Costantino Iadecola

Summary

Affiliation: Cornell University
Country: USA

Publications

  1. ncbi request reprint Neurovascular regulation in the normal brain and in Alzheimer's disease
    Costantino Iadecola
    Division of Neurobiology, Weill Medical College of Cornell University, room KB410, 411 East 69th Street, New York, New York 10021, USA
    Nat Rev Neurosci 5:347-60. 2004
  2. pmc The pathobiology of vascular dementia
    Costantino Iadecola
    Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10021, USA Electronic address
    Neuron 80:844-66. 2013
  3. pmc Circulating endothelin-1 alters critical mechanisms regulating cerebral microcirculation
    Giuseppe Faraco
    Brain and Mind Research Institute, 407 E 61st St, Room 303, New York, NY 10065
    Hypertension 62:759-66. 2013
  4. ncbi request reprint Cerebrovascular effects of amyloid-beta peptides: mechanisms and implications for Alzheimer's dementia
    Costantino Iadecola
    Division of Neurobiology, Weill Medical College of Cornell University, 411 East 69th Street, New York, New York 10021, USA
    Cell Mol Neurobiol 23:681-9. 2003
  5. ncbi request reprint Glial regulation of the cerebral microvasculature
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10021, USA
    Nat Neurosci 10:1369-76. 2007
  6. ncbi request reprint Hypertension, angiotensin, and stroke: beyond blood pressure
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021, USA
    Stroke 35:348-50. 2004
  7. pmc Neurovascular protection by ischaemic tolerance: role of nitric oxide
    Costantino Iadecola
    Division of Neurobiology, 407 East 61st Street, Room 304, New York, NY, USA
    J Physiol 589:4137-45. 2011
  8. ncbi request reprint Astrocytes take center stage in salt sensing
    Costantino Iadecola
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10021, USA
    Neuron 54:3-5. 2007
  9. pmc Stroke research at a crossroad: asking the brain for directions
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York, USA
    Nat Neurosci 14:1363-8. 2011
  10. ncbi request reprint The Janus face of cyclooxygenase-2 in ischemic stroke: shifting toward downstream targets
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 411 E 69th St, KB410, New York, NY 10021, USA
    Stroke 36:182-5. 2005

Research Grants

  1. Role of COX-2 Gene Expression in Ischemic Brain Damage
    Costantino Iadecola; Fiscal Year: 2007
  2. Prostanoid Receptors and Ischemic Brain Injury
    Costantino Iadecola; Fiscal Year: 2007
  3. NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGE
    Costantino Iadecola; Fiscal Year: 2007
  4. OVEREXPRESSION OF APP AND CEREBROVASCULAR REGULATION
    Costantino Iadecola; Fiscal Year: 2007
  5. NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGE
    Costantino Iadecola; Fiscal Year: 2009
  6. Role of COX-2 Gene Expression in Ischemic Brain Damage
    Costantino Iadecola; Fiscal Year: 2009
  7. Prostanoid Receptors and Ischemic Brain Injury
    Costantino Iadecola; Fiscal Year: 2009
  8. Prostanoid Receptors and Ischemic Brain Injury
    Costantino Iadecola; Fiscal Year: 2010
  9. Role of COX-2 Gene Expression in Ischemic Brain Damage
    Costantino Iadecola; Fiscal Year: 2010
  10. OVEREXPRESSION OF APP AND CEREBROVASCULAR REGULATION
    Costantino Iadecola; Fiscal Year: 2010

Collaborators

Detail Information

Publications100

  1. ncbi request reprint Neurovascular regulation in the normal brain and in Alzheimer's disease
    Costantino Iadecola
    Division of Neurobiology, Weill Medical College of Cornell University, room KB410, 411 East 69th Street, New York, New York 10021, USA
    Nat Rev Neurosci 5:347-60. 2004
  2. pmc The pathobiology of vascular dementia
    Costantino Iadecola
    Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10021, USA Electronic address
    Neuron 80:844-66. 2013
    ..Finally, preventative and therapeutic prospects will be examined, highlighting the importance of midlife vascular risk factor control in the prevention of late-life dementia. ..
  3. pmc Circulating endothelin-1 alters critical mechanisms regulating cerebral microcirculation
    Giuseppe Faraco
    Brain and Mind Research Institute, 407 E 61st St, Room 303, New York, NY 10065
    Hypertension 62:759-66. 2013
    ..The ET1-induced cerebrovascular dysfunction may increase cerebrovascular risk by lowering cerebrovascular reserves and increasing the vulnerability of the brain to cerebral ischemia...
  4. ncbi request reprint Cerebrovascular effects of amyloid-beta peptides: mechanisms and implications for Alzheimer's dementia
    Costantino Iadecola
    Division of Neurobiology, Weill Medical College of Cornell University, 411 East 69th Street, New York, New York 10021, USA
    Cell Mol Neurobiol 23:681-9. 2003
    ..4. The findings support the recently emerged notion that vascular factors play a pathogenic role in the early stages of Alzheimer dementia...
  5. ncbi request reprint Glial regulation of the cerebral microvasculature
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10021, USA
    Nat Neurosci 10:1369-76. 2007
    ..The involvement of astrocytes in neurovascular coupling has broad implications for the interpretation of functional imaging signals and for the understanding of brain diseases that are associated with neurovascular dysfunction...
