John R Cirrito

Summary

Affiliation: Washington University School of Medicine
Country: USA

Publications

  1. ncbi request reprint Synaptic activity regulates interstitial fluid amyloid-beta levels in vivo
    John R Cirrito
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Neuron 48:913-22. 2005
  2. pmc Acute stress increases interstitial fluid amyloid-beta via corticotropin-releasing factor and neuronal activity
    Jae Eun Kang
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 104:10673-8. 2007
  3. pmc Acute dosing of latrepirdine (Dimebon), a possible Alzheimer therapeutic, elevates extracellular amyloid-beta levels in vitro and in vivo
    John W Steele
    Departments of Neurology, Psychiatry and Alzheimer s Disease Research Center, Mount Sinai School of Medicine, New York, NY, 10029, USA
    Mol Neurodegener 4:51. 2009
  4. pmc ApoE mimetic peptide decreases Abeta production in vitro and in vivo
    S Sakura Minami
    Department of Neuroscience, Georgetown University, 3970 Reservoir Rd, NW, Washington, DC 20057, USA
    Mol Neurodegener 5:16. 2010
  5. pmc Endocytosis is required for synaptic activity-dependent release of amyloid-beta in vivo
    John R Cirrito
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neuron 58:42-51. 2008
  6. pmc Serotonin signaling is associated with lower amyloid-β levels and plaques in transgenic mice and humans
    John R Cirrito
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 108:14968-73. 2011
  7. pmc Neuronal activity regulates extracellular tau in vivo
    Kaoru Yamada
    Department of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer s Disease Research Center, Washington University School of Medicine, St Louis, MO 63110
    J Exp Med 211:387-93. 2014
  8. pmc Characterizing the appearance and growth of amyloid plaques in APP/PS1 mice
    Ping Yan
    Department of Neurology and the Hope Center for Neurological Disorders, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 29:10706-14. 2009
  9. pmc Opposing synaptic regulation of amyloid-β metabolism by NMDA receptors in vivo
    Deborah K Verges
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 31:11328-37. 2011
  10. pmc Neuronal activity regulates the regional vulnerability to amyloid-β deposition
    Adam W Bero
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri, USA
    Nat Neurosci 14:750-6. 2011

