Research Topics
Genomes and Genes
| Rashid DeaneSummaryAffiliation: University of Rochester Country: USA Publications
Research Grants
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Detail Information
Publications
The role of the cell surface LRP and soluble LRP in blood-brain barrier Abeta clearance in Alzheimer's diseaseR Deane
Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
Curr Pharm Des 14:1601-5. 2008....
Brain capillary endothelium and choroid plexus epithelium regulate transport of transferrin-bound and free iron into the rat brainRashid Deane
Frank P Smith Neurosurgical Research Laboratory, Department of Neurosurgery, University of Rochester Medical Center, Rochester, New York 14642, USA
J Neurochem 88:813-20. 2004....- Clearance of amyloid-beta peptide across the blood-brain barrier: implication for therapies in Alzheimer's diseaseR Deane
Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
CNS Neurol Disord Drug Targets 8:16-30. 2009.... - SRF and myocardin regulate LRP-mediated amyloid-beta clearance in brain vascular cellsRobert D Bell
Center for Neurodegenerative and Vascular Brain Disorders, Arthur Kornberg Medical Research Building, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, New York 14642, USA
Nat Cell Biol 11:143-53. 2009..Hypoxia stimulated SRF/MYOCD expression in human cerebral VSMCs and in animal models of AD. We suggest that SRF and MYOCD function as a transcriptional switch, controlling Abeta cerebrovascular clearance and progression of AD... - IgG-assisted age-dependent clearance of Alzheimer's amyloid beta peptide by the blood-brain barrier neonatal Fc receptorRashid Deane
Division of Neurovascular Biology, Department of Neurosurgery, Arthur Kornberg Medical Research Building, University of Rochester Medical Center, Rochester, New York 14642, USA
J Neurosci 25:11495-503. 2005..Our data suggest that the FcRn pathway at the BBB plays a crucial role in IgG-assisted Abeta removal from the aging brain... - Pericytes control key neurovascular functions and neuronal phenotype in the adult brain and during brain agingRobert D Bell
Department of Neurosurgery and Neurology, University of Rochester Medical Center, Center for Neurodegenerative and Vascular Brain Disorders, Rochester, NY 14642, USA
Neuron 68:409-27. 2010..Thus, pericytes control key neurovascular functions that are necessary for proper neuronal structure and function, and pericyte loss results in a progressive age-dependent vascular-mediated neurodegeneration... - Method for measurement of the blood-brain barrier permeability in the perfused mouse brain: application to amyloid-beta peptide in wild type and Alzheimer's Tg2576 miceBarbra LaRue
Department of Neurosurgery, Frank P. Smith Neurosurgical Research Laboratory, Center of Aging and Developmental Biology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 670, Rochester, NY 14642, USA
J Neurosci Methods 138:233-42. 2004.... 
Apolipoprotein E controls cerebrovascular integrity via cyclophilin ARobert D Bell
Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, Rochester, New York 14642, USA
Nature 485:512-6. 2012..Our data suggest that CypA is a key target for treating APOE4-mediated neurovascular injury and the resulting neuronal dysfunction and degeneration...- apoE isoform-specific disruption of amyloid beta peptide clearance from mouse brainRashid Deane
Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester Medical School, Rochester, New York 14642, USA
J Clin Invest 118:4002-13. 2008..Thus, apoE isoforms differentially regulate Abeta clearance from the brain, and this might contribute to the effects of APOE genotype on the disease process in both individuals with AD and animal models of AD... - Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cellsZhihui Zhong
Center for Neurodegenerative and Vascular Brain Disorders and Department of Neurological Surgery, University of Rochester Medical Center, Rochester, New York 14642, USA
J Clin Invest 119:3437-49. 2009..The delayed disease progression in mice after APC administration suggests that this approach may be of benefit to patients with familial, and possibly sporadic, ALS... - Clearance of amyloid-beta by circulating lipoprotein receptorsAbhay Sagare
Frank P Smith Laboratory for Neuroscience and Neurosurgical Research, Department of Neurosurgery, University of Rochester Medical School, Rochester, New York 14642, USA
Nat Med 13:1029-31. 2007.... - A multimodal RAGE-specific inhibitor reduces amyloid β-mediated brain disorder in a mouse model of Alzheimer diseaseRashid Deane
Center of Neurodegenerative and Vascular Brain Disorders, University of Rochester, Rochester, New York, USA
J Clin Invest 122:1377-92. 2012..Our data suggest that FPS-ZM1 is a potent multimodal RAGE blocker that effectively controls progression of Aβ-mediated brain disorder and that it may have the potential to be a disease-modifying agent for AD... - Endothelial protein C receptor-assisted transport of activated protein C across the mouse blood-brain barrierRashid Deane
Department of Neurosurgery, Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, Rochester, New York 14642, USA