  6. ncbi request reprint Hypertension, angiotensin, and stroke: beyond blood pressure
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021, USA
    Stroke 35:348-50. 2004
  7. pmc Neurovascular protection by ischaemic tolerance: role of nitric oxide
    Costantino Iadecola
    Division of Neurobiology, 407 East 61st Street, Room 304, New York, NY, USA
    J Physiol 589:4137-45. 2011
    ..The evidence suggests that NO can engage highly effective and multifunctional prosurvival pathways, which could be exploited for the prevention and treatment of cerebrovascular pathologies...
  8. ncbi request reprint Astrocytes take center stage in salt sensing
    Costantino Iadecola
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10021, USA
    Neuron 54:3-5. 2007
  9. pmc Stroke research at a crossroad: asking the brain for directions
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York, USA
    Nat Neurosci 14:1363-8. 2011
    ..Learning how the brain triggers and implements these protective measures may advance our quest to treat stroke...
  10. ncbi request reprint The Janus face of cyclooxygenase-2 in ischemic stroke: shifting toward downstream targets
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 411 E 69th St, KB410, New York, NY 10021, USA
    Stroke 36:182-5. 2005
  11. pmc The immunology of stroke: from mechanisms to translation
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York, USA
    Nat Med 17:796-808. 2011
    ....
  12. pmc The overlap between neurodegenerative and vascular factors in the pathogenesis of dementia
    Costantino Iadecola
    Division of Neurobiology, Weill Cornell Medical College, New York, NY 10065, USA
    Acta Neuropathol 120:287-96. 2010
    ....
  13. pmc Hypertension and cerebrovascular dysfunction
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10021, USA
    Cell Metab 7:476-84. 2008
    ..This review focuses on the mechanisms by which hypertension disrupts cerebral blood vessels, highlighting recent advances and outstanding issues...
  14. pmc Threats to the mind: aging, amyloid, and hypertension
    Costantino Iadecola
    Division of Neurobiology, Weill Medical College of Cornell University, 411 East 69th Street KB410, New York, NY 10021, USA
    Stroke 40:S40-4. 2009
    ....
  15. ncbi request reprint Converging pathogenic mechanisms in vascular and neurodegenerative dementia
    Costantino Iadecola
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021, USA
    Stroke 34:335-7. 2003
  16. ncbi request reprint NADPH-oxidase-derived reactive oxygen species mediate the cerebrovascular dysfunction induced by the amyloid beta peptide
    Laibaik Park
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Neurosci 25:1769-77. 2005
    ..Thus, a gp91phox-containing NADPH oxidase is the critical link between Abeta and cerebrovascular dysfunction, which may underlie the alteration in cerebral blood flow regulation observed in AD patients...
  17. pmc Cyclooxygenase 1-derived prostaglandin E2 and EP1 receptors are required for the cerebrovascular dysfunction induced by angiotensin II
    Carmen Capone
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, 407 East 61st St, New York, NY 10065, USA
    Hypertension 55:911-7. 2010
    ..The findings provide the first evidence that EP1Rs are involved in the deleterious cerebrovascular effects of Ang II and suggest new therapeutic approaches to counteract them...
  18. ncbi request reprint Angiotensin II impairs neurovascular coupling in neocortex through NADPH oxidase-derived radicals
    Ken Kazama
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY, USA
    Circ Res 95:1019-26. 2004
    ..The data provide the mechanistic basis for the cerebrovascular dysregulation induced by Ang II and suggest novel therapeutic strategies to counteract the effects of hypertension on the brain...
  19. pmc NMDA receptor activation increases free radical production through nitric oxide and NOX2
    Helene Girouard
    Division of Neurobiology, Weill Cornell Medical College, New York, New York 10021, USA
    J Neurosci 29:2545-52. 2009
    ..The findings establish a NOX2-containing NADPH oxidase as a major source of ROS produced by NMDA receptor activation, and identify NO as the critical link between NMDA receptor activity and NOX2-dependent ROS production...
  20. pmc COX-1-derived PGE2 and PGE2 type 1 receptors are vital for angiotensin II-induced formation of reactive oxygen species and Ca(2+) influx in the subfornical organ
    Gang Wang
    The Brain and Mind Research Institute, Weill Cornell Medical College, New York, New York
    Am J Physiol Heart Circ Physiol 305:H1451-61. 2013
    ..Our findings provide the first evidence of a spatial and functional framework that underlies ANG-II signaling in the SFO and reveal novel targets for antihypertensive therapies...
  21. pmc Membrane trafficking of NADPH oxidase p47(phox) in paraventricular hypothalamic neurons parallels local free radical production in angiotensin II slow-pressor hypertension
    Christal G Coleman
    Brain and Mind Research Institute, Weill Cornell Medical College of Cornell University, New York, New York 10065, USA
    J Neurosci 33:4308-16. 2013
    ....
  22. ncbi request reprint iNOS-derived NO and nox2-derived superoxide confer tolerance to excitotoxic brain injury through peroxynitrite
    Takayuki Kawano
    Division of Neurobiology, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Cereb Blood Flow Metab 27:1453-62. 2007
    ..Thus, peroxynitrite, in addition to its well-established deleterious role in ischemic brain injury and neurodegeneration, can also be beneficial by inducing tolerance to excitotoxicity...
  23. pmc Angiotensin II slow-pressor hypertension enhances NMDA currents and NOX2-dependent superoxide production in hypothalamic paraventricular neurons
    Gang Wang
    Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA
    Am J Physiol Regul Integr Comp Physiol 304:R1096-106. 2013
    ..The resulting enhancement of NMDAR activity may contribute to the neurohumoral dysfunction underlying the development of slow-pressor ANG II hypertension...
