Research Topics
Species | Berislav ZlokovicSummaryAffiliation: University of Rochester Country: USA Publications
Research Grants
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Publications
Brain clearance of Alzheimer's amyloid-beta40 in the squirrel monkey: a SPECT study in a primate model of cerebral amyloid angiopathyJames R Bading
Department of Radiology, USC School of Medicine, Los Angeles, CA 90033, USA
J Drug Target 10:359-68. 2002..Thus, vascular clearance plays an important role in reducing Abeta levels in the squirrel monkey brain and impaired Abeta40 elimination across the BBB may contribute to the development of CAA...
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...- Neurovascular mechanisms of Alzheimer's neurodegenerationBerislav V Zlokovic
Frank P Smith Laboratories for Neuroscience and Neurological Surgery Research, Department of Neurological Surgery and Division of Neurovascular Biology, University of Rochester Medical Center, Rochester, NY 14642, USA
Trends Neurosci 28:202-8. 2005.... - 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... - Clearing amyloid through the blood-brain barrierBerislav V Zlokovic
Frank P Smith Laboratories for Neuroscience, Department of Neurological Surgery, University of Rochester Medical Center, New York 14642, USA
J Neurochem 89:807-11. 2004..Thus, understanding A beta exchanges between brain and blood, and vice versa, and developing transport-based systemic A beta-lowering strategies may provide new important insights into pathogenesis and therapeutic control of AD... - Functional recovery after embolic stroke in rodents by activated protein CBerislav V Zlokovic
Department of Neurosurgery and Division of Neurovascular Biology, Frank P Smith Laboratory for Neuroscience and Neurosurgical Research, University of Rochester Medical Center, Rochester, NY 14642, USA
Ann Neurol 58:474-7. 2005..In contrast, tissue plasminogen activator alone was not protective. Thus, activated protein C may be useful as a new stand-alone therapy for clinical stroke and to extend the time window of thrombolytic therapy... - Pericyte-specific expression of PDGF beta receptor in mouse models with normal and deficient PDGF beta receptor signalingEthan A Winkler
Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery, University of Rochester, Rochester, NY, USA
Mol Neurodegener 5:32. 2010.... - New therapeutic targets in the neurovascular pathway in Alzheimer's diseaseBerislav V Zlokovic
Center for Neurodegenerative and Vascular Brain Disorders, Departments of Neurosurgery, University of Rochester Medical School, Rochester, New York 14642, USA
Neurotherapeutics 5:409-14. 2008..g., mesenchyme homeobox gene 2 and myocardin) are also discussed... - Protein S blocks the extrinsic apoptotic cascade in tissue plasminogen activator/N-methyl D-aspartate-treated neurons via Tyro3-Akt-FKHRL1 signaling pathwayHuang Guo
Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery and Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA
Mol Neurodegener 6:13. 2011..abstract:.. 
