R E Mrak

Summary

Affiliation: University of Arkansas for Medical Sciences
Country: USA

Publications

  1. 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
  2. pmc Reviewer acknowledgement
    SUE T GRIFFIN
    Department of Pathology, University of Toledo Health Sciences Campus, 300 Arlington Ave, MS 1090, OH 43614 2598, Toledo, USA
    J Neuroinflammation 10:17. 2013
  3. 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
  4. ncbi The role of activated astrocytes and of the neurotrophic cytokine S100B in the pathogenesis of Alzheimer's disease
    R E Mrak
    Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Neurobiol Aging 22:915-22. 2001
  5. ncbi Interleukin-1, neuroinflammation, and Alzheimer's disease
    R E Mrak
    Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Neurobiol Aging 22:903-8. 2001
  6. ncbi 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
  7. ncbi Glial-neuronal interactions in Alzheimer's disease: the potential role of a 'cytokine cycle' in disease progression
    W S Griffin
    Department of Veterans Affairs Medical Center, Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock 72205, USA
    Brain Pathol 8:65-72. 1998
  8. ncbi Neuronal DNA damage correlates with overexpression of interleukin-1beta converting enzyme in APPV717F mice
    J G Sheng
    Donald W. Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Neurobiol Aging 22:895-902. 2001
  9. pmc Life-long overexpression of S100beta in Down's syndrome: implications for Alzheimer pathogenesis
    W S Griffin
    Geriatric Research, Education, and Clinical Center of the Department of Veterans Affairs Medical Center, University of Arkansas for Medical Sciences, Little Rock 72205, USA
    Neurobiol Aging 19:401-5. 1998
  10. pmc Interleukin-1 promotion of MAPK-p38 overexpression in experimental animals and in Alzheimer's disease: potential significance for tau protein phosphorylation
    J G Sheng
    The Donald W. Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, 4301 W. Markham Street, Little Rock, AR 72205, USA
    Neurochem Int 39:341-8. 2001

