET K KNOWLES
    Department of Neurology and Neurological Science, Stanford University, Stanford, CA 94304, USA
    Neurobiol Aging 34:2052-63. 2013
    ..These studies reveal that p75(NTR) is an important and tractable in vivo drug target for AD, with LM11A-31 representing a novel class of therapeutic candidates...
  27. 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...
  28. pmc Inflammation in Alzheimer disease-a brief review of the basic science and clinical literature
    Tony Wyss-Coray
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305 5235, USA Geriatric Research Education and Clinical Center, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304, USA
    Cold Spring Harb Perspect Med 2:a006346. 2012
    ..The challenge will be to find ways of fine tuning inflammation to delay, prevent, or treat AD...
  29. 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. ..
  30. 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...
  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. doi request reprint Beclin 1 complex in autophagy and Alzheimer disease
    Philipp A Jaeger
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305 5235, USA
    Arch Neurol 67:1181-4. 2010
    ..It also provides a brief overview of the existing pharmacological interventions available to modulate autophagy activity in mammalian cells...
  33. 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...
  34. pmc Immune activation in brain aging and neurodegeneration: too much or too little?
    Kurt M Lucin
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    Neuron 64:110-22. 2009
    ....
  35. 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. ..
  36. doi request reprint Blood protein signature for the early diagnosis of Alzheimer disease
    Markus Britschgi
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, CA 94305 5235, USA
    Arch Neurol 66:161-5. 2009
    ..Herein, we describe these findings and discuss the potential for a more general application of our proteomic approach in understanding and diagnosing disease...
  37. pmc Modeling of pathological traits in Alzheimer's disease based on systemic extracellular signaling proteome
    Markus Britschgi
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305 5235, USA
    Mol Cell Proteomics 10:M111.008862. 2011
    ..Our study also points to proteins which were previously unknown to be associated with Alzheimer's disease thereby implicating novel signaling pathways in this disorder...
  38. pmc Bioactive TGF-beta can associate with lipoproteins and is enriched in those containing apolipoprotein E3
    Ina Tesseur
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA
    J Neurochem 110:1254-62. 2009
    ..Association of TGF-beta with different types of lipoproteins may facilitate its diffusion, regulate signaling, and offer additional specificity for this important growth factor...
  39. pmc Stem cells as vehicles for youthful regeneration of aged tissues
    Thomas A Rando
    Paul F Glenn Laboratories for the Biology of Aging and Department of Neurology and Neurological Sciences, Stanford University School of Medicine, California Rehabilitation R and D Program, REAP, VA Palo Alto Health Care System, Palo Alto, California
    J Gerontol A Biol Sci Med Sci 69:S39-42. 2014
    ....
  40. pmc Microglial dysfunction in brain aging and Alzheimer's disease
    Kira Irving Mosher
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA Neuroscience IDP Program, Stanford University School of Medicine, Stanford, California 94305, USA
    Biochem Pharmacol 88:594-604. 2014
    ..By calling attention to the commonalities of these two states, we hope to inspire new approaches for dissecting microglial mechanisms. ..
  41. 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...
  42. doi request reprint The circulatory systemic environment as a modulator of neurogenesis and brain aging
    Saul A Villeda
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    Autoimmun Rev 12:674-7. 2013
    ..Finally, we propose the possibility of combating brain aging by tapping into the 'rejuvenating' potential inherent in a young circulatory systemic environment...
  43. pmc APOE ε4 worsens hippocampal CA1 apical neuropil atrophy and episodic memory
    Geoffrey A Kerchner
    From the Departments of Neurology and Neurological Sciences G A K, D B, J C S, J D B, M C F, G K D, T W C and Radiology B K R, Stanford University School of Medicine, Stanford and Center for Tissue Regeneration, Repair and Restoration T W C, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA
    Neurology 82:691-7. 2014
    ..Using high-resolution structural MRI, we endeavored to study the relationships among APOE ε4, hippocampal subfield and stratal anatomy, and episodic memory...
  44. 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...