  24. ncbi request reprint Nox2-derived reactive oxygen species mediate neurovascular dysregulation in the aging mouse brain
    Laibaik Park
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Cereb Blood Flow Metab 27:1908-18. 2007
    ..These findings establish Nox2 as a critical source of the neurovascular oxidative stress mediating the deleterious cerebrovascular effects associated with increasing age...
  25. pmc Nuclear factor-kappaB activation and postischemic inflammation are suppressed in CD36-null mice after middle cerebral artery occlusion
    Alexander Kunz
    Division of Neurobiology, Weill Cornell Medical College, New York, New York 10021, USA
    J Neurosci 28:1649-58. 2008
    ..Inhibition of CD36 signaling may be a valuable therapeutic approach to counteract the deleterious effects of postischemic inflammation...
  26. pmc Chronic intermittent hypoxia induces NMDA receptor-dependent plasticity and suppresses nitric oxide signaling in the mouse hypothalamic paraventricular nucleus
    Christal G Coleman
    Department of Neurology and Neuroscience, Division of Neurobiology, Weill Cornell Medical College, New York, New York 10065, USA
    J Neurosci 30:12103-12. 2010
    ....
  27. ncbi request reprint Cerebrovascular nitrosative stress mediates neurovascular and endothelial dysfunction induced by angiotensin II
    Helene Girouard
    Division of Neurobiology, Weill Medical College of Cornell University, New York, NY 10021, USA
    Arterioscler Thromb Vasc Biol 27:303-9. 2007
    ..We tested the hypothesis that AngII-derived superoxide reacts with nitric oxide (NO) to form peroxynitrite, which, in turn, contributes to the vascular dysfunction...
  28. pmc Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein
    Laibaik Park
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10065, USA
    Proc Natl Acad Sci U S A 105:1347-52. 2008
    ..The findings unveil a previously unrecognized role of Nox2-derived radicals in the behavioral deficits of Tg2576 mice and provide a link between the neurovascular dysfunction and cognitive decline associated with amyloid pathology...
  29. pmc Estrous cycle-dependent neurovascular dysfunction induced by angiotensin II in the mouse neocortex
    Carmen Capone
    Division of Neurobiology, Weill Cornell Medical College, 407 East 61st St, New York, NY 10065, USA
    Hypertension 54:302-7. 2009
    ....
  30. pmc Sex differences in angiotensin signaling in bulbospinal neurons in the rat rostral ventrolateral medulla
    Gang Wang
    Division of Neurobiology, Weill Cornell Medical College, 411 East 69th St, New York, NY 10021, USA
    Am J Physiol Regul Integr Comp Physiol 295:R1149-57. 2008
    ....
  31. pmc Endothelin 1-dependent neurovascular dysfunction in chronic intermittent hypoxia
    Carmen Capone
    Division of Neurobiology, Department of Neurology and Neuroscience, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA
    Hypertension 60:106-13. 2012
    ..The ensuing cerebrovascular dysfunction may increase stroke risk in patients with sleep apnea by reducing cerebrovascular reserves and increasing the brain's susceptibility to cerebral ischemia...
  32. pmc Purinergic signaling induces cyclooxygenase-1-dependent prostanoid synthesis in microglia: roles in the outcome of excitotoxic brain injury
    Josef Anrather
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York, United States of America
    PLoS ONE 6:e25916. 2011
    ....
  33. ncbi request reprint Nox2, Ca2+, and protein kinase C play a role in angiotensin II-induced free radical production in nucleus tractus solitarius
    Gang Wang
    Division of Neurobiology, Weill Medical College of Cornell University, 411 East 69th St, New York, NY 10021, USA
    Hypertension 48:482-9. 2006
    ..Thus, a Nox2-containing NADPH oxidase is the critical link between Ang II and the enhancement of Ca(2+) currents that underlie the actions of Ang II on central autonomic regulation...
  34. pmc Scavenger receptor CD36 is essential for the cerebrovascular oxidative stress and neurovascular dysfunction induced by amyloid-beta
    Laibaik Park
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10065, USA
    Proc Natl Acad Sci U S A 108:5063-8. 2011
    ....
  35. ncbi request reprint Lipopolysaccharide induces early tolerance to excitotoxicity via nitric oxide and cGMP
    Marcello Orio
    Division of Neurobiology, Weill Medical College of Cornell University, 411 East 69th St, KB 410, New York, NY 10021, USA
    Stroke 38:2812-7. 2007
    ..We investigated whether the proinflammatory agent lipopolysaccharide (LPS), a well-established inducer of delayed tolerance, can also induce early tolerance and, if so, whether nitric oxide (NO) is involved in its mechanisms...
  36. ncbi request reprint Angiotensin II attenuates endothelium-dependent responses in the cerebral microcirculation through nox-2-derived radicals
    Helene Girouard
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College, Cornell University, New York, NY 10021, USA
    Arterioscler Thromb Vasc Biol 26:826-32. 2006
    ..We tested the hypothesis that Ang II impairs endothelium-dependent responses in the cerebral microcirculation through ROS generated in cerebrovascular cells by the enzyme NADPH oxidase...
  37. ncbi request reprint Prostaglandin E2 EP1 receptors: downstream effectors of COX-2 neurotoxicity
    Takayuki Kawano
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    Nat Med 12:225-9. 2006
    ..An EP1 receptor inhibitor reduces brain injury when administered 6 hours after MCA occlusion, suggesting that EP1 receptor inhibition may be a viable therapeutic option in ischemic stroke...
