Research Topics
Genomes and Genes | John R CirritoSummaryAffiliation: Washington University School of Medicine Country: USA Publications
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Publications
Synaptic activity regulates interstitial fluid amyloid-beta levels in vivoJohn 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...
Acute stress increases interstitial fluid amyloid-beta via corticotropin-releasing factor and neuronal activityJae 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...- Acute dosing of latrepirdine (Dimebon), a possible Alzheimer therapeutic, elevates extracellular amyloid-beta levels in vitro and in vivoJohn 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... - ApoE mimetic peptide decreases Abeta production in vitro and in vivoS 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... - Endocytosis is required for synaptic activity-dependent release of amyloid-beta in vivoJohn 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... - Serotonin signaling is associated with lower amyloid-β levels and plaques in transgenic mice and humansJohn 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... - Characterizing the appearance and growth of amyloid plaques in APP/PS1 micePing 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... - Opposing synaptic regulation of amyloid-β metabolism by NMDA receptors in vivoDeborah 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... - Neuronal activity regulates the regional vulnerability to amyloid-β depositionAdam 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... - Matrix metalloproteinases expressed by astrocytes mediate extracellular amyloid-beta peptide catabolismKe 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... - Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycleJae 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... - Dynamic analysis of amyloid β-protein in behaving mice reveals opposing changes in ISF versus parenchymal Aβ during age-related plaque formationSoyon Hong
Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
J Neurosci 31:15861-9. 2011.... - Abnormal glutamate homeostasis and impaired synaptic plasticity and learning in a mouse model of tuberous sclerosis complexLing 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... - Role of phosphatidylinositol clathrin assembly lymphoid-myeloid leukemia (PICALM) in intracellular amyloid precursor protein (APP) processing and amyloid plaque pathogenesisQingli 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... - Cerebrovascular dysfunction in amyloid precursor protein transgenic mice: contribution of soluble and insoluble amyloid-beta peptide, partial restoration via gamma-secretase inhibitionByung Hee Han
Department of Neurological Surgery, Washington University School of Medicine, St Louis, Missouri 63110, USA
J Neurosci 28:13542-50. 2008.... 
In vivo microdialysis reveals age-dependent decrease of brain interstitial fluid tau levels in P301S human tau transgenic miceKaoru 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...- Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 miceAndrew 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... - Anti-Abeta antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic miceRobert 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... - P-glycoprotein deficiency at the blood-brain barrier increases amyloid-beta deposition in an Alzheimer disease mouse modelJohn 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... - Loss of neprilysin function promotes amyloid plaque formation and causes cerebral amyloid angiopathyWesley 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.... - Bidirectional relationship between functional connectivity and amyloid-β deposition in mouse brainAdam W Bero
Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
J Neurosci 32:4334-40. 2012.... - Matrix metalloproteinase-9 degrades amyloid-beta fibrils in vitro and compact plaques in situPing 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... - In vivo assessment of brain interstitial fluid with microdialysis reveals plaque-associated changes in amyloid-beta metabolism and half-lifeJohn 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... - ApoE and clusterin cooperatively suppress Abeta levels and deposition: evidence that ApoE regulates extracellular Abeta metabolism in vivoRonald 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... - Traumatic brain injury reduces soluble extracellular amyloid-β in mice: a methodologically novel combined microdialysis-controlled cortical impact studyKatherine 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... - Amyloid beta and Alzheimer disease therapeutics: the devil may be in the detailsJohn 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 Grants
- Effect of Human AD Brain-Derived Abeta Species on Synaptic FunctionJohn Cirrito; Fiscal Year: 2007..Understanding the causes of synaptic dysfunction may provide new avenues for diagnosis and treatment of the disease. ..