  45. doi request reprint Bioluminescence analysis of Smad-dependent TGF-beta signaling in live mice
    Jian Luo
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA
    Methods Mol Biol 574:193-202. 2009
    ..SBE-luc and SBE-lucRT mice can be used to study temporal, tissue-specific activation of Smad2/3-dependent signaling in living mice as well as for the identification of endogenous or synthetic modulators of this pathway...
  46. 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...
  47. pmc Sorting through the roles of beclin 1 in microglia and neurodegeneration
    Caitlin E O'Brien
    Cell and Molecular Biology Program, Stanford University, Stanford, CA, 94305, USA
    J Neuroimmune Pharmacol 9:285-92. 2014
    ..Here we summarize these findings and discuss the implications for beclin 1-regulated receptor recycling in neurodegenerative disease. ..
  48. pmc Identification of a central role for complement in osteoarthritis
    Qian Wang
    Geriatric Research Education and Clinical Centers, Veteran s Affairs Palo Alto Health Care System, Palo Alto, California, USA
    Nat Med 17:1674-9. 2011
    ..Our findings indicate that dysregulation of complement in synovial joints has a key role in the pathogenesis of osteoarthritis...
  49. 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...
  50. 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...
  51. 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...
  52. 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...
  53. 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...
  54. 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
    ....
  55. ncbi request reprint Killing pain, killing neurons?
    Tony Wyss-Coray
    Nat Med 11:472-3. 2005
  56. 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
    ....
  57. 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...
  58. ncbi request reprint Immune cells may fend off Alzheimer disease
    Markus Britschgi
    Nat Med 13:408-9. 2007
  59. 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...
  60. 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
    ....
  61. 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...
  62. 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...
  63. 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...

Research Grants26

  1. Live Imaging of Neuronal Injury in Reporter Mice
    Tony Wyss Coray; Fiscal Year: 2006
    ..These, and other reporter mice could also be used to screen drugs for efficacy to interfere with or activate specific signaling pathways in living mice and to assess drug availability in the brain. ..
  2. TGFbeta Signaling in Neurodegeneration and Alzheimer's
    Tony Wyss Coray; Fiscal Year: 2007
    ..These in vivo studies will help us to assess the relevance and potential therapeutic implications of our hypothesis and will evaluate the TGF-bet1 signaling pathway as a potential target for the treatment of Alzheimer's disease. ..
  3. ROLE OF TGF B1 IN CEREBROVASCULAR AMYLOIDOSIS
    Tony Wyss Coray; Fiscal Year: 2002
    ..Our findings will have implications for the pathogenesis of human CAA and Alzheimer's disease in general and will help to assess whether TGF-ß1 could be a future target of therapeutic interventions. ..
  4. MECHANISMS OF APOLIPOPROTEIN E-INDUCED NEUROPROTECTION
    Tony Wyss Coray; Fiscal Year: 2002
    ..These results may help devise novel therapeutic strategies to mimic the beneficial Apo E3 effects or inhibit the detrimental Apo E4 effects in brain injury and neurodegeneration. ..
  5. MECHANISMS OF APOLIPOPROTEIN E-INDUCED NEUROPROTECTION
    Tony Wyss Coray; Fiscal Year: 2004
    ..These results may help devise novel therapeutic strategies to mimic the beneficial Apo E3 effects or inhibit the detrimental Apo E4 effects in brain injury and neurodegeneration. ..
  6. ROLE OF TGF B1 IN CEREBROVASCULAR AMYLOIDOSIS
    Tony Wyss Coray; Fiscal Year: 2001
    ..Our findings will have implications for the pathogenesis of human CAA and Alzheimer's disease in general and will help to assess whether TGF-ß1 could be a future target of therapeutic interventions. ..
  7. TGFbeta signaling in neurodegeneration and Alzhimer's
    Tony Wyss Coray; Fiscal Year: 2006
    ..These in vivo studies will help us to assess the relevance and potential therapeutic implications of our hypothesis and will evaluate the TGF-bet1 signaling pathway as a potential target for the treatment of Alzheimer's disease. ..