J Cereb Blood Flow Metab 29:25-33. 2009..APC brain uptake was reduced by 64% in severely deficient EPCR mice, but not in PAR1 null mice. These data suggest that APC and its variants with reduced anticoagulant activity cross the BBB via EPCR-mediated saturable transport... - Protein S controls hypoxic/ischemic blood-brain barrier disruption through the TAM receptor Tyro3 and sphingosine 1-phosphate receptorDonghui Zhu
Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester Medical Center, NY, USA
Blood 115:4963-72. 2010..Our findings indicate that PS protects the BBB integrity via Tyro3 and S1P(1), suggesting potentially novel treatments for neurovascular dysfunction resulting from hypoxic/ischemic BBB damage... - Neuroprotective activities of activated protein C mutant with reduced anticoagulant activityHuang Guo
Department for Neurosurgery and Neurology, Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, Rochester, NY 14642, USA
Eur J Neurosci 29:1119-30. 2009..Thus, 3K3A-APC offers a new approach for safer and more efficacious treatments of neurodegenerative disorders and stroke with APC... - Impaired spine formation and learning in GPCR kinase 2 interacting protein-1 (GIT1) knockout micePrashanthi Menon
Aab Cardiovascular Research Institute and Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Brain Res 1317:218-26. 2010..Thus, our data suggest that GIT1 plays an important role in brain in vivo by regulating spine density involved in synaptic plasticity that is required for processes involved in learning... - RAGE (yin) versus LRP (yang) balance regulates alzheimer amyloid beta-peptide clearance through transport across the blood-brain barrierRashid Deane
Frank P. Smith Laboratories for Neuroscience and Neurosurgical Research, Department of Neurological Surgery and Division of Neurovascular Biology, University of Rochester Medical Center, Rochester, NY, USA
Stroke 35:2628-31. 2004.... - Role of the MEOX2 homeobox gene in neurovascular dysfunction in Alzheimer diseaseZhenhua Wu
Frank P Smith Laboratories for Neuroscience and Neurosurgical Research, University of Rochester Medical Center, Arthur Kornberg Medical Research Building, 601 Elmwood Avenue, Box 670, Rochester, New York 14642, USA
Nat Med 11:959-65. 2005..The link of MEOX2 to neurovascular dysfunction in Alzheimer disease provides new mechanistic and therapeutic insights into this illness... - Role of the blood-brain barrier in the pathogenesis of Alzheimer's diseaseRashid Deane
Frank P Smith Laboratory for Neuroscience and Neurosurgical Research, University of Rochester Medical Center, Rochester, NY 14642, USA
Curr Alzheimer Res 4:191-7. 2007..These findings provide insights into new pathogenic pathways for the vascular dysfunction in AD and point to new therapeutic targets for AD... - Serum response factor and myocardin mediate arterial hypercontractility and cerebral blood flow dysregulation in Alzheimer's phenotypeNienwen Chow
Socratech Research Laboratories L L C, Department of Neurosurgery, University of Rochester School of Medicine, 601 Elmwood Avenue, Rochester, NY 14642, USA
Proc Natl Acad Sci U S A 104:823-8. 2007..Thus, SRF-MYOCD overexpression in small cerebral arteries appears to initiate independently of Abeta a pathogenic pathway mediating arterial hypercontractility and CBF dysregulation, which are associated with Alzheimer's dementia... - Transport pathways for clearance of human Alzheimer's amyloid beta-peptide and apolipoproteins E and J in the mouse central nervous systemRobert D Bell
Frank P Smith Laboratory for Neuroscience and Neurosurgical Research, Department of Neurosurgery, University of Rochester Medical Center, Rochester, New York 14642, USA
J Cereb Blood Flow Metab 27:909-18. 2007..7-fold, whereas Abeta42 binding to apoJ enhanced Abeta42 BBB clearance rate by 83%. Thus, Abeta, apoE, and apoJ are cleared from brain by different transport pathways, and apoE and apoJ may critically modify Abeta clearance at the BBB... - Low-density lipoprotein receptor-related protein-1: a serial clearance homeostatic mechanism controlling Alzheimer's amyloid β-peptide elimination from the brainBerislav V Zlokovic
Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, Rochester, New York 14642, USA
J Neurochem 115:1077-89. 2010..We suggest that LRP1 has a critical role in AD pathogenesis and is an important therapeutic target in AD... - LRP/amyloid beta-peptide interaction mediates differential brain efflux of Abeta isoformsRashid Deane
Frank P Smith Laboratories for Neuroscience and Neurosurgical Research, Department of Neurosurgery, Arthur Kornberg Medical Research Building, University of Rochester Medical Center, Rochester, NY 14642, USA
Neuron 43:333-44. 2004..Thus, low-affinity LRP/Abeta interaction and/or Abeta-induced LRP loss at the BBB mediate brain accumulation of neurotoxic Abeta... - ALS-causing SOD1 mutants generate vascular changes prior to motor neuron degenerationZhihui Zhong
Center for Neurodegenerative and Vascular Brain Disorders and Department of Neurosurgery, University of Rochester Medical Center, Kornberg Medical Research Bldg, 601 Elmwood Avenue, Box 670, Rochester, New York 14642, USA
