Stephen Scheff

Summary

Affiliation: University of Kentucky
Country: USA

Publications

  1. ncbi request reprint Synaptogenesis in the hippocampal CA1 field following traumatic brain injury
    S W Scheff
    Sanders Brown Center on Aging, University of Kentucky, Lexington, 40536, USA
    J Neurotrauma 22:719-32. 2005
  2. doi request reprint Synapse stability in the precuneus early in the progression of Alzheimer's disease
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    J Alzheimers Dis 35:599-609. 2013
  3. pmc Neuroprotective effect of Pycnogenol® following traumatic brain injury
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    Exp Neurol 239:183-91. 2013
  4. pmc Focal cerebral ischemia in the TNFalpha-transgenic rat
    L Creed Pettigrew
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA
    J Neuroinflammation 5:47. 2008
  5. pmc Effects of genetic deficiency of cyclooxygenase-1 or cyclooxygenase-2 on functional and histological outcomes following traumatic brain injury in mice
    Matthew L Kelso
    Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY, USA
    BMC Neurosci 10:108. 2009
  6. ncbi request reprint Alzheimer's disease-related alterations in synaptic density: neocortex and hippocampus
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky College of Medicine, Lexington, KY 40536 0230, USA
    J Alzheimers Dis 9:101-15. 2006
  7. ncbi request reprint Hippocampal synaptic loss in early Alzheimer's disease and mild cognitive impairment
    Stephen W Scheff
    Sanders Brown Center on Aging and the Alzheimer s Disease Research Center, University of Kentucky College of Medicine, 101 Sanders Brown, Lexington, KY 40536 0230, USA
    Neurobiol Aging 27:1372-84. 2006
  8. ncbi request reprint Synaptic alterations in CA1 in mild Alzheimer disease and mild cognitive impairment
    S W Scheff
    Sanders Brown Center on Aging and Alzheimer Disease Research Center, University of Kentucky College of Medicine, Lexington, KY 40536 0230, USA
    Neurology 68:1501-8. 2007
  9. ncbi request reprint Creatine-enhanced diet alters levels of lactate and free fatty acids after experimental brain injury
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky, 101 Sanders Brown, University of Kentucky, Lexington, Kentucky 40536 0230, USA
    Neurochem Res 29:469-79. 2004
  10. ncbi request reprint Synaptic pathology in Alzheimer's disease: a review of ultrastructural studies
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky College of Medicine, 800 S Limestone, Lexington, KY 40536 0230, USA
    Neurobiol Aging 24:1029-46. 2003

Research Grants

  1. SYNAPTIC CHANGE IN MILD COGNITIVE IMPAIRMENT
    Stephen Scheff; Fiscal Year: 2007
  2. RESPONSE OF THE AGING NERVOUS SYSTEM TO TRAUMA
    Stephen Scheff; Fiscal Year: 2007
  3. TRAUMATIC BRAIN INJURY AND CELLULAR HOMEOSTASIS
    Stephen Scheff; Fiscal Year: 2003
  4. SYNAPTIC CHANGE IN MILD COGNITIVE IMPAIRMENT
    Stephen W Scheff; Fiscal Year: 2010