  38. pmc The cerebrovascular dysfunction induced by slow pressor doses of angiotensin II precedes the development of hypertension
    Carmen Capone
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York, USA
    Am J Physiol Heart Circ Physiol 300:H397-407. 2011
    ....
  39. pmc Key role of tissue plasminogen activator in neurovascular coupling
    Laibaik Park
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 105:1073-8. 2008
    ..These findings unveil a previously unrecognized role of tPA in vital homeostatic mechanisms coupling NMDA receptor signaling with nitric oxide synthesis and local cerebral perfusion...
  40. ncbi request reprint Exogenous NADPH increases cerebral blood flow through NADPH oxidase-dependent and -independent mechanisms
    Laibaik Park
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021, USA
    Arterioscler Thromb Vasc Biol 24:1860-5. 2004
    ..We used a peptide inhibitor of NADPH oxidase (gp91ds-tat) and null mice lacking the gp91phox subunit of NADPH oxidase to examine the mechanisms of the cerebrovascular effects of exogenous NADPH...
  41. pmc The scavenger receptor CD36 contributes to the neurotoxicity of bone marrow-derived monocytes through peroxynitrite production
    Ping Zhou
    Division of Neurobiology, Weill Cornell Medical College, New York, NY 10065, USA
    Neurobiol Dis 42:292-9. 2011
    ..Accordingly, targeting CD36 in the vascular compartment may protect against neurotoxicity in the ischemic brain...
  42. pmc Prostaglandin E2 type 1 receptors contribute to neuronal apoptosis after transient forebrain ischemia
    Munehisa Shimamura
    Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA
    J Cereb Blood Flow Metab 33:1207-14. 2013
    ..These data implicate EP1R in postischemic neuronal apoptosis possibly by facilitating AKT inhibition. ..
  43. ncbi request reprint Neurovascular protection by ischemic tolerance: role of nitric oxide and reactive oxygen species
    Alexander Kunz
    Division of Neurobiology, Weill Cornell Medical College, KB 410, New York, New York 10021, USA
    J Neurosci 27:7083-93. 2007
    ..The data indicate that preservation of cerebrovascular function is an essential component of ischemic tolerance and suggest that combining neuroprotection and vasoprotection may be a valuable strategy for treating ischemic brain injury...
  44. pmc Angiotensin II-induced hypertension differentially affects estrogen and progestin receptors in central autonomic regulatory areas of female rats
    Teresa A Milner
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, 411 East 69th Street, New York, NY 10021, USA
    Exp Neurol 212:393-406. 2008
    ..Considering that ERalpha counteracts the central and peripheral effects of AngII, these receptor changes may underlie adaptive responses that protect females from the deleterious effects of hypertension...
  45. pmc Angiotensin II type 2 receptor-coupled nitric oxide production modulates free radical availability and voltage-gated Ca2+ currents in NTS neurons
    Gang Wang
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York 10065, USA
    Am J Physiol Regul Integr Comp Physiol 302:R1076-83. 2012
    ..The resulting NO production antagonizes AT(1)R-mediated ROS and dampens L-type Ca(2+) currents. The ensuing signaling changes in the NTS may counteract the deleterious effects of AT(1)R on cardiovascular function...
  46. pmc Changes in the subcellular distribution of NADPH oxidase subunit p47phox in dendrites of rat dorsomedial nucleus tractus solitarius neurons in response to chronic administration of hypertensive agents
    Michael J Glass
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 411 E 69th St, KB410, New York, NY 10021, USA
    Exp Neurol 205:383-95. 2007
    ....
  47. pmc Central cardiovascular circuits contribute to the neurovascular dysfunction in angiotensin II hypertension
    Carmen Capone
    Department of Neurology and Neuroscience, Division of Neurobiology, Weill Cornell Medical College, New York, New York 10021, USA
    J Neurosci 32:4878-86. 2012
    ....
  48. ncbi request reprint Abeta-induced vascular oxidative stress and attenuation of functional hyperemia in mouse somatosensory cortex
    Laibaik Park
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Cereb Blood Flow Metab 24:334-42. 2004
    ..Thus, vascular oxidative stress is an early event in the course of the brain dysfunction produced by APP overexpression and Abeta, and, as such, could be the target of early therapeutic interventions based on antioxidants...
  49. doi request reprint Lipoprotein receptor-related protein-6 protects the brain from ischemic injury
    Takato Abe
    Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY, USA
    Stroke 44:2284-91. 2013
    ..However, it remains to be established whether LRP6 is also involved in ischemic brain injury. We used LRP6+/- mice to examine the role of this receptor in the mechanisms of focal cerebral ischemia...
  50. pmc Innate immunity receptor CD36 promotes cerebral amyloid angiopathy
    Laibaik Park
    Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA
    Proc Natl Acad Sci U S A 110:3089-94. 2013
    ..These findings identify a previously unrecognized role of CD36 in the mechanisms of vascular amyloid deposition, and suggest that this scavenger receptor is a putative therapeutic target for CAA and related conditions...
  51. pmc Prohibitin reduces mitochondrial free radical production and protects brain cells from different injury modalities
    Ping Zhou
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10065, USA
    J Neurosci 32:583-92. 2012
    ..The protective effect of prohibitin has potential translational relevance in diseases of the nervous system associated with mitochondrial dysfunction and oxidative stress...
