Carol Anne Colton

Summary

Publications

  1. pmc Activation of matrix metalloproteinases following anti-Aβ immunotherapy; implications for microhemorrhage occurrence
    Donna M Wilcock
    University of Kentucky Sanders Brown Center on Aging, Department of Physiology, Lexington, KY 40536, USA
    J Neuroinflammation 8:115. 2011
  2. pmc The effects of NOS2 gene deletion on mice expressing mutated human AbetaPP
    Carol A Colton
    Division of Neurology, Duke University Medical Center, Durham, NC 27710, USA
    J Alzheimers Dis 15:571-87. 2008
  3. pmc NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease
    C A Colton
    Division of Neurology, and Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 103:12867-72. 2006
  4. ncbi request reprint Microglial contribution to oxidative stress in Alzheimer's disease
    C A Colton
    Department of Physiology, Georgetown University Medical School, Washington, DC 20007, USA
    Ann N Y Acad Sci 899:292-307. 2000
  5. ncbi request reprint Sex steroids, APOE genotype and the innate immune system
    Carol A Colton
    Division of Neurology, Duke University Medical Center, Box 2900, Bryan Research Bldg, Durham, NC 27710, USA
    Neurobiol Aging 26:363-72. 2005
  6. ncbi request reprint Disrupted spermine homeostasis: a novel mechanism in polyglutamine-mediated aggregation and cell death
    C A Colton
    Deane Laboratory, Division of Neurology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Neurosci 24:7118-27. 2004
  7. ncbi request reprint APOE genotype-specific differences in human and mouse macrophage nitric oxide production
    Carol A Colton
    Division of Neurology and the Alzheimer s Disease Research Center, Duke University Medical Center, Durham, NC 27710, USA
    J Neuroimmunol 147:62-7. 2004
  8. ncbi request reprint APOE and the regulation of microglial nitric oxide production: a link between genetic risk and oxidative stress
    Carol A Colton
    Division of Neurology, Duke University Medical Center, Box 2900, Bryan Research Building, Durham, NC 27710, USA
    Neurobiol Aging 23:777-85. 2002
  9. ncbi request reprint Nitroxyl anion regulation of the NMDA receptor
    C A Colton
    Division of Neurology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Neurochem 78:1126-34. 2001
  10. ncbi request reprint Apolipoprotein-E allele-specific regulation of nitric oxide production
    Carola A Colton
    Division of Neurology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Ann N Y Acad Sci 962:212-25. 2002

