Research Topics
Genomes and Genes
| Tony Wyss-CoraySummaryAffiliation: Stanford University Country: USA Publications
Research Grants
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Detail Information
Publications
Tgf-Beta pathway as a potential target in neurodegeneration and Alzheimer'sTony 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...- 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... - Transforming growth factor-beta signaling pathway as a therapeutic target in neurodegenerationTony 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... 
All-you-can-eat: autophagy in neurodegeneration and neuroprotectionPhilipp 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...- Loss of TGF-beta 1 leads to increased neuronal cell death and microgliosis in mouse brainThomas 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... - Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitisJian 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... - Neural progenitor cells regulate microglia functions and activityKira I Mosher
1 Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA 2 Neuroscience IDP Program, Stanford University School of Medicine, Stanford, California, USA 3
Nat Neurosci 15:1485-7. 2012..Thus, neural precursor cells may not only be shaped by microglia, but also regulate microglia functions and activity... - Global analysis of Smad2/3-dependent TGF-beta signaling in living mice reveals prominent tissue-specific responses to injuryAmy H Lin
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
J Immunol 175:547-54. 2005.... - Deficiency in neuronal TGF-beta signaling promotes neurodegeneration and Alzheimer's pathologyIna 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... - The p75 neurotrophin receptor promotes amyloid-beta(1-42)-induced neuritic dystrophy in vitro and in vivoJULIET K KNOWLES
Department of Neurology and Neurological Science, Stanford University, Stanford, California 94305, USA
J Neurosci 29:10627-37. 2009.... - The immunology of neurodegenerationEva Czirr
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305 5489, USA
J Clin Invest 122:1156-63. 2012.... - The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in miceFiona 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... - Complement receptor 2 is expressed in neural progenitor cells and regulates adult hippocampal neurogenesisMaiko 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... - Regulation of amyloid precursor protein processing by the Beclin 1 complexPhilipp 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... - Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1Marion 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... - Live imaging of Smad2/3 signaling in mouse skin wound healingAlphonsus 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... - Bioluminescence in vivo imaging of autoimmune encephalomyelitis predicts diseaseJian 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... 
Highly sensitive and specific bioassay for measuring bioactive TGF-betaIna 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...- Angiotensin II sustains brain inflammation in mice via TGF-betaTobias 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... - Chronically increased transforming growth factor-beta1 strongly inhibits hippocampal neurogenesis in aged miceMarion 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... 
Beclin 1 complex in autophagy and Alzheimer diseasePhilipp 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...- A role for TGF-beta signaling in neurodegeneration: evidence from genetically engineered modelsIna 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... - 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.... - Modeling of pathological traits in Alzheimer's disease based on systemic extracellular signaling proteomeMarkus 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... - The ageing systemic milieu negatively regulates neurogenesis and cognitive functionSaul 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... - Bioactive TGF-beta can associate with lipoproteins and is enriched in those containing apolipoprotein E3Ina 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... - Small molecule tgf-beta mimetics as potential neuroprotective factorsHui 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... - Bioluminescence imaging of Smad signaling in living mice shows correlation with excitotoxic neurodegenerationJian 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... - Deficiency of terminal complement pathway inhibitor promotes neuronal tau pathology and degeneration in miceMarkus 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..abstract:.. - Blood protein signature for the early diagnosis of Alzheimer diseaseMarkus 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... - 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.... - In vitro analysis of transforming growth factor-beta1 inhibition in novel transgenic SBE-luciferase miceThomas 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... - Systemic and acquired immune responses in Alzheimer's diseaseMarkus 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... - Adult mouse astrocytes degrade amyloid-beta in vitro and in situTony 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... - Bioluminescence analysis of Smad-dependent TGF-beta signaling in live miceJian 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... - Neurodegeneration and neuroprotection in multiple sclerosis and other neurodegenerative diseasesSuhayl 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... - Molecular and functional dissection of TGF-beta1-induced cerebrovascular abnormalities in transgenic miceMarion 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... - Inflammation in neurodegenerative disease--a double-edged swordTony 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... - Immune cells may fend off Alzheimer diseaseMarkus Britschgi
Nat Med 13:408-9. 2007 - Genes contributing to prion pathogenesisGULTEKIN TAMGUNEY
Institute for Neurodegenerative Diseases, University of California, San Francisco, CA, USA
J Gen Virol 89:1777-88. 2008.... - Killing pain, killing neurons?Tony Wyss-Coray
Nat Med 11:472-3. 2005 - Reduced brain tissue perfusion in TGF-beta 1 transgenic mice showing Alzheimer's disease-like cerebrovascular abnormalitiesRoger F Gaertner
Laboratoire de Recherches Cerebrovasculaires, CNRS UPR 646, Universite Paris 7, Paris, France
Neurobiol Dis 19:38-46. 2005.... - Insights into the pathogenesis of hydrocephalus from transgenic and experimental animal modelsLeslie 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... - Prominent neurodegeneration and increased plaque formation in complement-inhibited Alzheimer's miceTony 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.... - Neuron-specific apolipoprotein e4 proteolysis is associated with increased tau phosphorylation in brains of transgenic miceWalter 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... - Astroglial regulation of apolipoprotein E expression in neuronal cells. Implications for Alzheimer's diseaseFaith 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... - Selective expansion of foxp3-positive regulatory T cells and immunosuppression by suppressors of cytokine signaling 3-deficient dendritic cellsYumiko 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... - Orally administered TGF-beta is biologically active in the intestinal mucosa and enhances oral toleranceTakashi 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... - Classification and prediction of clinical Alzheimer's diagnosis based on plasma signaling proteinsSandip 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... - Carboxyl-terminal-truncated apolipoprotein E4 causes Alzheimer's disease-like neurodegeneration and behavioral deficits in transgenic miceFaith 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...
Research Grants
- Live Imaging of Neuronal Injury in Reporter MiceTony 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. ..
- Controlled Activation of Complement to Treat Alzheimer'sTony 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. ..
- Drug Agonists of TGFbeta Signaling to Treat Alzheimer'sTony 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. ..
- TGFbeta Signaling in Neurodegeneration and Alzheimer'sTony 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. ..
- Beclin 1 Neurodegeneration and Alzheimer's DiseaseTony 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. ..
- MECHANISMS OF APOLIPOPROTEIN E-INDUCED NEUROPROTECTIONTony 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. ..
- ROLE OF TGF B1 IN CEREBROVASCULAR AMYLOIDOSISTony 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. ..
- TGFbeta signaling in neurodegeneration and Alzhimer'sTony 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. ..