  52. pmc Amyloid β-induced impairments in hippocampal synaptic plasticity are rescued by decreasing mitochondrial superoxide
    Tao Ma
    Center for Neural Science, New York University, New York, New York 10003, USA
    J Neurosci 31:5589-95. 2011
    ..Our data suggest a causal relationship between mitochondrial ROS imbalance and Aβ-induced impairments in hippocampal synaptic plasticity...
  53. pmc The neuroprotective effect of prostaglandin E2 EP1 receptor inhibition has a wide therapeutic window, is sustained in time and is not sexually dimorphic
    Takato Abe
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10021, USA
    J Cereb Blood Flow Metab 29:66-72. 2009
    ..The data provide proof of principle that EP1 receptor inhibition is a potentially valuable strategy for neuroprotection that deserves further preclinical investigation for therapeutic application in human stroke...
  54. ncbi request reprint The class B scavenger receptor CD36 mediates free radical production and tissue injury in cerebral ischemia
    Sunghee Cho
    Division of Neurobiology, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Neurosci 25:2504-12. 2005
    ..The data unveil a previously unrecognized role of CD36 in ischemia-induced ROS production and brain injury. Modulation of CD36 signaling may provide a new strategy for the treatment of ischemic stroke...
  55. pmc Key role of CD36 in Toll-like receptor 2 signaling in cerebral ischemia
    Takato Abe
    Division of Neurobiology, Weill Cornell Medical College, 407 E 61st St, Room RR303, New York, NY 10065, USA
    Stroke 41:898-904. 2010
    ..Because CD36 may act as a coreceptor for TLR2 heterodimers (TLR2/1 or TLR2/6), we tested whether such interaction plays a role in ischemic brain injury...
  56. pmc Angiotensin II-dependent hypertension requires cyclooxygenase 1-derived prostaglandin E2 and EP1 receptor signaling in the subfornical organ of the brain
    Xian Cao
    Department of Cell and Developmental Biology, Weill Cornell Medical College, New York, NY, USA
    Hypertension 59:869-76. 2012
    ..Thus, COX 1-derived PGE(2) signaling through EP(1)R in the SFO is required for the ROS-mediated HTN induced by systemic infusion of Ang II and suggests that EP(1)R in the SFO may provide a novel target for antihypertensive therapy...
  57. pmc Neuronal nitric oxide contributes to neuroplasticity-associated protein expression through cGMP, protein kinase G, and extracellular signal-regulated kinase
    Eduardo F Gallo
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10065, USA
    J Neurosci 31:6947-55. 2011
    ..Our data unveil a previously unrecognized link between neuronal NO and the molecular machinery responsible for the sustained synaptic changes underlying neuroplasticity...
  58. ncbi request reprint Angiotensin II attenuates functional hyperemia in the mouse somatosensory cortex
    Ken Kazama
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 411 E 69th Street, Rm KB410, New York, NY 10021, USA
    Am J Physiol Heart Circ Physiol 285:H1890-9. 2003
    ..The imbalance between CBF and neural activity induced by ANG II may alter the homeostasis of the neuronal microenvironment and contribute to brain dysfunction during ANG II-induced hypertension...
  59. ncbi request reprint NF-kappaB regulates phagocytic NADPH oxidase by inducing the expression of gp91phox
    Josef Anrather
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021, USA
    J Biol Chem 281:5657-67. 2006
    ..The findings raise the possibility of a positive feedback loop in which NF-kappaB activation by oxidative stress leads to further radical production via NADPH oxidase...
  60. ncbi request reprint Obligatory role of inducible nitric oxide synthase in ischemic preconditioning
    Sunghee Cho
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10021, USA
    J Cereb Blood Flow Metab 25:493-501. 2005
    ....
  61. pmc Exaggerated inflammation, impaired host defense, and neuropathology in progranulin-deficient mice
    Fangfang Yin
    Department of Microbiology and Immunology, Weill Cornell Medical College, New York, NY 10065, USA
    J Exp Med 207:117-28. 2010
    ..FTD associated with PGRN insufficiency may result from many years of reduced neutrotrophic support together with cumulative damage in association with dysregulated inflammation...
  62. pmc Early postnatal exposure to methylphenidate alters stress reactivity and increases hippocampal ectopic granule cells in adult rats
    Annelyn Torres-Reveron
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, 411 East 69th Street, New York, NY 10021, United States
    Brain Res Bull 78:175-81. 2009
    ....
  63. ncbi request reprint Cellular and subcellular localization of androgen receptor immunoreactivity relative to C1 adrenergic neurons in the rostral ventrolateral medulla of male and female rats
    Teresa A Milner
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    Synapse 61:268-78. 2007
    ....
  64. pmc Brain and circulating levels of Aβ1-40 differentially contribute to vasomotor dysfunction in the mouse brain
    Laibaik Park
    Brain and Mind Research Institute, Weill Medical College of Cornell University, 411 E 69th St, KB410, New York, NY 10021, USA
    Stroke 44:198-204. 2013
    ..However, the contributions of brain and circulating Aβ1-40 to the vascular dysfunction have not been elucidated...
  65. pmc Reperfusion rather than ischemia drives the formation of ubiquitin aggregates after middle cerebral artery occlusion
    Karin Hochrainer
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
    Stroke 43:2229-35. 2012
    ..Here we investigate the relationship between ubiquitin aggregation and duration of ischemia/reperfusion, infarct volume, and proteasomal activity in a mouse model of focal ischemia...