Detail Information

Publications52

  1. ncbi request reprint Synaptogenesis in the hippocampal CA1 field following traumatic brain injury
    S W Scheff
    Sanders Brown Center on Aging, University of Kentucky, Lexington, 40536, USA
    J Neurotrauma 22:719-32. 2005
    ....
  2. doi request reprint Synapse stability in the precuneus early in the progression of Alzheimer's disease
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    J Alzheimers Dis 35:599-609. 2013
    ..These results support the idea that despite increased amyloid load, the precuneus region does not show early changes in synaptic decline during the progression of AD...
  3. pmc Neuroprotective effect of Pycnogenol® following traumatic brain injury
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    Exp Neurol 239:183-91. 2013
    ..These results are the first to show a neuroprotective effect of PYC following TBI. They also suggest that the diverse effects of bioflavonoids may provide a unique avenue for possible therapeutic intervention following head trauma...
  4. pmc Focal cerebral ischemia in the TNFalpha-transgenic rat
    L Creed Pettigrew
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA
    J Neuroinflammation 5:47. 2008
    ..To determine if chronic elevation of the inflammatory cytokine, tumor necrosis factor-alpha (TNFalpha), will affect infarct volume or cortical perfusion after focal cerebral ischemia...
  5. pmc Effects of genetic deficiency of cyclooxygenase-1 or cyclooxygenase-2 on functional and histological outcomes following traumatic brain injury in mice
    Matthew L Kelso
    Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY, USA
    BMC Neurosci 10:108. 2009
    ..The purpose of the current study was to determine the role of the COX isoforms in contributing to pathological processes resulting from TBI by utilizing mice deficient in COX-1 or COX-2...
  6. ncbi request reprint Alzheimer's disease-related alterations in synaptic density: neocortex and hippocampus
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky College of Medicine, Lexington, KY 40536 0230, USA
    J Alzheimers Dis 9:101-15. 2006
    ..This article reviews the ultrastructural studies assessing AD-related synaptic loss and the possible compensatory changes in the synaptic complex that occur as a result of the loss in brain connectivity...
  7. ncbi request reprint Hippocampal synaptic loss in early Alzheimer's disease and mild cognitive impairment
    Stephen W Scheff
    Sanders Brown Center on Aging and the Alzheimer s Disease Research Center, University of Kentucky College of Medicine, 101 Sanders Brown, Lexington, KY 40536 0230, USA
    Neurobiol Aging 27:1372-84. 2006
    ..This study supports the concept that synapse loss is an early event in the disease process and suggests that MCI may be a transition stage between eAD and NCI with synaptic loss a structural correlate involved in cognitive decline...
  8. ncbi request reprint Synaptic alterations in CA1 in mild Alzheimer disease and mild cognitive impairment
    S W Scheff
    Sanders Brown Center on Aging and Alzheimer Disease Research Center, University of Kentucky College of Medicine, Lexington, KY 40536 0230, USA
    Neurology 68:1501-8. 2007
    ....
  9. ncbi request reprint Creatine-enhanced diet alters levels of lactate and free fatty acids after experimental brain injury
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky, 101 Sanders Brown, University of Kentucky, Lexington, Kentucky 40536 0230, USA
    Neurochem Res 29:469-79. 2004
    ..Animals fed a 1% Cr-diet were afforded greater neuroprotection than animals fed a 0.5% Cr diet. These results support the idea that a Cr-enriched diet can provide substantial neuroprotection in part by suppressing secondary brain injury...
  10. ncbi request reprint Synaptic pathology in Alzheimer's disease: a review of ultrastructural studies
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky College of Medicine, 800 S Limestone, Lexington, KY 40536 0230, USA
    Neurobiol Aging 24:1029-46. 2003
    ..Comparisons are made between results observed with ultrastructural technique and those utilizing immunohistochemistry to assess changes in synaptic pathology. Possible reasons underlying the synaptic neuropathology are discussed...
  11. pmc Synaptic loss in the inferior temporal gyrus in mild cognitive impairment and Alzheimer's disease
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA
    J Alzheimers Dis 24:547-57. 2011
    ..These results demonstrate that the inferior temporal gyrus is affected during the prodromal stage of the disease and may underlie some of the early AD-related clinical dysfunctions...
  12. ncbi request reprint Reactive synaptogenesis in aging and Alzheimer's disease: lessons learned in the Cotman laboratory
    Stephen Scheff
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA
    Neurochem Res 28:1625-30. 2003
    ..In Alzheimer's disease, one observes a marked reduction in the number of synaptic contacts in important association areas of the cortex and hippocampus. This reduction may be the result of an altered reactive plasticity response...
  13. pmc Age-related mitochondrial changes after traumatic brain injury
    Lesley K Gilmer
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536 0230, USA
    J Neurotrauma 27:939-50. 2010