Detail Information

Publications33

  1. pmc Activation of matrix metalloproteinases following anti-Aβ immunotherapy; implications for microhemorrhage occurrence
    Donna M Wilcock
    University of Kentucky Sanders Brown Center on Aging, Department of Physiology, Lexington, KY 40536, USA
    J Neuroinflammation 8:115. 2011
    ..Also, vasogenic edema was reported in phase 2 of a passive immunization clinical trial. In order to overcome these vascular adverse effects it is critical that we understand the mechanism(s) by which they occur...
  2. pmc The effects of NOS2 gene deletion on mice expressing mutated human AbetaPP
    Carol A Colton
    Division of Neurology, Duke University Medical Center, Durham, NC 27710, USA
    J Alzheimers Dis 15:571-87. 2008
    ..As APP/NOS2(-/-) bigenic mice more fully model the human AD disease pathology, they may serve as a tool to better understand disease progression in AD and the role of NO in altering chronic neurological disease processes...
  3. pmc NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease
    C A Colton
    Division of Neurology, and Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 103:12867-72. 2006
    ....
  4. ncbi request reprint Microglial contribution to oxidative stress in Alzheimer's disease
    C A Colton
    Department of Physiology, Georgetown University Medical School, Washington, DC 20007, USA
    Ann N Y Acad Sci 899:292-307. 2000
    ....
  5. ncbi request reprint Sex steroids, APOE genotype and the innate immune system
    Carol A Colton
    Division of Neurology, Duke University Medical Center, Box 2900, Bryan Research Bldg, Durham, NC 27710, USA
    Neurobiol Aging 26:363-72. 2005
    ..These data re-enforce the concept that classical activation in macrophages has multiple levels of regulation, dictated by competing or synergistic factors and genotype...
  6. ncbi request reprint Disrupted spermine homeostasis: a novel mechanism in polyglutamine-mediated aggregation and cell death
    C A Colton
    Deane Laboratory, Division of Neurology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Neurosci 24:7118-27. 2004
    ..Inhibition of ODC by difluoromethylornithine prevented basal and induced cell death in Q57 cells, demonstrating a central role for polyamines in this process...
  7. ncbi request reprint APOE genotype-specific differences in human and mouse macrophage nitric oxide production
    Carol A Colton
    Division of Neurology and the Alzheimer s Disease Research Center, Duke University Medical Center, Durham, NC 27710, USA
    J Neuroimmunol 147:62-7. 2004
    ....
  8. ncbi request reprint APOE and the regulation of microglial nitric oxide production: a link between genetic risk and oxidative stress
    Carol A Colton
    Division of Neurology, Duke University Medical Center, Box 2900, Bryan Research Building, Durham, NC 27710, USA
    Neurobiol Aging 23:777-85. 2002
    ....
  9. ncbi request reprint Nitroxyl anion regulation of the NMDA receptor
    C A Colton
    Division of Neurology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Neurochem 78:1126-34. 2001
    ..Our data suggest that the regulation of NMDA-r function by nitroxyl anion is distinctly different from NO and may result in different cellular outcomes compared with NO...
  10. ncbi request reprint Apolipoprotein-E allele-specific regulation of nitric oxide production
    Carola A Colton
    Division of Neurology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Ann N Y Acad Sci 962:212-25. 2002
    ..The inappropriate levels of arginine transport and of NO in the presence of the APOE4 compared to the APOE3 gene and its products are likely to have significant impact in the CNS...
  11. ncbi request reprint Apolipoprotein E acts to increase nitric oxide production in macrophages by stimulating arginine transport
    C A Colton
    Department of Physiology, Georgetown University Medical School, Washington, DC 20007, USA
    Biochim Biophys Acta 1535:134-44. 2001
    ..Regulation of arginine availability is a novel action of apoE on the regulation of macrophage function and the immune response...
  12. ncbi request reprint Androgen-mediated immune function is altered by the apolipoprotein E gene
    Candice M Brown
    Division of Neurology, Duke University Medical Center, Box 2900, Durham, North Carolina 27710, USA
    Endocrinology 148:3383-90. 2007
    ..Thus, our data suggest that DHT modulation of kinase activity is altered in microglia from mice expressing an APOE4 genotype and may impact androgen treatment therapies in individuals with an APOE4 genotype...
  13. ncbi request reprint Characterization of NO and cytokine production in immune-activated microglia and peritoneal macrophages derived from a mouse model expressing the human NOS2 gene on a mouse NOS2 knockout background
    Michael P Vitek
    Division of Neurology, Duke University Medical Center, Durham North Carolina 27710, USA
    Antioxid Redox Signal 8:893-901. 2006
    ....
  14. ncbi request reprint Apolipoprotein E isoform mediated regulation of nitric oxide release
    Candice M Brown
    University Program in Genetics, Department of Medicine Neurology, Duke University Medical Center, Durham, NC 27710, USA
    Free Radic Biol Med 32:1071-5. 2002
    ..These data suggest a potentially novel mechanism for gender-dependent and apoE isoform-dependent immune responses that parallel the genetic susceptibility of APOE4 carriers for the development of Alzheimer's disease...
  15. pmc APOE genotype-specific differences in the innate immune response
    Michael P Vitek
    Duke University Medical Center, Durham, NC 27710, USA
    Neurobiol Aging 30:1350-60. 2009
    ..Overall, these data emphasize the important role of apolipoprotein E and of the APOE genotype on the immune responses that are evident in most, if not all, neurological disease...
  16. pmc The APOE4 genotype alters the response of microglia and macrophages to 17beta-estradiol
    Candice M Brown
    Division of Neurology, Duke University Medical Center, Durham, NC 27710, United States
    Neurobiol Aging 29:1783-94. 2008
    ....
  17. pmc Amyloid reduction by amyloid-beta vaccination also reduces mouse tau pathology and protects from neuron loss in two mouse models of Alzheimer's disease
    Donna M Wilcock
