Hyoung gon Lee

Summary

Affiliation: Case Western Reserve University
Country: USA

Publications

  1. pmc The effect of mGluR2 activation on signal transduction pathways and neuronal cell survival
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Brain Res 1249:244-50. 2009
  2. pmc The neuronal expression of MYC causes a neurodegenerative phenotype in a novel transgenic mouse
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, 2103 Cornell Rd, Cleveland, OH 44106, USA
    Am J Pathol 174:891-7. 2009
  3. pmc Cell cycle re-entry and mitochondrial defects in myc-mediated hypertrophic cardiomyopathy and heart failure
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, United States of America
    PLoS ONE 4:e7172. 2009
  4. pmc Cell cycle re-entry mediated neurodegeneration and its treatment role in the pathogenesis of Alzheimer's disease
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, Cleveland, OH, USA
    Neurochem Int 54:84-8. 2009
  5. ncbi request reprint Aberrant localization of importin alpha1 in hippocampal neurons in Alzheimer disease
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Brain Res 1124:1-4. 2006
  6. ncbi request reprint Aberrant expression of metabotropic glutamate receptor 2 in the vulnerable neurons of Alzheimer's disease
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Acta Neuropathol 107:365-71. 2004
  7. ncbi request reprint Tau modifiers as therapeutic targets for Alzheimer's disease
    Quan Liu
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
    Biochim Biophys Acta 1739:211-5. 2005
  8. ncbi request reprint Ectopic localization of phosphorylated histone H3 in Alzheimer's disease: a mitotic catastrophe?
    Osamu Ogawa
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Acta Neuropathol 105:524-8. 2003
  9. ncbi request reprint Mitogen- and stress-activated protein kinase 1: convergence of the ERK and p38 pathways in Alzheimer's disease
    Kate M Webber
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurosci Res 79:554-60. 2005
  10. ncbi request reprint Signal transduction cascades associated with oxidative stress in Alzheimer's disease
    Robert B Petersen
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    J Alzheimers Dis 11:143-52. 2007