    ..Data indicate that cortical synaptic mitochondria appear to have an increased susceptibility to perturbation with age, suggesting that the increased mitochondrial dysfunction observed following injury may impede recovery in aged animals...
  14. pmc Protective effect of Pycnogenol in human neuroblastoma SH-SY5Y cells following acrolein-induced cytotoxicity
    Mubeen A Ansari
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    Free Radic Biol Med 45:1510-9. 2008
    ..These findings provide support that PYC may provide a promising approach for the treatment of oxidative stress-related neurodegenerative diseases such as AD...
  15. ncbi request reprint Oxidative stress in head trauma in aging
    Changxing Shao
    Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA
    Free Radic Biol Med 41:77-85. 2006
    ..Glutathione reductase activity also showed an age-dependent decrease. Overall, our data show increased levels of oxidative damage, diminished antioxidant capacities, and increased tissue loss in TBI in aging...
  16. ncbi request reprint The pathophysiology of traumatic brain injury in alpha7 nicotinic cholinergic receptor knockout mice
    Matthew L Kelso
    College of Pharmacy, University of Kentucky, Lexington, KY 40536, USA
    Brain Res 1083:204-10. 2006
    ..However, when null mutant mice develop in the absence of central alpha7 expression, it is possible that compensatory changes occur that confound the results obtained...
  17. pmc Oxidative stress and modification of synaptic proteins in hippocampus after traumatic brain injury
    Mubeen A Ansari
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    Free Radic Biol Med 45:443-52. 2008
    ..Early onset of oxidative stress suggests that the initial therapeutic window following TBI appears to be relatively short, and it may be necessary to stagger selective types of antioxidant therapy to target specific oxidative components...
  18. ncbi request reprint Nicotine attenuates morphological deficits in a contusion model of spinal cord injury
    R Ravikumar
    Department of Surgery, University of Kentucky Medical Center, Lexington, Kentucky 40536, USA
    J Neurotrauma 22:240-51. 2005
    ..These results suggest that agonists of neuronal nicotinic receptors can be attractive candidates for SCI therapy...
  19. pmc Efficacy of progesterone following a moderate unilateral cortical contusion injury
    Lesley K Gilmer
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    J Neurotrauma 25:593-602. 2008
    ..Failure to modify two major sequelae associated with TBI brings into question the clinical usefulness of PROG as an effective treatment for all types of brain injury...
  20. pmc Oxidative stress in the progression of Alzheimer disease in the frontal cortex
    Mubeen A Ansari
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536 0230, USA
    J Neuropathol Exp Neurol 69:155-67. 2010
    ..Oxidative stress was more localized to the synapses, with levels increasing in a disease-dependent fashion. These correlations implicate an involvement of oxidative stress in Alzheimer disease-related synaptic loss...
  21. pmc Regionally localized recurrent excitation in the dentate gyrus of a cortical contusion model of posttraumatic epilepsy
    Robert F Hunt
    Dept of Physiology, University of Kentucky, Lexington, KY 40536, USA
    J Neurophysiol 103:1490-500. 2010
    ..These results suggest that a new regionally localized excitatory network forms between dentate granule cells near the injury site within weeks after cortical contusion head injury...
  22. doi request reprint A time course of contusion-induced oxidative stress and synaptic proteins in cortex in a rat model of TBI
    Mubeen A Ansari
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536 0230, USA
    J Neurotrauma 25:513-26. 2008
    ..The initial therapeutic window following TBI appears relatively short since oxidative damage occurs as early as 3 h...
  23. pmc Age-related changes in mitochondrial respiration and oxidative damage in the cerebral cortex of the Fischer 344 rat
    Lesley K Gilmer
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536 0230, United States
    Mech Ageing Dev 131:133-43. 2010
    ..Levels of oxidative damage that accumulates in the cortex with age does not appear to significantly impair cortical mitochondrial respiration of F344 rats...
  24. pmc Human cerebral neuropathology of Type 2 diabetes mellitus
    Peter T Nelson
    Department of Pathology, Division of Neuropathology, University of Kentucky Medical Center, Sanders Brown Center on Aging and Alzheimer s Disease Center, University of Kentucky, Lexington, KY 40536 0230, USA
    Biochim Biophys Acta 1792:454-69. 2009
    ..These preliminary, correlative, and descriptive studies may help develop new hypotheses about CNDM2. We conclude that more work should be performed on human material in the context of CNDM2...
  25. pmc Alzheimer's disease is not "brain aging": neuropathological, genetic, and epidemiological human studies
    Peter T Nelson
    Department of Pathology, University of Kentucky, Lexington, KY 40536 0230, USA
    Acta Neuropathol 121:571-87. 2011
    ..In conclusion, it may be most fruitful to focus attention on specific pathways involved in AD rather than attributing it to an inevitable consequence of aging...
  26. ncbi request reprint Experimental modeling of spinal cord injury: characterization of a force-defined injury device
    Stephen W Scheff
    The Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536 0230, USA
