Markus Britschgi

Summary

Affiliation: F. Hoffmann-La Roche Ltd

Publications

  1. 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
  2. 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
  3. 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
  4. 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
  5. doi 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
  6. 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
  7. ncbi 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
  8. 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

Collaborators

Detail Information

Publications8

  1. 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...
  2. 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...
  3. 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...
  4. 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...
  5. doi 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...
  6. 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...
  7. ncbi 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...
  8. 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...