    Division of Neurology, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Neurosci 29:7957-65. 2009
    ..Nevertheless, by providing evidence that reducing amyloid pathology also reduces nonmutant tau pathology and blocks neuron loss, these data support the development of amyloid-lowering therapies for disease-modifying treatment of AD...
  18. pmc Progression of amyloid pathology to Alzheimer's disease pathology in an amyloid precursor protein transgenic mouse model by removal of nitric oxide synthase 2
    Donna M Wilcock
    Division of Neurology, Duke University Medical Center, Durham, North Carolina 27710, USA
    J Neurosci 28:1537-45. 2008
    ..These data show that removal of NOS2 from an APP transgenic mouse results in development of a much greater spectrum of AD-like pathology and behavioral impairments...
  19. pmc Interaction of NG2(+) glial progenitors and microglia/macrophages from the injured spinal cord
    Junfang Wu
    Department of Neuroscience, Georgetown University Medical Center, Washington, District of Columbia, USA
    Glia 58:410-22. 2010
    ..Thus, the nonreplacement of lost glial cells in the central lesion zone may involve, at least in part, inhibitory factors produced by microglia/macrophages that are concentrated within the lesion...
  20. pmc Anti-amyloid-beta immunotherapy in Alzheimer's disease: relevance of transgenic mouse studies to clinical trials
    Donna M Wilcock
    Duke University Medical Center, Department of Medicine Division of Neurology, Durham, NC 27710, USA
    J Alzheimers Dis 15:555-69. 2008
    ..Reports from the active immunization clinical trial indicated that, similarly to effects observed in mouse studies, amyloid levels in brain were reduced...
  21. ncbi request reprint Assessing activation states in microglia
    Carol A Colton
    Duke University Medical Center, Durham, NC 27710, USA
    CNS Neurol Disord Drug Targets 9:174-91. 2010
    ..A broad-based functional view is provided that is designed to more fully explore the balance between inflammo-toxic and inflammo-resolution factors that govern chronic disease progression...
  22. pmc Immunotherapy, vascular pathology, and microhemorrhages in transgenic mice
    Donna M Wilcock
    Duke University Medical Center, Division of Neurology, Research Dr, Durham, NC 27710, USA
    CNS Neurol Disord Drug Targets 8:50-64. 2009
    ..Understanding the type of damage to the neurovascular unit caused by CAA in AD and the underlying cause of microhemorrhage after immunotherapy is essential to the success of therapeutic vaccines as a treatment for AD...
  23. ncbi request reprint Apolipoprotein E-derived peptides ameliorate clinical disability and inflammatory infiltrates into the spinal cord in a murine model of multiple sclerosis
    Feng Qiao Li
    Division of Neurology, Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    J Pharmacol Exp Ther 318:956-65. 2006
    ....
  24. ncbi request reprint Nitric oxide production and regulation of neuronal NOS in tyrosine hydroxylase containing neurons
    Qing Xu
    Division of Neurology, Duke University Medical Center, Durham, NC 27710, USA
    Exp Neurol 188:341-50. 2004
    ..However, NO was not the primary mediator of cell death since NOS inhibitors rescued only less than 10% of the cells. These data suggest that endogenous NO production by nNOS is not a major factor in CAD cell death under these conditions...
  25. pmc Heterogeneity of microglial activation in the innate immune response in the brain
    Carol A Colton
    Division of Neurology, Duke University Medical Center, Durham, 27710 NC, USA
    J Neuroimmune Pharmacol 4:399-418. 2009
    ..The immunosuppressive and repair processes of each of these states and how alternative activation and acquired deactivation participate in chronic neuroinflammation in the brain are discussed...
  26. ncbi request reprint Mitochondria and nitric oxide
    Pedram Ghafourifar
    Antioxid Redox Signal 5:249-50. 2003
  27. ncbi request reprint Redox regulation of neuronal migration in a Down Syndrome model
    Toby N Behar
    Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
    Free Radic Biol Med 35:566-75. 2003
    ..Our data indicate that oxidative stress may play a key role in the abnormal glutamate-mediated responses during cortical development in the Ts16 mouse and may have an impact on neuronal migration at critical stages...
  28. pmc Human apolipoprotein E redistributes fibrillar amyloid deposition in Tg-SwDI mice
    Feng Xu
    Department of Medicine, Stony Brook University, Stony Brook, New York 11794 8153, USA
    J Neurosci 28:5312-20. 2008
    ....
  29. ncbi request reprint Orthogonal properties of the redox siblings nitroxyl and nitric oxide in the cardiovascular system: a novel redox paradigm
    David A Wink
    Tumor Biology Section, Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bldg 10, Rm B3 B69, Bethesda, MD 20892, USA
    Am J Physiol Heart Circ Physiol 285:H2264-76. 2003
    ..This article discusses the emerging aspects of HNO chemistry and attempts to provide a framework for the distinct effects of NO and HNO in vivo...
  30. ncbi request reprint Guide for the use of nitric oxide (NO) donors as probes of the chemistry of NO and related redox species in biological systems
    Douglas D Thomas
    Tumor Biology Section, Radiation Biology Branch, National Institutes of Health National Cancer Institute, Bethesda, Maryland 20892, USA
    Methods Enzymol 359:84-105. 2002
  31. ncbi request reprint Compartmentalized nitrosation and nitration in mitochondria
    Pedram Ghafourifar
    Department of Pharmacology and Therapeutics, LSU Health Sciences Center, Shreveport, LA 71130, USA
    Antioxid Redox Signal 5:349-54. 2003
    ..The reversibility and the suborganelle preference of these reactions will be discussed...
  32. ncbi request reprint Heme proteins and nitric oxide (NO): the neglected, eloquent chemistry in NO redox signaling and regulation
    Douglas D Thomas
    Tumor Biology Section, Radiation Biology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Antioxid Redox Signal 5:307-17. 2003
    ..Here the basic chemistry of nitrosylation and the interactions of NO and other nitrogen oxides with metal-oxo species such as found in peroxidases and monoxygenases are discussed...