  8. Drug Agonists of TGFbeta Signaling to Treat Alzheimer's
    Tony Wyss Coray; Fiscal Year: 2007
    ..This would for the first time bring a novel neuroprotective and amyloid reducing drug based on the TGF-p signaling pathway towards testing in AD. ..
  9. Beclin 1 Neurodegeneration and Alzheimer's Disease
    Tony Wyss Coray; Fiscal Year: 2009
    ..If we inhibit this protein degradation process in AD mice they develop more disease. We propose to study this process to try to reduce disease in mice and possibly in AD. ..
  10. TGFbeta Signaling in Neurodegeneration and Alzheimer's
    Tony Wyss Coray; Fiscal Year: 2009
    ..These in vivo studies will help us to assess the relevance and potential therapeutic implications of our hypothesis and will evaluate the TGF-bet1 signaling pathway as a potential target for the treatment of Alzheimer's disease. ..
  11. Beclin 1 Neurodegeneration and Alzheimer's Disease
    Tony Wyss Coray; Fiscal Year: 2010
    ..If we inhibit this protein degradation process in AD mice they develop more disease. We propose to study this process to try to reduce disease in mice and possibly in AD. ..
  12. ROLE OF TGF B1 IN CEREBROVASCULAR AMYLOIDOSIS
    Tony Wyss Coray; Fiscal Year: 1999
    ..Our findings will have implications for the pathogenesis of human CAA and Alzheimer's disease in general and will help to assess whether TGF-ß1 could be a future target of therapeutic interventions. ..
  13. Controlled Activation of Complement to Treat Alzheimer's
    Tony Wyss Coray; Fiscal Year: 2006
    ..Importantly, the role of complement in the removal of protein aggregates from the brain and in neurodegeneration is of fundamental interest to CNS biology. ..
  14. MECHANISMS OF APOLIPOPROTEIN E-INDUCED NEUROPROTECTION
    Tony Wyss Coray; Fiscal Year: 2005
    ..These results may help devise novel therapeutic strategies to mimic the beneficial Apo E3 effects or inhibit the detrimental Apo E4 effects in brain injury and neurodegeneration. ..
  15. MECHANISMS OF APOLIPOPROTEIN E-INDUCED NEUROPROTECTION
    Tony Wyss Coray; Fiscal Year: 2003
    ..These results may help devise novel therapeutic strategies to mimic the beneficial Apo E3 effects or inhibit the detrimental Apo E4 effects in brain injury and neurodegeneration. ..
  16. ROLE OF TGF B1 IN CEREBROVASCULAR AMYLOIDOSIS
    Tony Wyss Coray; Fiscal Year: 2002
    ..Our findings will have implications for the pathogenesis of human CAA and Alzheimer's disease in general and will help to assess whether TGF-ß1 could be a future target of therapeutic interventions. ..
  17. Controlled Activation of Complement to Treat Alzheimer's
    Tony Wyss Coray; Fiscal Year: 2002
    ..Importantly, the role of complement in the removal of protein aggregates from the brain and in neurodegeneration is of fundamental interest to CNS biology. ..
  18. ROLE OF TGF B1 IN CEREBROVASCULAR AMYLOIDOSIS
    Tony Wyss Coray; Fiscal Year: 2000
    ..Our findings will have implications for the pathogenesis of human CAA and Alzheimer's disease in general and will help to assess whether TGF-ß1 could be a future target of therapeutic interventions. ..
  19. MECHANISMS OF APOLIPOPROTEIN E-INDUCED NEUROPROTECTION
    Tony Wyss Coray; Fiscal Year: 2001
    ..These results may help devise novel therapeutic strategies to mimic the beneficial Apo E3 effects or inhibit the detrimental Apo E4 effects in brain injury and neurodegeneration. ..
  20. TGFbeta signaling in neurodegeneration and Alzhimer's
    Tony Wyss Coray; Fiscal Year: 2010
    ..These in vivo studies will help us to assess the relevance and potential therapeutic implications of our hypothesis and will evaluate the TGF-bet1 signaling pathway as a potential target for the treatment of Alzheimer's disease. ..