  66. ncbi request reprint Inducible nitric oxide synthase contributes to gender differences in ischemic brain injury
    Eun Mi Park
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, 10021, USA
    J Cereb Blood Flow Metab 26:392-401. 2006
    ..Such attenuation could result from the potent antiinflammatory effects of estrogens that downregulate iNOS expression via transcriptional or posttranscriptional mechanisms...
  67. pmc MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival
    Younghwa Kim
    Department of Microbiology and Immunology, Weill Medical College of Cornell University, New York, NY 10021, USA
    J Exp Med 204:2063-74. 2007
    ..In contrast, MyD88-5-null macrophages behaved like wild-type cells in their response to microbial products. Thus, MyD88-5 appears unique among MyD88s in functioning to mediate stress-induced neuronal toxicity...
  68. ncbi request reprint Prostanoids, not reactive oxygen species, mediate COX-2-dependent neurotoxicity
    Yasuhiro Manabe
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY, USA
    Ann Neurol 55:668-75. 2004
    ....
  69. ncbi request reprint Nitric oxide inhibits caspase activation and apoptotic morphology but does not rescue neuronal death
    Ping Zhou
    Division of Neurobiology, Weill Medical College of Cornell University, New York, NY 10021, USA
    J Cereb Blood Flow Metab 25:348-57. 2005
    ..A better understanding of this form of cell death may provide new strategies for neuroprotection in neuropathologies, such as ischemic brain injury, associated with apoptosis...
  70. pmc Neuroprotection by PGE2 receptor EP1 inhibition involves the PTEN/AKT pathway
    Ping Zhou
    Division of Neurobiology, Weill Cornell Medical College, New York, NY 10021, USA
    Neurobiol Dis 29:543-51. 2008
    ..The findings provide evidence for a link between EP1 receptors and the PI3K/AKT survival pathway and shed light on the molecular mechanisms of the prosurvival effect of EP1 receptor inhibition...
  71. ncbi request reprint Cyclooxygenase-2 does not contribute to postischemic production of reactive oxygen species
    Alexander Kunz
    Division of Neurobiology, Weill Medical College of Cornell University, New York, NY 10021, USA
    J Cereb Blood Flow Metab 27:545-51. 2007
    ....
  72. ncbi request reprint Evidence that estrogen directly and indirectly modulates C1 adrenergic bulbospinal neurons in the rostral ventrolateral medulla
    Gang Wang
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021, USA
    Brain Res 1094:163-78. 2006
    ..These findings provide a structural and functional basis for the effects of estrogens on blood pressure control and suggest a mechanism for the modulation of cardiovascular function by estrogen in women...
  73. pmc Brain dendritic cells in ischemic stroke: time course, activation state, and origin
    Jennifer C Felger
    Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY 10065, USA
    Brain Behav Immun 24:724-37. 2010
    ..High levels of MHC II and the co-stimulatory molecule CD80 on bDC at 72 h corresponded to peak lymphocyte infiltration, and suggested a functional interaction between these two immune cell populations...
  74. ncbi request reprint Attenuation of activity-induced increases in cerebellar blood flow by lesion of the inferior olive
    Yi Zhang
    Division of Neurobiology, Department of Neurobiology and Neuroscience, Weill Medical College of Cornell University, 411 East 69th Street, New York, NY 10021, USA
    Am J Physiol Heart Circ Physiol 285:H1177-82. 2003
    ..Thus the hemodynamic response evoked by functional activation of the cerebellar cortex reflects, in large part, CF activity...
  75. pmc Occlusion of cortical ascending venules causes blood flow decreases, reversals in flow direction, and vessel dilation in upstream capillaries
    John Nguyen
    Department of Biomedical Engineering, Cornell University, Ithaca, New York 14853, USA
    J Cereb Blood Flow Metab 31:2243-54. 2011
    ....
  76. ncbi request reprint Mitochondria are involved in the neurogenic neuroprotection conferred by stimulation of cerebellar fastigial nucleus
    Ping Zhou
    Division of Neurobiology, Weill Medical College of Cornell University, New York, NY 10021, USA
    J Neurochem 95:221-9. 2005
    ..These mitochondrial mechanisms are likely to play a role in the neuroprotection exerted by FN stimulation...
  77. ncbi request reprint Neurovascular coupling in the normal brain and in hypertension, stroke, and Alzheimer disease
    Helene Girouard
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA
    J Appl Physiol 100:328-35. 2006
    ..These findings, collectively, highlight the importance of neurovascular coupling to the health of the normal brain and suggest a therapeutic target for improving brain function in pathologies associated with cerebrovascular dysfunction...
  78. ncbi request reprint NADPH oxidase contributes to angiotensin II signaling in the nucleus tractus solitarius
    Gang Wang
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Neurosci 24:5516-24. 2004
    ....
  79. doi request reprint Spreading depolarization: a possible new culprit in the delayed cerebral ischemia of subarachnoid hemorrhage
    Lewis Z Leng
    Department of Neurological Surgery, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY 10065, USA
    Arch Neurol 68:31-6. 2011
    ....
  80. pmc Ultrastructural localization of extranuclear progestin receptors relative to C1 neurons in the rostral ventrolateral medulla
    Teresa A Milner
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, 411 East 69th Street, New York, NY 10021, United States
    Neurosci Lett 431:167-72. 2008
    ..Moreover, they suggest that PR activation may contribute to progestin's effects on arterial blood pressure during pregnancy as well as to sex differences in central cardiovascular regulation...