Research Grants17

  1. Regulation of Microglial Activation
    Carol Colton; Fiscal Year: 2001
    ....
  2. The amyloid cascade in a novel mouse model of Alzheimer's disease
    Carol Anne Colton; Fiscal Year: 2010
    ..The method used will involve the generation of a novel mouse model for potential therapeutic value and will provide a useful to tool to fully investigate therapeutics in the pre-clinical stage. ..
  3. A Mouse Model of Inflammation in Alzheimer's Disease
    Carol Colton; Fiscal Year: 2009
    ..PUBLIC HEALTH REVELANCE: This project will examine the role of the brain's innate immune state in generating the neuropathology associated with chronic neurodegenerative diseases such as Alzheimer's disease. ..
  4. The amyloid cascade in a novel mouse model of Alzheimer's disease
    Carol Colton; Fiscal Year: 2009
    ..The method used will involve the generation of a novel mouse model for potential therapeutic value and will provide a useful to tool to fully investigate therapeutics in the pre-clinical stage. ..
  5. Immune Responsiveness, APOE/Gender in Neurodegeneration
    Carol Colton; Fiscal Year: 2007
    ..Thus, we will examine the role of hormones in the regulation of microglial and peritoneal macrophage immune activation in mice expressing only human apoE3 protein or expressing only human apoE4 protein. ..
  6. Immune Responsiveness, APOE/Gender in Neurodegeneration
    Carol Colton; Fiscal Year: 2006
    ..Thus, we will examine the role of hormones in the regulation of microglial and peritoneal macrophage immune activation in mice expressing only human apoE3 protein or expressing only human apoE4 protein. ..
  7. Regulation of neuronal NO by apolipoprotein E
    Carol Colton; Fiscal Year: 2006
    ....
  8. Immune Responsiveness, APOE/Gender in Neurodegeneration
    Carol Colton; Fiscal Year: 2005
    ..Thus, we will examine the role of hormones in the regulation of microglial and peritoneal macrophage immune activation in mice expressing only human apoE3 protein or expressing only human apoE4 protein. ..
  9. Regulation of neuronal NO by apolipoprotein E
    Carol Colton; Fiscal Year: 2005
    ....
  10. Immune Responsiveness, APOE/Gender in Neurodegeneration
    Carol Colton; Fiscal Year: 2004
    ..Thus, we will examine the role of hormones in the regulation of microglial and peritoneal macrophage immune activation in mice expressing only human apoE3 protein or expressing only human apoE4 protein. ..
  11. Regulation of neuronal NO by apolipoprotein E
    Carol Colton; Fiscal Year: 2004
    ....
  12. Regulation of Microglial Activation
    Carol Colton; Fiscal Year: 2003
    ....
  13. Regulation of neuronal NO by apolipoprotein E
    Carol Colton; Fiscal Year: 2003
    ....
  14. Regulation of Microglial Activation
    Carol Colton; Fiscal Year: 2002
    ....
  15. Regulation of neuronal NO by apolipoprotein E
    Carol Colton; Fiscal Year: 2002
    ....
  16. A Mouse Model of Inflammation in Alzheimer's Disease
    Carol Anne Colton; Fiscal Year: 2010
    ..PUBLIC HEALTH REVELANCE: This project will examine the role of the brain's innate immune state in generating the neuropathology associated with chronic neurodegenerative diseases such as Alzheimer's disease. ..