Collaborators

Detail Information

Publications30

  1. 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...
  2. pmc Reviewer acknowledgement
    SUE T GRIFFIN
    Department of Pathology, University of Toledo Health Sciences Campus, 300 Arlington Ave, MS 1090, OH 43614 2598, Toledo, USA
    J Neuroinflammation 10:17. 2013
    ..CONTRIBUTING REVIEWERS: The editors of Journal of Neuroinflammation would like to thank all the reviewers who have contributed to the journal in Volume 9 (2012)...
  3. 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...
  4. ncbi The role of activated astrocytes and of the neurotrophic cytokine S100B in the pathogenesis of Alzheimer's disease
    R E Mrak
    Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Neurobiol Aging 22:915-22. 2001
    ..These cells and molecules are an important components of a cytokine cycle of molecular and cellular cascades that may drive disease progression in Alzheimer's disease...
  5. ncbi Interleukin-1, neuroinflammation, and Alzheimer's disease
    R E Mrak
    Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Neurobiol Aging 22:903-8. 2001
    ....
  6. ncbi 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...
  7. ncbi Glial-neuronal interactions in Alzheimer's disease: the potential role of a 'cytokine cycle' in disease progression
    W S Griffin
    Department of Veterans Affairs Medical Center, Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock 72205, USA
    Brain Pathol 8:65-72. 1998
    ..Chronic propagation of this cytokine cycle represents a possible mechanism for progression of neurodegenerative changes culminating in Alzheimer's disease...
  8. ncbi Neuronal DNA damage correlates with overexpression of interleukin-1beta converting enzyme in APPV717F mice
    J G Sheng
    Donald W. Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Neurobiol Aging 22:895-902. 2001
    ..These findings are consistent with the idea that increases in ICE activity and expression contribute to neuronal injury in Alzheimer's disease...
  9. pmc Life-long overexpression of S100beta in Down's syndrome: implications for Alzheimer pathogenesis
    W S Griffin
    Geriatric Research, Education, and Clinical Center of the Department of Veterans Affairs Medical Center, University of Arkansas for Medical Sciences, Little Rock 72205, USA
    Neurobiol Aging 19:401-5. 1998
    ..05). Our findings are consistent with the idea that conditions--including Down's syndrome--that promote chronic overexpression of S100beta may confer increased risk for later development of Alzheimer's disease...
  10. pmc Interleukin-1 promotion of MAPK-p38 overexpression in experimental animals and in Alzheimer's disease: potential significance for tau protein phosphorylation
    J G Sheng
    The Donald W. Reynolds Department of Geriatrics, University of Arkansas for Medical Sciences, 4301 W. Markham Street, Little Rock, AR 72205, USA
    Neurochem Int 39:341-8. 2001
    ....
  11. ncbi Vitamin E suppression of microglial activation is neuroprotective
    Y Li
    Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    J Neurosci Res 66:163-70. 2001
    ....
  12. ncbi Senescence-accelerated overexpression of S100beta in brain of SAMP6 mice
    W S Griffin
    Department of Veterans Affairs Medical Center, and the Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock 72205, USA
    Neurobiol Aging 19:71-6. 1998
    ....
  13. pmc The pervasiveness of interleukin-1 in alzheimer pathogenesis: a role for specific polymorphisms in disease risk
    W S Griffin
    Departments of Geriatrics, Medicine, Psychiatry, and Pathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
    Exp Gerontol 35:481-7. 2000
    ..This increase is associated with earlier age of onset. Homozygosity for this polymorphism plus another in the IL-1B gene further increases risk...
  14. doi Neuropathology and the neuroinflammation idea
    Robert E Mrak
    Department of Pathology, 2280 Dowling Hall, University of Toledo Health Science Campus MS 1090, 3000 Arlington Avenue, Toledo, OH 43614, USA
    J Alzheimers Dis 18:473-81. 2009
    ..Further observations have extended these ideas to alpha-synuclein-based diseases (Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy) as well as other neurodegenerative diseases and conditions...
  15. 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...
  16. doi Pituitary adenoma with craniopharyngioma component
    Murat Gokden
    Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Hum Pathol 40:1189-93. 2009
    ..It was clinically a nonfunctioning adenoma, which was also negative for pituitary hormones by immunohistochemistry. Its histogenesis and implications are discussed with a review of the literature...
  17. ncbi Overexpression of the neuritotrophic cytokine S100beta precedes the appearance of neuritic beta-amyloid plaques in APPV717F mice
    J G Sheng
    Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, USA
    J Neurochem 74:295-301. 2000
    ..Accelerated age-related overexpression of S100beta may interact with age-associated overexpression of mutant betaAPP in transgenic mice to promote development of Alzheimer-like neuropathological changes...
  18. 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
    ....
  19. 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...
  20. ncbi Alzheimer-type neuropathological changes in morbidly obese elderly individuals
    R E Mrak
    Department of Pathology, University of Toledo College of Medicine, 3000 Arlington Avenue, Toledo, OH 43614, USA
    Clin Neuropathol 28:40-5. 2009
    ..Middle age obesity increases risk for Alzheimer disease (AD). This study evaluated neuropathological changes in morbidly obese patients ranging in age from 21-70 years...
  21. ncbi Phospholipid abnormalities in postmortem schizophrenic brains detected by 31P nuclear magnetic resonance spectroscopy: a preliminary study
    R A Komoroski
    Department of Radiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Psychiatry Res 106:171-80. 2001
    ..Although these results are not in complete agreement with previous studies, they support the idea that PL abnormalities occur in the brain in schizophrenia and that fatty acid metabolism may be abnormal...
  22. ncbi 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
    ....
  23. 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...
  24. pmc Trafficking of glucose, lactate, and amyloid-beta from the inferior colliculus through perivascular routes
    Kelly K Ball
    Department of Neurology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    J Cereb Blood Flow Metab 30:162-76. 2010
    ..Convergence of 'watershed' drainage to common pathways may facilitate perivascular amyloid plaque formation and pathway obstruction in Alzheimer's disease...
  25. ncbi 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
    ....
  26. ncbi Heparanase expression and TrkC/p75NTR ratios in human medulloblastoma
    Neeta D Sinnappah-Kang
    Division of Pediatrics, University of Texas M D Anderson Cancer Center, Houston, TX 77030, USA
    Clin Exp Metastasis 23:55-63. 2006
    ..Of note, TrkC was significantly present in 100% of MB female patients (P = 0.0313; n = 6). These studies support the role of p75(NTR) and HPSE-1 as two novel molecular determinants involved in the biology and clinical progression of MB...
  27. ncbi Postmortem locus coeruleus neuron count in three American veterans with probable or possible war-related PTSD
    H Stefan Bracha
    National Center for Posttraumatic Stress Disorder, Department of Veterans Affairs, Pacific Islands Health Care System, Spark M Matsunaga VA Medical Center, 1132 Bishop St 307, Honolulu, HI, USA
    J Neuropsychiatry Clin Neurosci 17:503-9. 2005
    ..Larger neuromorphometric studies of the LC in veterans with WR-PTSD and in other development-stress-induced and fear-circuitry disorders are warranted, especially using VA registries...