    J Neurotrauma 20:179-93. 2003
    ..This novel rodent model of SCI provides a significant improvement over existing devices for SCI by reducing variability with a constant preset force to define the injury...
  27. pmc Alzheimer's-type neuropathology in the precuneus is not increased relative to other areas of neocortex across a range of cognitive impairment
    Peter T Nelson
    Department of Pathology and Division of Neuropathology, University of Kentucky Medical Center, Sanders Brown Center on Aging and Alzheimer s Disease Center, University of Kentucky, Lexington, KY 40536, USA
    Neurosci Lett 450:336-9. 2009
    ..Our results are not consistent with the idea that the precuneus is involved in a special way with plaques or tangles relative to other areas of neocortex...
  28. pmc Early mitochondrial dysfunction after cortical contusion injury
    Lesley K Gilmer
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536 0230, USA
    J Neurotrauma 26:1271-80. 2009
    ..This study stresses the importance of early therapeutic intervention and suggests a window of approximately 1-3 h before greater dysfunction occurs...
  29. pmc Recovery of afferent function and synaptic strength in hippocampal CA1 following traumatic brain injury
    Christopher M Norris
    Sanders Brown Center on Aging, University of Kentucky College of Medicine, Lexington, Kentucky, USA
    J Neurotrauma 26:2269-78. 2009
    ..Although plasticity mechanisms appear to remain intact, synaptic strength deficits in CA1 could limit information throughput in the hippocampus, leading to persistent memory dysfunction...
  30. ncbi request reprint Rat models of traumatic spinal cord injury to assess motor recovery
    Stephen M Onifer
    Spinal Cord and Brain Injury Research Center, Biomedical and Biological Sciences Research Building, University of Kentucky, 741 South Limestone Street, Lexington, KY 40536 0509, USA
    ILAR J 48:385-95. 2007
    ....
  31. ncbi request reprint Gender differences in spinal cord injury are not estrogen-dependent
    Karin R Swartz
    Division of Neurosurgery, Department of Surgery, University of Kentucky Medical Center, Lexington, Kentucky 40536, USA
    J Neurotrauma 24:473-80. 2007
    ..These results suggest that E(2) does not provide a viable therapy following SCI...
  32. ncbi request reprint Efficacy of methylprednisolone therapy for the injured rat spinal cord
    Alexander G Rabchevsky
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536 0298, USA
    J Neurosci Res 68:7-18. 2002
    ..Equally important, our results caution the use of lesion volume dimensions or percent tissue sparing at the epicenter as indicators of therapeutic efficacy because neither reflects the actual amount of tissue sparing...
  33. ncbi request reprint A statistical method for analyzing rating scale data: the BBB locomotor score
    Stephen W Scheff
    Sanders Brown Center on Aging, University of Kentucky, Lexington 40536, USA
    J Neurotrauma 19:1251-60. 2002
    ..Specifically, it defines appropriate statistical analysis of these data in order to facilitate interpretation of results between laboratories and to provide a common methodology for the correct interpretation of SCI behavioral data...
  34. ncbi request reprint Creatine diet supplement for spinal cord injury: influences on functional recovery and tissue sparing in rats
    Alexander G Rabchevsky
    Sanders Brown Center on Aging, Department of Physiology, University of Kentucky, 236 Health Sciences Research Building, Lexington, Kentucky 40536 0305, USA
    J Neurotrauma 20:659-69. 2003
    ..The relationship between the efficacy of creatine and the magnitude of the insults is discussed...
  35. ncbi request reprint Intrinsic differences in brain and spinal cord mitochondria: Implication for therapeutic interventions
    Patrick G Sullivan
    Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky 40536, USA
    J Comp Neurol 474:524-34. 2004
    ....
  36. ncbi request reprint Mitochondrial uncoupling as a therapeutic target following neuronal injury
    P G Sullivan
    Spinal Cord and Brain Injury Research Center and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky 40536 0305, USA
    J Bioenerg Biomembr 36:353-6. 2004
    ..These findings raise the possibility that mitochondrial uncoupling could be a potential novel treatment for acute CNS injuries...
  37. ncbi request reprint Pathobiology of dynorphins in trauma and disease
    Kurt F Hauser
    Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, Kentucky 40536 0298, USA
    Front Biosci 10:216-35. 2005
    ..Evidence outlined in this review suggests that a variety of CNS pathologies alter dynorphin biogenesis. Such alterations are likely maladaptive and contribute to secondary injury and the pathogenesis of disease...
  38. ncbi request reprint Spatial and temporal characteristics of neurodegeneration after controlled cortical impact in mice: more than a focal brain injury
    Edward D Hall
    Spinal Cord and Brain Injury Research Center, University of Kentucky Chandler Medical Center, Lexington, Kentucky 40536 0305, USA
    J Neurotrauma 22:252-65. 2005
    ....
  39. ncbi request reprint Effects of progesterone on experimental spinal cord injury
    Dominic B Fee
    Department of Neurology, University of Kentucky Chandler Medical Center, Lexington, KY 40536, USA
    Brain Res 1137:146-52. 2007