The blood-brain barrier in health and chronic neurodegenerative disordersBerislav V Zlokovic
Center for Neurodegenerative and Vascular Brain Disorders, Frank P Smith Laboratory for Neuroscience and Neurosurgical Research, University of Rochester Medical School, Rochester, NY 14642, USA
Neuron 57:178-201. 2008..These findings support developments of new therapeutic approaches for chronic neurodegenerative disorders directed at the BBB and other nonneuronal cells of the neurovascular unit...- Cytoprotective protein C pathways and implications for stroke and neurological disordersBerislav V Zlokovic
Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurological Surgery, University of Rochester Medical Center, Rochester, New York, USA
Trends Neurosci 34:198-209. 2011.... - Current treatments and therapeutic targets in Alzheimer's diseaseBerislav V Zlokovic
Department of Neurological Surgery, Division of Neurovascular Biology, University of Rochester Medical Center, NY 14642, USA
Adv Drug Deliv Rev 54:1533-7. 2002 - Vascular disorder in Alzheimer's disease: role in pathogenesis of dementia and therapeutic targetsBerislav V Zlokovic
Frank P Smith Laboratories for Neurosurgery and Division of Neurovascular Biology, Center for Aging and Developmental Biology, University of Rochester Medical Center, Rochester, NY 14642, USA
Adv Drug Deliv Rev 54:1553-9. 2002..In addition, vascularly-based therapeutic strategies to limit the development of beta-amyloidosis and to remove amyloid and plaques from the CNS of AD individuals are discussed... - 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.... - 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.... - Activated protein C promotes neovascularization and neurogenesis in postischemic brain via protease-activated receptor 1Meenakshisundaram Thiyagarajan
Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, Rochester, New York 14642, USA
J Neurosci 28:12788-97. 2008..e., neovascularization and neurogenesis), suggesting a significant extension of the therapeutic window for APC intervention in postischemic brain... - Activated protein C analog with reduced anticoagulant activity improves functional recovery and reduces bleeding risk following controlled cortical impactCorey T Walker
Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, Arthur Kornberg Medical Research Building, 601 Elmwood Ave, Box 670, Rochester, New York 14642, USA
Brain Res 1347:125-31. 2010..Thus, compared to wt-APC, 3K3A-APC is more efficacious and safer therapy for TBI with no risk for intracerebral hemorrhage... - Activated protein C is neuroprotective and mediates new blood vessel formation and neurogenesis after controlled cortical impactAnthony L Petraglia
Department of Neurosurgery, University of Rochester Medical Center, Rochester, New York, USA
Neurosurgery 66:165-71; discussion 171-2. 2010..We used a controlled cortical impact (CCI) in mice to determine the effects of APC on neuroprotection and angiogenesis and neurogenesis after traumatic brain injury (TBI)... - 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... - 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... - Neurovascular mechanisms and blood-brain barrier disorder in Alzheimer's diseaseRobert D Bell
Arthur Kornberg Medical Research Building, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Box 670, Rochester, New York 14642, USA
Acta Neuropathol 118:103-13. 2009..The data reviewed here support an essential role of neurovascular and BBB mechanisms in contributing to both, onset and progression of AD... - 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... - Circulating amyloid-beta peptide crosses the blood-brain barrier in aged monkeys and contributes to Alzheimer's disease lesionsJasmina B Mackic
Department of Neurological Surgery, USC School of Medicine, Los Angeles, CA 90033, USA
Vascul Pharmacol 38:303-13. 2002..Negligible capillary binding, rapid systemic and brain degradation, and accelerated body elimination of blood-borne A beta, may prevent the development of CAA in rhesus in contrast to squirrel monkeys... - 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 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.... - 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... - 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... - 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... - 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.... - 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... - 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... - 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... - Activated protein C prevents neuronal apoptosis via protease activated receptors 1 and 3Huang Guo
Socratech Laboratories, Rochester, NY 14620, USA