Nat Neurosci 11:420-2. 2008..SOD1 mutant-mediated endothelial damage accumulated before motor neuron degeneration and the neurovascular inflammatory response occurred, indicating that it was a central contributor to disease initiation... - Impaired lipoprotein receptor-mediated peripheral binding of plasma amyloid-β is an early biomarker for mild cognitive impairment preceding Alzheimer's diseaseAbhay P Sagare
Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester, Rochester, NY, USA
J Alzheimers Dis 24:25-34. 2011.... - Neurovascular pathways and Alzheimer amyloid beta-peptideBerislav V Zlokovic
Frank R Smith Laboratories for Neuroscience and Neurosurgical Research, University of Rochester Medical Center, Rochester, NY 14642, USA
Brain Pathol 15:78-83. 2005..We suggest that there is a link between neurovascular dysfunction and elevated brain Abeta which provides a new scenario for therapeutic interventions to control Alzheimer mental deterioration... - Activated protein C inhibits tissue plasminogen activator-induced brain hemorrhageTong Cheng
Frank P. Smith Laboratory for Neuroscience and Neurosurgical Research, Department of Neurosurgery, University of Rochester Medical Center, Rochester, New York 14642, USA
Nat Med 12:1278-85. 2006..The present findings suggest that APC may improve thrombolytic therapy for stroke, in part, by reducing tPA-mediated hemorrhage... - Methamphetamine causes sustained depression in cerebral blood flowOksana Polesskaya
Department of Microbiology and Immunology, The University of Rochester Medical Center, 575 Elmwood Avenue, Rochester, NY 14642, USA
Brain Res 1373:91-100. 2011..These findings show that even a single, acute exposure to MA can result in profound changes in CBF, with potentially deleterious consequences for brain function... - RAGE mediates amyloid-beta peptide transport across the blood-brain barrier and accumulation in brainRashid Deane
Frank P Smith Laboratories for Neurosurgery, Department of Neurosurgery and Division of Neurovascular Biology, Center for Aging and Developmental Biology, University of Rochester Medical Center, Rochester, New York 14642, USA
Nat Med 9:907-13. 2003..These findings suggest that vascular RAGE is a target for inhibiting pathogenic consequences of Abeta-vascular interactions, including development of cerebral amyloidosis... - Two-photon imaging of astrocytic Ca2+ signaling and the microvasculature in experimental mice models of Alzheimer's diseaseTakahiro Takano
Department of Neurosurgery, Center for Aging and Developmental Biology, University of Rochester Medical Center, 601 Elmwood Ave, Box 645, Rochester, NY 14642, USA
Ann N Y Acad Sci 1097:40-50. 2007.... - 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... - Early-onset and robust cerebral microvascular accumulation of amyloid beta-protein in transgenic mice expressing low levels of a vasculotropic Dutch/Iowa mutant form of amyloid beta-protein precursorJudianne Davis
Department of Medicine, Health Sciences Center, Stony Brook University, Stony Brook, NY 11794 8153, USA
J Biol Chem 279:20296-306. 2004..These results with Tg-SwDI mice demonstrate that overexpression of human AbetaPP is not required for early-onset and robust accumulation of both vascular and parenchymal Abeta in mouse brain... - Role of transthyretin in thyroxine transfer from cerebrospinal fluid to brain and choroid plexusNouhad A Kassem
King s College London, Institute of Gerontology and Wolfson Centre for Age Related Diseases, Hodgkin Bldg, Guy s Hospital Campus, London SE1 1UL, UK
Am J Physiol Regul Integr Comp Physiol 291:R1310-5. 2006..These results support a role for TTR in the distribution of T4 from CSF into brain sites around the ventricular system, indicating those areas involved in neurogenesis (ER and HC)... - Thyroxine (T4) transfer from CSF to choroid plexus and ventricular brain regions in rabbit: contributory role of P-glycoprotein and organic anion transporting polypeptidesNouhad A Kassem
King s College London, Pharmaceutical Sciences Research Division, Hodgkin Building, Guy s Campus London SE1 1UL, UK
Brain Res 1181:44-50. 2007..We conclude that P-gp and oatps contribute to the transfer of 125I-T4 between the CSF, CP and brain, hence regulating 125I-T4 availability in CSF... - Transport of L-[125I]thyroxine by in situ perfused ovine choroid plexus: inhibition by lead exposureWei Zheng
Department of Environmental Health Sciences, School of Public Health, Columbia University, New York, New York, USA
J Toxicol Environ Health A 66:435-51. 2003..Data suggest that the choroid plexus may serve as a significant site for T4 transport into the CSF, and Pb exposure may hinder the influx of T4 from the blood into the choroid plexus...
Research Grants
- Iron regulation at the CNS vascular barriers and agingRashid Deane; Fiscal Year: 2006..abstract_text> ..
- Copper's Role in Brain LRP-mediated Abeta Efflux and AgingRashid Deane; Fiscal Year: 2010..These studies may provide new therapeutic insights on how to lower brain A by controlling its CNS barriers transport in Cu-potentiated neurodegenerative disorders. ..