Donna M Wilcock

Summary

Affiliation: University of Kentucky
Country: USA

Publications

  1. pmc Lithium treatment of APPSwDI/NOS2-/- mice leads to reduced hyperphosphorylated tau, increased amyloid deposition and altered inflammatory phenotype
    Tiffany L Sudduth
    Department of Physiology, University of Kentucky Sanders Brown Center on Aging, Lexington, Kentucky, United States of America
    PLoS ONE 7:e31993. 2012
  2. pmc Neuroinflammation in the aging down syndrome brain; lessons from Alzheimer's disease
    Donna M Wilcock
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, 800 S Limestone Street, Lexington, KY 40536, USA
    Curr Gerontol Geriatr Res 2012:170276. 2012
  3. pmc A changing perspective on the role of neuroinflammation in Alzheimer's disease
    Donna M Wilcock
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    Int J Alzheimers Dis 2012:495243. 2012
  4. 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
  5. pmc Induction of hyperhomocysteinemia models vascular dementia by induction of cerebral microhemorrhages and neuroinflammation
    Tiffany L Sudduth
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536, USA
    J Cereb Blood Flow Metab 33:708-15. 2013
  6. pmc Intracranial injection of Gammagard, a human IVIg, modulates the inflammatory response of the brain and lowers Aβ in APP/PS1 mice along a different time course than anti-Aβ antibodies
    Tiffany L Sudduth
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536, USA
    J Neurosci 33:9684-92. 2013
  7. pmc Down's syndrome, neuroinflammation, and Alzheimer neuropathogenesis
    Donna M Wilcock
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    J Neuroinflammation 10:84. 2013
  8. pmc APOE-ε2 and APOE-ε4 correlate with increased amyloid accumulation in cerebral vasculature
    Peter T Nelson
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA
    J Neuropathol Exp Neurol 72:708-15. 2013
  9. pmc Neuroinflammatory phenotype in early Alzheimer's disease
    Tiffany L Sudduth
    Department of Physiology, University of Kentucky Sanders Brown Center on Aging, Lexington, KY 40536, USA
    Neurobiol Aging 34:1051-9. 2013
  10. pmc Early stage drug treatment that normalizes proinflammatory cytokine production attenuates synaptic dysfunction in a mouse model that exhibits age-dependent progression of Alzheimer's disease-related pathology
    Adam D Bachstetter
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536, USA
    J Neurosci 32:10201-10. 2012

Collaborators

Detail Information

Publications10

  1. pmc Lithium treatment of APPSwDI/NOS2-/- mice leads to reduced hyperphosphorylated tau, increased amyloid deposition and altered inflammatory phenotype
    Tiffany L Sudduth
    Department of Physiology, University of Kentucky Sanders Brown Center on Aging, Lexington, Kentucky, United States of America
    PLoS ONE 7:e31993. 2012
    ..Our data suggest that lithium may be beneficial for the treatment of tauopathies but may not be beneficial for the treatment of Alzheimer's disease...
  2. pmc Neuroinflammation in the aging down syndrome brain; lessons from Alzheimer's disease
    Donna M Wilcock
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, 800 S Limestone Street, Lexington, KY 40536, USA
    Curr Gerontol Geriatr Res 2012:170276. 2012
    ....
  3. pmc A changing perspective on the role of neuroinflammation in Alzheimer's disease
    Donna M Wilcock
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    Int J Alzheimers Dis 2012:495243. 2012
    ..Overall, it is clear that more focused, cause-effect studies need to be performed to better establish how each inflammatory state can modulate the pathologies of AD...
  4. 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...
  5. pmc Induction of hyperhomocysteinemia models vascular dementia by induction of cerebral microhemorrhages and neuroinflammation
    Tiffany L Sudduth
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536, USA
    J Cereb Blood Flow Metab 33:708-15. 2013
    ..Overall, we have developed a dietary model of VaD that will be valuable for studying the pathophysiology of VaD and also for studying the comorbidity of VaD with other dementias and other neurodegenerative disorders...
  6. pmc Intracranial injection of Gammagard, a human IVIg, modulates the inflammatory response of the brain and lowers Aβ in APP/PS1 mice along a different time course than anti-Aβ antibodies
    Tiffany L Sudduth
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536, USA
    J Neurosci 33:9684-92. 2013
    ....
  7. pmc Down's syndrome, neuroinflammation, and Alzheimer neuropathogenesis
    Donna M Wilcock
    Department of Physiology, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    J Neuroinflammation 10:84. 2013
    ....
  8. pmc APOE-ε2 and APOE-ε4 correlate with increased amyloid accumulation in cerebral vasculature
    Peter T Nelson
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA
    J Neuropathol Exp Neurol 72:708-15. 2013
    ..These data demonstrate that APOE genotype correlations with Aβ deposition in CAA only incompletely correspond to other AD-linked brain pathologies...
  9. pmc Neuroinflammatory phenotype in early Alzheimer's disease
    Tiffany L Sudduth
    Department of Physiology, University of Kentucky Sanders Brown Center on Aging, Lexington, KY 40536, USA
    Neurobiol Aging 34:1051-9. 2013
    ..We were able to detect differences in AD neuropathology, and changes in serum proteins that distinguished the individuals with apparent M1 versus M2 brain inflammatory polarization...
  10. pmc Early stage drug treatment that normalizes proinflammatory cytokine production attenuates synaptic dysfunction in a mouse model that exhibits age-dependent progression of Alzheimer's disease-related pathology
    Adam D Bachstetter
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536, USA
    J Neurosci 32:10201-10. 2012
    ....