W Sue T Griffin

Summary

Affiliation: University of Arkansas for Medical Sciences
Country: USA

Publications

  1. pmc Perispinal etanercept: potential as an Alzheimer therapeutic
    W Sue T Griffin
    Geriatric Research, Education and Clinical Center, Neurobiology, Physiology, and Psychiatry, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    J Neuroinflammation 5:3. 2008
  2. pmc Alzheimer's - Looking beyond plaques
    W Sue T Griffin
    Geriatric Research, Education and Clinical Center, Neurobiology, Physiology, and Psychiatry, University of Arkansas for Medical Sciences, and the Geriatrics, Education Clinical Center, Central Arkansas Veterans Healthcare System Little Rock, Arkansas 72205 USA
    F1000 Med Rep 3:24. 2011
  3. doi request reprint Epilepsy: neuroinflammation, neurodegeneration, and APOE genotype
    Orwa Aboud
    Donald W, Reynolds Department of Geriatrics, University of Arkansas College of Medicine, Little Rock, AR 72205, USA
    Acta Neuropathol Commun 1:41. 2013
  4. 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
  5. pmc Interleukin-1 mediates Alzheimer and Lewy body pathologies
    W Sue T Griffin
    Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    J Neuroinflammation 3:5. 2006
  6. pmc Apolipoprotein epsilon 3 alleles are associated with indicators of neuronal resilience
    Orwa Aboud
    Donald W, Reynolds Department of Geriatrics, Reynolds Institute on Aging, 629 Jack Stephens Drive, Little Rock, AR 72205, USA
    BMC Med 10:35. 2012
  7. pmc Generation of reactive oxygen species in 1-methyl-4-phenylpyridinium (MPP+) treated dopaminergic neurons occurs as an NADPH oxidase-dependent two-wave cascade
    W Michael Zawada
    Donald W, Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    J Neuroinflammation 8:129. 2011
  8. pmc The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective
    Solomon S Shaftel
    Department of Neurobiology and Anatomy, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA
    J Neuroinflammation 5:7. 2008
  9. pmc Interleukin-1 in the genesis and progression of and risk for development of neuronal degeneration in Alzheimer's disease
    W Sue T Griffin
    Department of Geriatrics, Medicine, and Psychiatry, University of Arkansas for Medical Sciences, Veterans Affairs Medical Center, Little Rock, USA
    J Leukoc Biol 72:233-8. 2002
  10. ncbi request reprint Inflammation and neurodegenerative diseases
    W Sue T Griffin
    Donald W Reynolds Department of Geriatrics, The University of Arkansas for Medical Sciences, and the Geriatric Research Education Clinical Center, Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA
    Am J Clin Nutr 83:470S-474S. 2006