Detail Information

Publications87

  1. pmc The effect of mGluR2 activation on signal transduction pathways and neuronal cell survival
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Brain Res 1249:244-50. 2009
    ..Additionally, our findings lend support to the notion that tau phosphorylation is a neuroprotective antioxidant response to cellular insults...
  2. pmc The neuronal expression of MYC causes a neurodegenerative phenotype in a novel transgenic mouse
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, 2103 Cornell Rd, Cleveland, OH 44106, USA
    Am J Pathol 174:891-7. 2009
    ....
  3. pmc Cell cycle re-entry and mitochondrial defects in myc-mediated hypertrophic cardiomyopathy and heart failure
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, United States of America
    PLoS ONE 4:e7172. 2009
    ....
  4. pmc Cell cycle re-entry mediated neurodegeneration and its treatment role in the pathogenesis of Alzheimer's disease
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, Cleveland, OH, USA
    Neurochem Int 54:84-8. 2009
    ..Therefore, the study of aberrant cell cycle regulation in model systems, both cellular and animal, may provide extremely important insights into the pathogenesis of AD and also serve as a means to test novel therapeutic approaches...
  5. ncbi request reprint Aberrant localization of importin alpha1 in hippocampal neurons in Alzheimer disease
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Brain Res 1124:1-4. 2006
    ..These data suggest a hindrance in importin-mediated cytoplasmic-nuclear transport in AD...
  6. ncbi request reprint Aberrant expression of metabotropic glutamate receptor 2 in the vulnerable neurons of Alzheimer's disease
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Acta Neuropathol 107:365-71. 2004
    ..Immunocytochemical examination revealed considerable overlap between mGluR2 and neurofibrillary alterations. Thus, it is likely that mGluR2 represents a novel therapeutic target for AD...
  7. ncbi request reprint Tau modifiers as therapeutic targets for Alzheimer's disease
    Quan Liu
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
    Biochim Biophys Acta 1739:211-5. 2005
    ..Biochemical findings show that tau oxidative modifications are regulated by phosphorylation and that tau found in neurofibrillary tangles is oxidatively modified, suggesting that tau is closely linked to the biology, not toxicity, of AD...
  8. ncbi request reprint Ectopic localization of phosphorylated histone H3 in Alzheimer's disease: a mitotic catastrophe?
    Osamu Ogawa
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Acta Neuropathol 105:524-8. 2003
    ..Therefore, the aberrant cytoplasmic localization of phosphorylated histone H3 indicates a mitotic catastrophe that leads to neuronal dysfunction and neurodegeneration in AD...
  9. ncbi request reprint Mitogen- and stress-activated protein kinase 1: convergence of the ERK and p38 pathways in Alzheimer's disease
    Kate M Webber
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurosci Res 79:554-60. 2005
    ....
  10. ncbi request reprint Signal transduction cascades associated with oxidative stress in Alzheimer's disease
    Robert B Petersen
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    J Alzheimers Dis 11:143-52. 2007
    ..In this review, we present the evidence of oxidative stress and compensatory responses that occur in Alzheimer's disease with a particular focus on the roles and mechanism of activation of stress-activated protein kinase pathways...
  11. ncbi request reprint Ectopic expression of phospho-Smad2 in Alzheimer's disease: uncoupling of the transforming growth factor-beta pathway?
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    J Neurosci Res 84:1856-61. 2006
    ....
  12. ncbi request reprint Increased p27, an essential component of cell cycle control, in Alzheimer's disease
    Osamu Ogawa
    Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Aging Cell 2:105-10. 2003
    ..The findings presented here suggest that dysregulation of the cell cycle plays a crucial role in the pathogenesis of Alzheimer's disease that may provide a novel mechanistic basis for therapeutic intervention...
  13. pmc Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer's disease
    Baiyang Sheng
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurochem 120:419-29. 2012
    ..Overall, this study demonstrated that impaired mitochondrial biogenesis likely contributes to mitochondrial dysfunction in AD...
  14. doi request reprint Chronic oxidative stress causes increased tau phosphorylation in M17 neuroblastoma cells
    Bo Su
    Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA
    Neurosci Lett 468:267-71. 2010
    ..In conclusion we suggest that chronic oxidative stress contributes to increased tau phosphorylation in vitro and could play a critical role in neurofibrillary pathology in vivo...
  15. ncbi request reprint Oxidative stress and neuronal adaptation in Alzheimer disease: the role of SAPK pathways
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, Cleveland, OH, USA
    Antioxid Redox Signal 5:571-6. 2003
    ....
  16. pmc The cell cycle regulator phosphorylated retinoblastoma protein is associated with tau pathology in several tauopathies
    Jeremy G Stone
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    J Neuropathol Exp Neurol 70:578-87. 2011
    ..These observations further implicate aberrant neuronal cell cycle progression in neurodegenerative diseases, particularly tauopathies, and suggest a novel target for therapeutic intervention...