  81. ncbi request reprint Synaptic and vascular associations of neurons containing cyclooxygenase-2 and nitric oxide synthase in rat somatosensory cortex
    Hong Wang
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021, USA
    Cereb Cortex 15:1250-60. 2005
    ..Thus, COX-2 has a compartmental distribution in somatosensory cortical neurons consistent with the local neuronal synthesis of prostanoids that are involved in neurovascular coupling and whose actions are modulated by nitric oxide...
  82. ncbi request reprint cis-acting, element-specific transcriptional activity of differentially phosphorylated nuclear factor-kappa B
    Josef Anrather
    Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Biol Chem 280:244-52. 2005
    ..This study shows for the first time that site-specific phosphorylation can target a transcription factor to a particular subset of genes...
  83. ncbi request reprint Herbal alkaloid tetrandrine: fron an ion channel blocker to inhibitor of tumor proliferation
    Gang Wang
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY 10021, USA
    Trends Pharmacol Sci 25:120-3. 2004
  84. ncbi request reprint The role of neuronal signaling in controlling cerebral blood flow
    Carrie T Drake
    Department of Neurology and Neuroscience, Division of Neurobiology, Weill Medical College of Cornell University, 411 East 69th St, New York, NY 10128, USA
    Brain Lang 102:141-52. 2007
    ..Here, we review the mechanisms of functional hyperemia and their implications for interpreting the blood oxygen level-dependent (BOLD) contrast signal used in functional magnetic resonance imaging (fMRI)...
  85. ncbi request reprint Attenuation of activity-induced increases in cerebellar blood flow in mice lacking neuronal nitric oxide synthase
    Guang Yang
    Department of Neuroloy and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    Am J Physiol Heart Circ Physiol 285:H298-304. 2003
    ..These data provide the first nonpharmacological evidence that nNOS-derived NO is a critical link between glutamatergic synaptic activity and blood flow in the activated cerebellum...
  86. pmc Recommendations of the National Heart, Lung, and Blood Institute working group on cerebrovascular biology and disease
    Costantino Iadecola
    Weill Cornell Medical College, New York, NY, USA
    Stroke 37:1578-81. 2006
    ....
  87. ncbi request reprint L-Arginine increases ischemic injury in wild-type mice but not in iNOS-deficient mice
    Xueren Zhao
    Department of Neurology, University of Minnesota Medical School, Minneapolis, MN 55455, USA
    Brain Res 966:308-11. 2003
    ..The findings support the hypothesis that L-arginine worsens ischemic injury by increasing the catalytic output of iNOS and suggest that administration of L-arginine should be avoided in patients with acute stroke...
  88. ncbi request reprint Delayed effect of administration of COX-2 inhibitor in mice with acute cerebral ischemia
    Koreaki Sugimoto
    Department of Neurology, University of Minnesota Medical School, Minneapolis, MN 55455, USA
    Brain Res 960:273-6. 2003
    ..Our results showed that the beneficial effect of NS398 on reduction of infarct volume and improvement of neurologic deficits were noted more than 24 h after the injection regardless of the administration timing...
  89. ncbi request reprint The neural basis of functional brain imaging signals
    David Attwell
    Dept of Physiology, University College London, Gower Street, UK
    Trends Neurosci 25:621-5. 2002
    ..A firm understanding of the BOLD response will require investigation to be focussed on the neural signalling mechanisms controlling blood flow rather than on the locus of energy use...
  90. ncbi request reprint Effects of aminoguanidine on cerebral ischemia in mice: comparison between mice with and without inducible nitric oxide synthase gene
    Koreaki Sugimoto
    Department of Neurology, Center for Clinical and Molecular Neurobiology, University of Minnesota Medical School, Minneapolis, MN 55455, USA
    Neurosci Lett 331:25-8. 2002
    ..Our results indicated that AG suppresses iNOS activity in mice with brain ischemia to level equivalent to those seen in iNOS knockout mice, confirming that this enzyme is involved in ischemic brain injury...
  91. ncbi request reprint Interferon regulatory factor-1 immunoreactivity in neurons and inflammatory cells following ischemic stroke in rodents and humans
    Mihaela Alexander
    Department of Neurology, University of Minnesota, Minneapolis, MN 55455, USA
    Acta Neuropathol 105:420-4. 2003
    ..The neuronal expression of IRF-1, in conjunction with the finding that IRF-1 deletion is beneficial to the post-ischemic brain, suggests that expression of IRF-1-dependent genes in neurons plays a role in ischemic neuronal death...
  92. ncbi request reprint Cerebrovascular autoregulation is profoundly impaired in mice overexpressing amyloid precursor protein
    Kiyoshi Niwa
    Department of Neurology, University of Minnesota, Minneapolis, Minnesota 55455, USA
    Am J Physiol Heart Circ Physiol 283:H315-23. 2002
    ..The resulting alterations in cerebral perfusion may play a role in the brain dysfunction and periventricular white-matter changes associated with Alzheimer's dementia...
  93. ncbi request reprint Interaction between inducible nitric oxide synthase and poly(ADP-ribose) polymerase in focal ischemic brain injury
    Eun Mi Park
    Department of Pharmacology, College of Medicine, Ewha Women s University, Seoul, Republic of Korea
    Stroke 35:2896-901. 2004
    ....