Research Grants

Detail Information

Publications26

  1. pmc Perispinal etanercept: potential as an Alzheimer therapeutic
    W Sue T Griffin
    Geriatric Research, Education and Clinical Center, Neurobiology, Physiology, and Psychiatry, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    J Neuroinflammation 5:3. 2008
    ....
  2. pmc Alzheimer's - Looking beyond plaques
    W Sue T Griffin
    Geriatric Research, Education and Clinical Center, Neurobiology, Physiology, and Psychiatry, University of Arkansas for Medical Sciences, and the Geriatrics, Education Clinical Center, Central Arkansas Veterans Healthcare System Little Rock, Arkansas 72205 USA
    F1000 Med Rep 3:24. 2011
    ..This review is a personal account of the quest to prove that inflammation plays a critical role in causing Alzheimer's disease...
  3. doi request reprint Epilepsy: neuroinflammation, neurodegeneration, and APOE genotype
    Orwa Aboud
    Donald W, Reynolds Department of Geriatrics, University of Arkansas College of Medicine, Little Rock, AR 72205, USA
    Acta Neuropathol Commun 1:41. 2013
    ....
  4. 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
    ....
  5. pmc Interleukin-1 mediates Alzheimer and Lewy body pathologies
    W Sue T Griffin
    Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    J Neuroinflammation 3:5. 2006
    ..Glial activation, with overexpression of interleukin-1 (IL-1) and other proinflammatory cytokines, has been increasingly implicated in the pathogenesis of both AD and PD...
  6. pmc Apolipoprotein epsilon 3 alleles are associated with indicators of neuronal resilience
    Orwa Aboud
    Donald W, Reynolds Department of Geriatrics, Reynolds Institute on Aging, 629 Jack Stephens Drive, Little Rock, AR 72205, USA
    BMC Med 10:35. 2012
    ....
  7. pmc Generation of reactive oxygen species in 1-methyl-4-phenylpyridinium (MPP+) treated dopaminergic neurons occurs as an NADPH oxidase-dependent two-wave cascade
    W Michael Zawada
    Donald W, Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    J Neuroinflammation 8:129. 2011
    ....
  8. pmc The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective
    Solomon S Shaftel
    Department of Neurobiology and Anatomy, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA
    J Neuroinflammation 5:7. 2008
    ..Potentially adaptive functions of IL-1 elevation in AD warrant further mechanistic studies, and provide evidence that enhancement of these effects may help to alleviate the pathologic burden of disease...
  9. pmc Interleukin-1 in the genesis and progression of and risk for development of neuronal degeneration in Alzheimer's disease
    W Sue T Griffin
    Department of Geriatrics, Medicine, and Psychiatry, University of Arkansas for Medical Sciences, Veterans Affairs Medical Center, Little Rock, USA
    J Leukoc Biol 72:233-8. 2002
    ..Moreover, this increased risk is associated with earlier age of onset of the disease. Homozygosity for this polymorphism in combination with another in the IL-1B gene further increases risk...
  10. ncbi request reprint Inflammation and neurodegenerative diseases
    W Sue T Griffin
    Donald W Reynolds Department of Geriatrics, The University of Arkansas for Medical Sciences, and the Geriatric Research Education Clinical Center, Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA
    Am J Clin Nutr 83:470S-474S. 2006
    ..Over a period of years, this slow, smoldering inflammation in the brain destroys sufficient neurons to cause the clinical signs of Alzheimer disease...
  11. pmc Relationships between expression of apolipoprotein E and beta-amyloid precursor protein are altered in proximity to Alzheimer beta-amyloid plaques: potential explanations from cell culture studies
    Steven W Barger
    Department of Geriatrics, Geriatric Research Education and Clinical Center, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA
    J Neuropathol Exp Neurol 67:773-83. 2008
    ....
  12. pmc Apolipoprotein E expression is elevated by interleukin 1 and other interleukin 1-induced factors
    Ling Liu
    Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    J Neuroinflammation 8:175. 2011
    ..These stressors include interleukin-1 (IL-1)-mediated neuroinflammation and glutamate-mediated excitotoxicity. Such circumstances are especially powerful when they transpire in the context of an APOE ε4 allele...
  13. ncbi request reprint S100B-induced microglial and neuronal IL-1 expression is mediated by cell type-specific transcription factors
    Ling Liu
    Department of Geriatrics, University of Arkansas for Medical Sciences, 629 Jack Stephens Drive 807, Little Rock, AR 72205, USA
    J Neurochem 92:546-53. 2005
    ....
  14. pmc Microglial activation by uptake of fDNA via a scavenger receptor
    Yuekui Li
    Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    J Neuroimmunol 147:50-5. 2004
    ..These results suggest that the brain rids itself of fDNA from dying neurons through microglial uptake, activation, and overexpression of IL-1. Such overexpression of IL-1 in Alzheimer brain has been linked to Alzheimer pathogenesis...
  15. pmc Interleukin-1 mediates pathological effects of microglia on tau phosphorylation and on synaptophysin synthesis in cortical neurons through a p38-MAPK pathway
    Yuekui Li
    Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    J Neurosci 23:1605-11. 2003
    ....
  16. ncbi request reprint Potential inflammatory biomarkers in Alzheimer's disease
    Robert E Mrak
    Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    J Alzheimers Dis 8:369-75. 2005
    ....
  17. pmc Trisomy 21 and the brain
    Robert E Mrak
    Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
    J Neuropathol Exp Neurol 63:679-85. 2004
    ..IL-1 upregulates betaAPP and S100B expression and drives numerous neurodegenerative and self-amplifying cascades that support a neuroinflammatory component in the pathogenesis of sporadic and Down syndrome-related Alzheimer disease...
  18. ncbi request reprint Common inflammatory mechanisms in Lewy body disease and Alzheimer disease
    Robert E Mrak
    Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    J Neuropathol Exp Neurol 66:683-6. 2007
    ..These neuroinflammatory processes may be a common link driving progression in both diseases and explaining the frequent overlap between the 2 diseases...
  19. ncbi request reprint Glia and their cytokines in progression of neurodegeneration
    Robert E Mrak
    Department of Pathology, University of Arkansas for Medical Sciences, 629 South Elm Street, Room 3103, Little Rock, AR 72205, USA
    Neurobiol Aging 26:349-54. 2005
    ....
  20. pmc Nox4-generated superoxide drives angiotensin II-induced neural stem cell proliferation
    Elena Topchiy
    Department of Behavioral Neuroscience, Oregon Health and Sciences University, 3181 SW Sam Jackson Park Rd, Mail Code L470, Portland, OR 97239, USA
    Dev Neurosci 35:293-305. 2013
    ....
  21. pmc APP-BP1 inhibits Abeta42 levels by interacting with Presenilin-1
    Yuzhi Chen
    Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Mol Neurodegener 2:3. 2007
    ..Increased Abeta42/Abeta40 ratios trigger amyloid plaque formations in Alzheimer's disease (AD). APP binds to APP-BP1, but the biological consequence is not well understood...
  22. ncbi request reprint Increased susceptibility of S100B transgenic mice to perinatal hypoxia-ischemia
    Mark S Wainwright
    Department of Pediatrics, Division of Neurology, Children s Memorial Hospital, Chicago, IL, USA
    Ann Neurol 56:61-7. 2004
    ..This is the first demonstration to our knowledge that overexpression of S100B in vivo enhances pathological response to injury...
  23. ncbi request reprint Apolipoprotein E co-localizes with newly formed amyloid beta-protein (Abeta) deposits lacking immunoreactivity against N-terminal epitopes of Abeta in a genotype-dependent manner
    Dietmar Rudolf Thal
    Department of Neuropathology, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
    Acta Neuropathol 110:459-71. 2005
    ..Moreover, apoE-positive newly formed plaques were seen more frequently in APOE epsilon4/4 cases than in non-APOE epsilon4/4 individuals, thereby underlining the potentially crucial role of apoE for the development of Abeta deposits...
  24. ncbi request reprint [Relationship between apoptosis of neurons and microglia activation in Alzheimer's disease]
    Dong ge Liu
    Department of Pathology, Beijing Hospital, Beijing 100730, China
    Zhonghua Bing Li Xue Za Zhi 33:404-7. 2004
    ..To assess the relationship between microglia activation and apoptosis of neurons, and the significance of activated microglias in the formation and progression of senile plaques in Alzheimer's disease...
  25. ncbi request reprint Association of the glutathione S-transferase omega-1 Ala140Asp polymorphism with cerebrovascular atherosclerosis and plaque-associated interleukin-1 alpha expression
    Heike Kolsch
    Stroke 38:2847-50. 2007
    ..The objective of this study is to address the question of whether common vessel disorders known to cause vascular dementia are modified in their severity by this polymorphism...
  26. doi request reprint Cerebral amyloid angiopathy and its relationship to Alzheimer's disease
    Dietmar Rudolf Thal
    Laboratory of Neuropathology, Institute of Pathology, University of Ulm, Albert Einstein Allee 7, 89081 Ulm, Germany
    Acta Neuropathol 115:599-609. 2008
    ..Thus, blood flow alterations with subsequent hypoperfusion induced by CAA-related capillary occlusion presumably point to a second mechanism in which A beta adversely affects the brain in AD in addition to its direct neurotoxic effects...