    ..This study does not support progesterone as a potential therapeutic agent in spinal cord injury...
  40. ncbi request reprint Gender and estrogen manipulation do not affect traumatic brain injury in mice
    Annadora J Bruce-Keller
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536, USA
    J Neurotrauma 24:203-15. 2007
    ....
  41. ncbi request reprint Temporal-spatial dynamics in oligodendrocyte and glial progenitor cell numbers throughout ventrolateral white matter following contusion spinal cord injury
    Alexander G Rabchevsky
    Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky 40536 0509, USA
    Glia 55:831-43. 2007
    ....
  42. pmc Dietary choline supplementation improves behavioral, histological, and neurochemical outcomes in a rat model of traumatic brain injury
    Maria V Guseva
    Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, Kentucky 40536 0082, USA
    J Neurotrauma 25:975-83. 2008
    ..The results of this study suggest that alpha7 nAChR agonists may be useful drugs to enhance recovery following brain injury...
  43. doi request reprint Posttraumatic epilepsy after controlled cortical impact injury in mice
    Robert F Hunt
    Department of Physiology, University of Kentucky, MS 508 Chandler Medical Center, 800 Rose St, Lexington, KY 40536 0298, USA
    Exp Neurol 215:243-52. 2009
    ..Identifying experimental injury models that exhibit similar pathology to injury-induced epilepsy in humans should help to elucidate the mechanisms by which the injured brain becomes epileptic...
  44. ncbi request reprint Cytochrome c release and caspase activation after traumatic brain injury
    Patrick G Sullivan
    229 Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536 0230, USA
    Brain Res 949:88-96. 2002
    ..Our data suggest that several pro-apoptotic events occur following TBI, however the translocation of cytochrome c itself and/or other events upstream of caspase activation/inhibition may be sufficient to induce neuronal cell death...
  45. ncbi request reprint Fluoro-jade B stains quiescent and reactive astrocytes in the rodent spinal cord
    Kevin J Anderson
    Sanders Brown Center on Aging, and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky 40536 0230, USA
    J Neurotrauma 20:1223-31. 2003
    ....
  46. pmc University of Kentucky Sanders-Brown healthy brain aging volunteers: donor characteristics, procedures and neuropathology
    Frederick A Schmitt
    Department of Neurology and the Sanders Brown Center on Aging, 303 Sanders Brown Building, 800 S Limestone, University of Kentucky, Lexington, USA
    Curr Alzheimer Res 9:724-33. 2012
    ..We also explain some of the evolving methodologies and the academic contributions that have been made due to this motivated group of older Kentuckians...
  47. ncbi request reprint Time-dependent changes in rat brain cholinergic receptor expression after experimental brain injury
    S Leigh Verbois
    Division of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, Kentucky 40536 0082, USA
    J Neurotrauma 19:1569-85. 2002
    ..Persistent deficits in alpha7* nAChr expression following TBI may contribute to impaired functional outcome following brain injury...
  48. doi request reprint Melatonin-analog, beta-methyl-6-chloromelatonin, supplementation in spinal cord injury
    Dominic B Fee
    Department of Neurology, University of Kentucky Chandler Medical Center, Lexington, KY, USA
    Brain Res 1340:81-5. 2010
    ..The 10mg/kg supplementation demonstrated benefit; the 100mg/kg dosage was limited by toxicity. This is the first work to assess a melatonin analog in SCI...
  49. ncbi request reprint Regional distribution of fluoro-jade B staining in the hippocampus following traumatic brain injury
    Kevin J Anderson
    Sanders Brown Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536, USA
    Exp Neurol 193:125-30. 2005
    ..In both injury groups and in all hippocampal regions, more FJB-positive neurons were seen at the earlier times post injury (1 and 2 days) than at 7 days. FJB appears to be a reliable marker for neuronal vulnerability following TBI...
  50. ncbi request reprint Traumatic brain injury regulates adrenocorticosteroid receptor mRNA levels in rat hippocampus
    Deanna L McCullers
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536, USA
    Brain Res 947:41-9. 2002
    ..Regulation of MR and GR expression following TBI may influence hippocampal neuron viability by modulating glucocorticoid signaling after injury...
  51. ncbi request reprint Early effects of tribromoethanol, ketamine/xylazine, pentobarbitol, and isoflurane anesthesia on hepatic and lymphoid tissue in ICR mice
    John S Thompson
    Department of Internal Medicine and Sanders Brown Center on Aging, University of Kentucky, Lexington 40536 0298, USA
    Comp Med 52:63-7. 2002
    ..In addition, they also should be avoided in experiments testing effects on hepatic tissue...
  52. ncbi request reprint Cleaved-tau: a biomarker of neuronal damage after traumatic brain injury
    S Prasad Gabbita
    Department of Psychiatry, College of Medicine, University of Cincinnati, Cincinnati, Ohio 45267, USA
    J Neurotrauma 22:83-94. 2005
    ..Serum data suggests that C-tau levels are dependent both on a compromised blood-brain barrier as well as release of TBI biomarkers from the brain, which has implications for the study of human serum TBI biomarkers...