  94. ncbi request reprint Alterations in cerebral blood flow and glucose utilization in mice overexpressing the amyloid precursor protein
    Kiyoshi Niwa
    Center for Clinical and Molecular Neurobiology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA
    Neurobiol Dis 9:61-8. 2002
    ..These observations support the hypothesis that cerebrovascular and metabolic abnormalities are early events in the pathogenesis of Alzheimer's disease...
  95. ncbi request reprint Farnesyl transferase inhibitors induce neuroprotection by inhibiting Ha-Ras signalling pathway
    Antonio Ruocco
    Department of Clinical and Experimental Medicine, Federico II University, Naples, Italy
    Eur J Neurosci 26:3261-6. 2007
    ..Thus, Ha-Ras inhibition plays a role in the pathology of neuroprotection, suggesting a potential role of FTIs in the treatment of cerebrovascular diseases...
  96. ncbi request reprint Heat shock proteins and p53 play a critical role in K+ channel-mediated tumor cell proliferation and apoptosis
    Xiaobing Han
    Cancer Biology Reseach Center, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China
    Apoptosis 12:1837-46. 2007
    ....
  97. ncbi request reprint Atherosclerosis and neurodegeneration: unexpected conspirators in Alzheimer's dementia
    Costantino Iadecola
    Arterioscler Thromb Vasc Biol 23:1951-3. 2003
  98. ncbi request reprint Rescuing troubled vessels in Alzheimer disease
    Costantino Iadecola
    Nat Med 11:923-4. 2005
  99. ncbi request reprint Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress
    Ben A Weissman
    Department of Pharmacology, Israel Institute for Biological Research, Ness Ziona, Israel
    Am J Physiol Endocrinol Metab 292:E615-20. 2007
    ..These results support the hypothesis that CORT, but not NO, is a plausible candidate to mediate rapid stress-induced suppression of Leydig cell steroidogenesis...
  100. ncbi request reprint Intrinsic signals and functional brain mapping: caution, blood vessels at work
    Costantino Iadecola
    Cereb Cortex 12:223-4. 2002

Research Grants39

  1. Role of COX-2 Gene Expression in Ischemic Brain Damage
    Costantino Iadecola; Fiscal Year: 2007
    ....
  2. Prostanoid Receptors and Ischemic Brain Injury
    Costantino Iadecola; Fiscal Year: 2007
    ..End of Abstract) ..
  3. NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGE
    Costantino Iadecola; Fiscal Year: 2007
    ..The proposed studies will provide insight into poorly understood aspects of the mechanisms of ischemic preconditioning that may have important implications for the prevention and treatment of ischemic stroke. ..
  4. OVEREXPRESSION OF APP AND CEREBROVASCULAR REGULATION
    Costantino Iadecola; Fiscal Year: 2007
    ....
  5. NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGE
    Costantino Iadecola; Fiscal Year: 2009
    ..The proposed studies will provide insight into poorly understood aspects of the mechanisms of ischemic preconditioning that may have important implications for the prevention and treatment of ischemic stroke. ..
  6. Role of COX-2 Gene Expression in Ischemic Brain Damage
    Costantino Iadecola; Fiscal Year: 2009
    ..abstract_text> ..
  7. Prostanoid Receptors and Ischemic Brain Injury
    Costantino Iadecola; Fiscal Year: 2009
    ..abstract_text> ..
  8. Prostanoid Receptors and Ischemic Brain Injury
    Costantino Iadecola; Fiscal Year: 2010
    ..abstract_text> ..
  9. Role of COX-2 Gene Expression in Ischemic Brain Damage
    Costantino Iadecola; Fiscal Year: 2010
    ..abstract_text> ..
  10. OVEREXPRESSION OF APP AND CEREBROVASCULAR REGULATION
    Costantino Iadecola; Fiscal Year: 2010
    ....
  11. Overexpression of APP and Cerebrovasuclar Regulation
    Costantino Iadecola; Fiscal Year: 2006
    ..These studies will continue to expand our understanding of the biological effects of AB and constitute a necessary step toward elucidating the contribution of vascular factors to the pathogenesis of AD. ..
  12. COX2 GENE EXPRESSION AND ISCHEMIC BRAIN DAMAGE
    Costantino Iadecola; Fiscal Year: 2000
    ..Preliminary results suggest that this is a most promising area of research that will advance our understanding of the fundamental mechanisms of cerebral ischemia and may unveil new avenues for stroke treatment. ..
  13. SYNAPTIC ACTIVITY AND BLOOD FLOW IN CEREBELLAR CORTEX
    Costantino Iadecola; Fiscal Year: 2003
    ..abstract_text> ..
  14. Neurovascular Coupling in Hypertension
    Costantino Iadecola; Fiscal Year: 2004
    ..The results of these studies will enhance our understanding of the effects of hypertension on the brain and may provide new insights into treatment strategies aimed at counteracting these detrimental actions. ..
  15. Role of Cox2 Gene Expression in Ischemic Brain Damage
    Costantino Iadecola; Fiscal Year: 2004
    ..While the proposed studies will expand our understanding of the involvement of COX-2 in ischemic brain injury, they will also provide the rational basis for new neuroprotective strategies for human stroke. ..
  16. NO SYNTHASE GENE EXPRESSION AND CEREBRAL ISCHEMIC DAMAGE
    Costantino Iadecola; Fiscal Year: 2011
    ..The proposed studies will provide insight into poorly understood aspects of the mechanisms of ischemic preconditioning that may have important implications for the prevention and treatment of ischemic stroke. ..