Research Grants

Collaborators

Detail Information

Publications32

  1. ncbi request reprint Synaptic activity regulates interstitial fluid amyloid-beta levels in vivo
    John R Cirrito
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Neuron 48:913-22. 2005
    ..The findings also have important implications for treatment development...
  2. pmc Acute stress increases interstitial fluid amyloid-beta via corticotropin-releasing factor and neuronal activity
    Jae Eun Kang
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 104:10673-8. 2007
    ..Thus, behavioral stressors can rapidly increase ISF Abeta through neuronal activity in a CRF-dependent manner, and the results suggest a mechanism by which behavioral stress may affect Alzheimer's disease pathogenesis...
  3. pmc Acute dosing of latrepirdine (Dimebon), a possible Alzheimer therapeutic, elevates extracellular amyloid-beta levels in vitro and in vivo
    John W Steele
    Departments of Neurology, Psychiatry and Alzheimer s Disease Research Center, Mount Sinai School of Medicine, New York, NY, 10029, USA
    Mol Neurodegener 4:51. 2009
    ..In the current study, we assessed the effect of acute dosing of latrepirdine on levels of extracellular Abeta using in vitro and in vivo experimental systems...
  4. pmc ApoE mimetic peptide decreases Abeta production in vitro and in vivo
    S Sakura Minami
    Department of Neuroscience, Georgetown University, 3970 Reservoir Rd, NW, Washington, DC 20057, USA
    Mol Neurodegener 5:16. 2010
    ..Here, we further examined whether peptides containing tandem repeats of the apoE receptor-binding region (amino acids 141-149) affected APP trafficking, APP processing, and Abeta production...
  5. pmc Endocytosis is required for synaptic activity-dependent release of amyloid-beta in vivo
    John R Cirrito
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neuron 58:42-51. 2008
    ..These findings have implications for AD pathogenesis and may provide insights into therapeutic intervention...
  6. pmc Serotonin signaling is associated with lower amyloid-β levels and plaques in transgenic mice and humans
    John R Cirrito
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 108:14968-73. 2011
    ..Cumulative time of antidepressant use within the 5-y period preceding the scan correlated with less plaque load. These data suggest that serotonin signaling was associated with less Aβ accumulation in cognitively normal individuals...
  7. pmc Neuronal activity regulates extracellular tau in vivo
    Kaoru Yamada
    Department of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer s Disease Research Center, Washington University School of Medicine, St Louis, MO 63110
    J Exp Med 211:387-93. 2014
    ..The in vivo results provide one mechanism underlying neuronal tau release and may link trans-synaptic spread of tau pathology with synaptic activity itself...
  8. pmc Characterizing the appearance and growth of amyloid plaques in APP/PS1 mice
    Ping Yan
    Department of Neurology and the Hope Center for Neurological Disorders, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 29:10706-14. 2009
    ..Together, these findings indicate that individual amyloid plaque growth in vivo occurs over a period of weeks and may be influenced by interstitial Abeta concentration as well as reactive gliosis...
  9. pmc Opposing synaptic regulation of amyloid-β metabolism by NMDA receptors in vivo
    Deborah K Verges
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 31:11328-37. 2011
    ..NMDA receptor antagonists increase ISF Aβ levels, suggesting that basal activity at these receptors normally suppresses Aβ levels in vivo. This has implications for understanding normal Aβ metabolism as well as AD pathogenesis...
  10. pmc Neuronal activity regulates the regional vulnerability to amyloid-β deposition
    Adam W Bero
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri, USA
    Nat Neurosci 14:750-6. 2011
    ..Long-term unilateral vibrissal deprivation decreased amyloid plaque formation and growth. Our results suggest a mechanism to account for the vulnerability of specific brain regions to Aβ deposition in Alzheimer's disease...
  11. pmc Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle
    Jae Eun Kang
    Department of Neurology, Washington University, St Louis, MO 63110, USA
    Science 326:1005-7. 2009
    ..Thus, the sleep-wake cycle and orexin may play a role in the pathogenesis of Alzheimer's disease...
  12. ncbi request reprint Matrix metalloproteinases expressed by astrocytes mediate extracellular amyloid-beta peptide catabolism
    Ke Jie Yin
    Department of Neurology and the Hope Center for Neurological Disorders, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 26:10939-48. 2006
    ..These results suggest that MMP-2 and -9 may contribute to extracellular brain Abeta clearance by promoting Abeta catabolism...
  13. pmc Dynamic analysis of amyloid β-protein in behaving mice reveals opposing changes in ISF versus parenchymal Aβ during age-related plaque formation
    Soyon Hong
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 31:15861-9. 2011
    ....
  14. pmc Abnormal glutamate homeostasis and impaired synaptic plasticity and learning in a mouse model of tuberous sclerosis complex
    Ling Hui Zeng
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurobiol Dis 28:184-96. 2007
    ..These results suggest that abnormal glutamate homeostasis predisposes to excitotoxic cell death, impaired synaptic plasticity and learning deficits in Tsc1 GFAP CKO mice...
  15. pmc Neuronal clearance of amyloid-β by endocytic receptor LRP1
    Takahisa Kanekiyo
    Department of Neuroscience, Mayo Clinic, Jacksonville, Florida 32224, Department of Neurology, Knight Alzheimer s Disease Research Center, and Hope Center for Neurological Disorders, Washington University, St Louis, Missouri 63110, and Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen 361005, China
    J Neurosci 33:19276-83. 2013
    ..Together, our results demonstrate that LRP1 plays an important role in receptor-mediated clearance of Aβ and indicate that neurons not only produce but also clear Aβ. ..
  16. pmc Role of phosphatidylinositol clathrin assembly lymphoid-myeloid leukemia (PICALM) in intracellular amyloid precursor protein (APP) processing and amyloid plaque pathogenesis
    Qingli Xiao
    Hope Center for Neurological Disorders and Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 287:21279-89. 2012
    ..PICALM contributes to amyloid plaque load in brain likely via its effect on Aβ metabolism...
  17. pmc Antisense reduction of tau in adult mice protects against seizures
    Sarah L DeVos
    Department of Neurology, Hope Center for Neurological Disorders, Washington University, St Louis, Missouri 63110, USA
    J Neurosci 33:12887-97. 2013
    ....
  18. pmc Amyloid-β oligomerization in Alzheimer dementia versus high-pathology controls
    Thomas J Esparza
    Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
    Ann Neurol 73:104-19. 2013
    ..However, the lack of a sensitive, specific, and quantitative assay for Aβ oligomers has hampered rigorous tests of this hypothesis...
  19. pmc Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice
    Andrew W Kraft
    The Hope Center for Neurological Disorders, Knight Alzheimer s Disease Research Center, Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63124, USA
    FASEB J 27:187-98. 2013
    ..These results suggest that astrocyte activation limits plaque growth and attenuates plaque-related dystrophic neurites. These activities may require intimate contact between astrocyte and plaque...
  20. doi request reprint In vivo microdialysis reveals age-dependent decrease of brain interstitial fluid tau levels in P301S human tau transgenic mice
    Kaoru Yamada
    Department of Neurology, Hope Center for Neurological Disorders, Washington University, St Louis, Missouri 63110, USA
    J Neurosci 31:13110-7. 2011
    ..This technique should facilitate further studies of tau secretion, spread of tau pathology, the effects of different disease states on ISF tau, and the efficacy of experimental treatments...
  21. pmc Cerebrovascular dysfunction in amyloid precursor protein transgenic mice: contribution of soluble and insoluble amyloid-beta peptide, partial restoration via gamma-secretase inhibition
    Byung Hee Han
    Department of Neurological Surgery, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 28:13542-50. 2008
    ....
  22. pmc In vivo measurement of apolipoprotein E from the brain interstitial fluid using microdialysis
    JASON D ULRICH
    Department of Neurology, Saint Louis, MO, USA
    Mol Neurodegener 8:13. 2013
    ..We have developed an assay to measure apoE levels in the brain interstitial fluid of awake and freely moving mice using large molecular weight cut-off microdialysis probes...
  23. pmc Loss of neprilysin function promotes amyloid plaque formation and causes cerebral amyloid angiopathy
    Wesley Farris
    Center for Neurologic Diseases, Department of Neurology, Harvard Institutes of Medicine, Room 730, Boston, MA 02115, USA
    Am J Pathol 171:241-51. 2007
    ....
  24. pmc P-glycoprotein deficiency at the blood-brain barrier increases amyloid-beta deposition in an Alzheimer disease mouse model
    John R Cirrito
    Department of Neurology, Washington University Medical School, St Louis, Missouri 63110, USA
    J Clin Invest 115:3285-90. 2005
    ..These data establish a direct link between Pgp and Abeta metabolism in vivo and suggest that Pgp activity at the BBB could affect risk for developing AD as well as provide a novel diagnostic and therapeutic target...
  25. pmc Anti-Abeta antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice
    Robert P Brendza
    Department of Neurology and Hope Center for Neurological Disorders, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Clin Invest 115:428-33. 2005
    ..This analysis suggests that ongoing axonal and dendritic damage is secondary to Abeta and is, in part, rapidly reversible...
  26. pmc Genetic suppression of transgenic APP rescues Hypersynchronous network activity in a mouse model of Alzeimer's disease
    Heather A Born
    Department of Neuroscience, Department of Neurology, Department of Molecular and Cellular Biology, Department of Human and Molecular Genetics, Department of Neurosurgery, The Jan and Dan Duncan Neurological Research Institute, and the Huffington Center on Aging, Baylor College of Medicine, Houston, Texas 77030, Texas A and M Health Science Center, College Station, Texas 77843, Department of Neuroscience, Mayo Clinic, Jacksonville, Florida 32224, Department of Computational and Applied Mathematics, Rice University, Houston, Texas 77251, Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, and Department of Neuroscience, University of Florida, Gainesville, Florida 32610
    J Neurosci 34:3826-40. 2014
    ..Our results suggest that APP overexpression, and not Aβ overproduction, is responsible for EEG abnormalities in our transgenic mice and can be rescued independently of pathology. ..
  27. pmc Bidirectional relationship between functional connectivity and amyloid-β deposition in mouse brain
    Adam W Bero
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Neurosci 32:4334-40. 2012
    ....
  28. ncbi request reprint Matrix metalloproteinase-9 degrades amyloid-beta fibrils in vitro and compact plaques in situ
    Ping Yan
    Department of Neurology and the Hope Center for Neurological Disorders, Division of Endocrinology, Diabetes, Metabolism, and Lipid Research, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 281:24566-74. 2006
    ..These findings suggest that MMP-9 can degrade fAbeta and may contribute to ongoing clearance of plaques from amyloid-laden brains...
  29. ncbi request reprint In vivo assessment of brain interstitial fluid with microdialysis reveals plaque-associated changes in amyloid-beta metabolism and half-life
    John R Cirrito
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 23:8844-53. 2003
    ..This now measurable in vivo pool is a likely target for new diagnostic and therapeutic strategies...
  30. ncbi request reprint ApoE and clusterin cooperatively suppress Abeta levels and deposition: evidence that ApoE regulates extracellular Abeta metabolism in vivo
    Ronald B DeMattos
    Neuroscience Discovery Research, Lilly Research Laboratories, Indianapolis, IN 46285, USA
    Neuron 41:193-202. 2004
    ..These findings demonstrate additive effects of apoE and clusterin on influencing Abeta deposition and that apoE plays an important role in regulating extracellular CNS Abeta metabolism independent of Abeta synthesis...
  31. pmc Traumatic brain injury reduces soluble extracellular amyloid-β in mice: a methodologically novel combined microdialysis-controlled cortical impact study
    Katherine E Schwetye
    Washington University School of Medicine, Department of Neurology and Hope Center for Neurological Disorders, 660 S Euclid Ave Box 8111, St Louis, MO 63110, USA
    Neurobiol Dis 40:555-64. 2010
    ..Reduced neuronal activity may contribute, though the underlying mechanisms have not been definitively determined. Further work will be needed to assess the dynamics of insoluble and oligomeric Aβ after TBI...
  32. pmc Amyloid beta and Alzheimer disease therapeutics: the devil may be in the details
    John R Cirrito
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Clin Invest 112:321-3. 2003
    ..The work suggests that further testing of the therapeutic utility of these types of compounds for the potential treatment of AD is warranted...

Research Grants2

  1. Effect of Human AD Brain-Derived Abeta Species on Synaptic Function
    John Cirrito; Fiscal Year: 2007
    ..Understanding the causes of synaptic dysfunction may provide new avenues for diagnosis and treatment of the disease. ..