Neuron 41:563-72. 2004..Thus, PAR1 and PAR3 mediate anti-apoptotic signaling by APC in neurons, which may suggest novel treatments for neurodegenerative disorders... - 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... - 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... - Activated protein C blocks p53-mediated apoptosis in ischemic human brain endothelium and is neuroprotectiveTong Cheng
Frank P Smith Neurosurgical Research Laboratory, Department of Neurosurgery and Center for Aging and Developmental Biology, Division of Neurovascular Biology, University of Rochester Medical Center, Rochester, New York, USA
Nat Med 9:338-42. 2003..9). Moreover, the in vivo neuroprotective effects of low-dose mouse APC seemed to be independent of its anti-coagulant activity. Thus, APC protects the brain from ischemic injury by acting directly on brain cells... - Species-dependent neuroprotection by activated protein C mutants with reduced anticoagulant activityHuang Guo
Department for Neurosurgery and Neurology, Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, Rochester, New York 14642, USA
J Neurochem 109:116-24. 2009..Thus, 3K3A-APC exhibits species-dependent neuroprotection which should be taken into account when designing human trials for ischemic stroke with APC mutants... - Differential neuroprotection and risk for bleeding from activated protein C with varying degrees of anticoagulant activityYaoming Wang
Department for Neurosurgery, Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, Rochester, NY 14642, USA
Stroke 40:1864-9. 2009..How changes in APC anticoagulant activity influence APC's neuroprotection and risk for bleeding is not clear... - Activated protein C alters cytosolic calcium flux in human brain endothelium via binding to endothelial protein C receptor and activation of protease activated receptor-1Eszter Domotor
Frank P Smith Neurological Research Laboratory, Department of Neurosurgery and Division of Neurovascular Biology, University of Rochester Medical Center, NY 14642, USA
Blood 101:4797-801. 2003..These data suggest that APC regulates [Ca2+]i in human brain endothelium and in HUVECs by binding to EPCR and signaling via PAR-1... - Protein S confers neuronal protection during ischemic/hypoxic injury in miceDong Liu
Frank P. Smith Neurosurgical Research Laboratory, Division of Neurovascular Biology, University of Rochester Medical Center, 601 Elmwood Ave, Box 645, Rochester, NY 14642, USA
Circulation 107:1791-6. 2003..Thus, protein S could be a prototype of a new class of agents for clinical stroke with combined direct neuronal protective effects and systemic antithrombotic and antiinflammatory activities... - 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... - 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... - 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... - 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... - Tissue plasminogen activator neurovascular toxicity is controlled by activated protein CDong Liu
Frank P Smith Laboratory for Neuroscience and Neurosurgical Research, Department of Neurosurgery and Division of Neurovascular Biology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 645, Rochester, New York 14642, USA
Nat Med 10:1379-83. 2004..APC blocks tPA's neurovascular toxicity and may add substantially to the effectiveness of tPA therapy for stroke... - Presence and functional activity of the aryl hydrocarbon receptor in isolated murine cerebral vascular endothelial cells and astrocytesCarissa R Filbrandt
Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Box EHSC, 575 Elmwood Avenue, Rochester, NY 14642, USA
Neurotoxicology 25:605-16. 2004..Together these data indicate endothelial cells and astrocytes are responsive to TCDD through the AhR-mediated pathway and therefore could be targets of toxicity... - 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... - Protein S protects neurons from excitotoxic injury by activating the TAM receptor Tyro3-phosphatidylinositol 3-kinase-Akt pathway through its sex hormone-binding globulin-like regionZhihui Zhong
Center for Neurodegenerative and Vascular Brain Disorders, Department of Neurosurgery and Neurology, University of Rochester Medical Center, Rochester, New York 14642, USA
J Neurosci 30:15521-34. 2010.... - 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... - A simple method for isolation and characterization of mouse brain microvascular endothelial cellsZhenhua Wu
Frank P. Smith Laboratories for Neurosurgery, Department of Neurosurgery and Division for Neurovascular Biology, Center for Aging and Developmental Biology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 645, Rochester, NY 14642, USA
J Neurosci Methods 130:53-63. 2003.... - 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... - Effect of endothelial cell polarity on beta-amyloid-induced migration of monocytes across normal and AD endotheliumRanjit Giri
Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles 90033, USA
Am J Physiol Cell Physiol 283:C895-904. 2002..We suggest that Abeta in the AD brain parenchyma or cerebrovasculature initiates cellular signaling that induces PBM to transmigrate across the BBB and accumulate in the brain... - Recombinant murine-activated protein C is neuroprotective in a murine ischemic stroke modelJose A Fernandez
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
Blood Cells Mol Dis 30:271-6. 2003..The results imply that murine APC is notably superior to human APC for studies of murine disease models, including thrombosis and ischemic brain injury... - 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... - The promise of protein CJohn H Griffin
Department of Molecular and Experimental Medicine, The Scripps Research Institute, MEM180, 10550 N Torrey Pines Road, La Jolla, CA 92037, USA
Blood Cells Mol Dis 36:211-6. 2006..This review summarizes data from clinical observations, from in vitro studies, and from animal models of focal ischemic injury that provide a compelling rationale for clinical trials of APC for ischemic stroke... - Remodeling after strokeBerislav V Zlokovic
Nat Med 12:390-1. 2006 - Mechanism of amyloid peptide induced CCR5 expression in monocytes and its inhibition by siRNA for Egr-1Ranjit K Giri
Department of Biochemistry and Molecular Biology, USC Keck School of Medicine, Los Angeles, CA 90033, USA
Am J Physiol Cell Physiol 289:C264-76. 2005..We suggest that inhibition of Egr-1 by either Egr-1 siRNA or pharmacological agents may reduce activation of monocytes/microglia and possibly ameliorate the inflammation and progression of AD... - Activated protein C and ischemic strokeJohn H Griffin
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA, USA
Crit Care Med 32:S247-53. 2004..CONCLUSIONS: There is compelling evidence that ischemic stroke is an attractive target for therapy with APC... - 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... - The cytoprotective protein C pathwayLaurent O Mosnier
Department of Molecular and Experimental Medicine MEM 180, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA, USA
Blood 109:3161-72. 2007.... - Endothelial cell protein C receptor: role beyond endothelium?Meenakshisundaram Thiyagarajan
Circ Res 100:155-7. 2007 - Coupling of angiogenesis and neurogenesis in cultured endothelial cells and neural progenitor cells after strokeHua Teng
Department of Neurology, Henry Ford Health System, Detroit, Michigan 48202, USA
J Cereb Blood Flow Metab 28:764-71. 2008..These data suggest that angiogenesis couples to neurogenesis after stroke and vascular endothelial growth factor likely mediates this coupling...
Research Grants
- REGULATION OF BRAIN THROMBOSIS IN STROKE MODELSBerislav Zlokovic; Fiscal Year: 2003..Proposed studies will define the role of hypercoagulable state in ischemic stroke and evaluate potential protective vs. deleterious effects of anticoagulant and fibrinolytic therapies for stroke. ..
- Alzheimer's Abeta, apolipoproteins and blood-brain barrierBerislav Zlokovic; Fiscal Year: 2007....
- Protein S: Neurovascular Protection in StrokeBerislav Zlokovic; Fiscal Year: 2007..B. Berk (Rochester) (Tyro 3 RTK-Akt signaling) and Dr. M. Chopp (Henry Ford) (rat stroke model). The results will provide mechanistic insights and test therapeutic agents that may be translated to improved therapy for ischemic stroke. ..
- Cerebrovascular beta-Amyloidosis: A-beta CNS Transport PathwaysBerislav Zlokovic; Fiscal Year: 2007..These studies will provide new therapeutic insights to lower Abeta and prevent development of beta-amyloidosis in AD and familial Abeta-disorders by controlling Abeta CNS transport pathways. ..
- Protein S: Neurovascular Protection in StrokeBerislav Zlokovic; Fiscal Year: 2009..B. Berk (Rochester) (Tyro 3 RTK-Akt signaling) and Dr. M. Chopp (Henry Ford) (rat stroke model). The results will provide mechanistic insights and test therapeutic agents that may be translated to improved therapy for ischemic stroke. ..
- REGULATION OF BRAIN THROMBOSIS IN STROKE MODELSBerislav Zlokovic; Fiscal Year: 2009....
- Protein S: Neurovascular Protection in StrokeBerislav V Zlokovic; Fiscal Year: 2010..B. Berk (Rochester) (Tyro 3 RTK-Akt signaling) and Dr. M. Chopp (Henry Ford) (rat stroke model). The results will provide mechanistic insights and test therapeutic agents that may be translated to improved therapy for ischemic stroke. ..
- REGULATION OF BRAIN THROMBOSIS IN STROKE MODELSBerislav Zlokovic; Fiscal Year: 2007..abstract_text> ..
- AGING BRAIN--CEREBROVASCULAR MECHANISM & AMYLOID BETABerislav Zlokovic; Fiscal Year: 2003..abstract_text> ..
- Alzheimer's ABeta, Apolipoproteins & Blood-Brain BarrierBerislav Zlokovic; Fiscal Year: 2004....
- REGULATION OF BRAIN THROMBOSIS IN STROKE MODELSBerislav V Zlokovic; Fiscal Year: 2010....