Research Grants15

  1. SYNAPTIC CHANGE IN MILD COGNITIVE IMPAIRMENT
    Stephen Scheff; Fiscal Year: 2007
    ..Successful completion of the proposed studies will lead to new insights into the mechanisms underlying MCI and early AD and contribute to the development of effective pharmacologic therapies for AD. ..
  2. RESPONSE OF THE AGING NERVOUS SYSTEM TO TRAUMA
    Stephen Scheff; Fiscal Year: 2007
    ..Specific aim #4 will use a 'creatine-supplemented' dietary intervention that enhances cytosolic phosphocreatine and increases the ability of neurons to produce ATP, an intervention to reverse the age-related response to TBI. ..
  3. TRAUMATIC BRAIN INJURY AND CELLULAR HOMEOSTASIS
    Stephen Scheff; Fiscal Year: 2003
    ..These studies will significantly enhance our understanding of the mechanisms following TBI and hopefully lead to therapies resulting in increased recovery. ..
  4. SYNAPTIC CHANGE IN MILD COGNITIVE IMPAIRMENT
    Stephen W Scheff; Fiscal Year: 2010
    ..Successful completion of the proposed studies will lead to new insights into the mechanisms underlying MCI and early AD and contribute to the development of effective pharmacologic therapies for AD. ..