Research Grants7

  1. CYTOKINES, NEURODEGENERATION AND DOWN'S SYNDROME
    Sue Griffin; Fiscal Year: 2000
    ..Accomplishment of our aims will elucidate the pathogenic mechanisms underlying the cognitive decline apparent at middle age in Down's patients and provide targets for possible therapeutic intervention. ..
  2. CYTOKINES, NEURODEGENERATION AND DOWN'S SYNDROME
    Sue Griffin; Fiscal Year: 2001
    ..Accomplishment of our aims will elucidate the pathogenic mechanisms underlying the cognitive decline apparent at middle age in Down's patients and provide targets for possible therapeutic intervention. ..
  3. CYTOKINES, NEURODEGENERATION AND DOWN'S SYNDROME
    Sue Griffin; Fiscal Year: 2002
    ..Accomplishment of our aims will elucidate the pathogenic mechanisms underlying the cognitive decline apparent at middle age in Down's patients and provide targets for possible therapeutic intervention. ..
  4. CYTOKINES, NEURODEGENERATION AND DOWN'S SYNDROME
    Sue Griffin; Fiscal Year: 2003
    ..Accomplishment of our aims will elucidate the pathogenic mechanisms underlying the cognitive decline apparent at middle age in Down's patients and provide targets for possible therapeutic intervention. ..
  5. CYTOKINES, NEURODEGENERATION AND DOWN'S SYNDROME
    Sue Griffin; Fiscal Year: 2004
    ..Accomplishment of our aims will elucidate the pathogenic mechanisms underlying the cognitive decline apparent at middle age in Down's patients and provide targets for possible therapeutic intervention. ..
  6. EARLY EVENTS IN ALZHEIMER PATHOGENESIS
    Sue Griffin; Fiscal Year: 2006
    ..Accomplishment of the goals of this Program Project will yield results that directly identify basic mechanisms in Alzheimer pathogenesis and provide targets for developing therapeutic strategies for degenerative conditions in general...