  17. ncbi request reprint Redox metals and oxidative abnormalities in human prion diseases
    Robert B Petersen
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Acta Neuropathol 110:232-8. 2005
    ..These findings suggest an important distinction in prion-related oxidative stress, indicating that different neurodegenerative pathways are involved in different prion diseases...
  18. pmc Cellular prion protein is essential for oligomeric amyloid-β-induced neuronal cell death
    Wataru Kudo
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Hum Mol Genet 21:1138-44. 2012
    ..These findings are the first to demonstrate that PrP(C) is required for Aβ oligomer-induced neuronal cell death, the pathology essential to cognitive loss...
  19. pmc Reexamining Alzheimer's disease: evidence for a protective role for amyloid-beta protein precursor and amyloid-beta
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, MD 21201, USA
    J Alzheimers Dis 18:447-52. 2009
    ..It is now long overdue that the neuroscientists avoid the pitfall of perseverating on "proteinopathies'' and recognize that the continued targeting of end stage lesions in the face of repeated failure, or worse, is a losing proposition...
  20. pmc Evidence for the progression through S-phase in the ectopic cell cycle re-entry of neurons in Alzheimer disease
    David J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Aging (Albany NY) 1:382-8. 2009
    ....
  21. ncbi request reprint Tau phosphorylation in Alzheimer's disease: pathogen or protector?
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106 USA
    Trends Mol Med 11:164-9. 2005
    ....
  22. ncbi request reprint Will preventing protein aggregates live up to its promise as prophylaxis against neurodegenerative diseases?
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Brain Pathol 13:630-8. 2003
    ..In this review, we weigh the evidence of whether removal of amyloids, aggregates and neuronal inclusions represent a reasonable strategy for protecting neurons...
  23. pmc Impaired balance of mitochondrial fission and fusion in Alzheimer's disease
    Xinglong Wang
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurosci 29:9090-103. 2009
    ..Based on these findings, we suggest that an altered balance in mitochondrial fission and fusion is likely an important mechanism leading to mitochondrial and neuronal dysfunction in AD brain...
  24. pmc Biomarkers in Alzheimer's disease: past, present and future
    Katarzyna Gustaw-Rothenberg
    University Hospitals, Case Medical Center and University Memory and Cognitive Center, Case Western Reserve University, Cleveland, OH, USA
    Biomark Med 4:15-26. 2010
    ....
  25. pmc Indoleamine 2,3-dioxygenase and 3-hydroxykynurenine modifications are found in the neuropathology of Alzheimer's disease
    David J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Redox Rep 15:161-8. 2010
    ....
  26. ncbi request reprint Amyloid-beta in Alzheimer disease: the null versus the alternate hypotheses
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA
    J Pharmacol Exp Ther 321:823-9. 2007
    ..To determine which hypothesis relates best to Alzheimer disease requires a broader view of disease pathogenesis and is discussed herein...
  27. ncbi request reprint Neuroprotective properties of Bcl-w in Alzheimer disease
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    J Neurochem 89:1233-40. 2004
    ..Taken together, these series of results suggest that Bcl-w may play an important protective role in neurons in the diseased brain and that this aspect could be therapeutically harnessed to afford neuroprotection...
  28. ncbi request reprint The role of mitogen-activated protein kinase pathways in Alzheimer's disease
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Neurosignals 11:270-81. 2002
    ..e., tau phosphorylation and amyloid-beta deposition, as well as the functional association to amyloid beta protein precursor. We suggest that regulation of these pathways may be a central facet to any potential treatment for the disease...
  29. ncbi request reprint Perspectives on the amyloid-beta cascade hypothesis
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    J Alzheimers Dis 6:137-45. 2004
    ..These findings bring into serious doubt the validity of the Amyloid Cascade Hypothesis as the central cause of Alzheimer disease and, consequently, the potential usefulness of therapeutic targets against amyloid-beta...
  30. ncbi request reprint Challenging the amyloid cascade hypothesis: senile plaques and amyloid-beta as protective adaptations to Alzheimer disease
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Ann N Y Acad Sci 1019:1-4. 2004
    ..With this in mind, we suspect that current therapeutic efforts targeted toward lowering amyloid-beta production or removal of deposited amyloid-beta will only serve to exacerbate the disease process...
  31. ncbi request reprint Therapeutic opportunities in Alzheimer disease: one for all or all for one?
    Michael W Marlatt
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
    Curr Med Chem 12:1137-47. 2005
    ..In this review, the scientific basis for common AD therapeutics as well as the efficacy of these treatments will be discussed...
  32. doi request reprint Neuronal cell cycle re-entry markers are altered in the senescence accelerated mouse P8 (SAMP8)
    Gemma Casadesus
    Departments of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA
    J Alzheimers Dis 30:573-83. 2012
    ....
  33. doi request reprint Antioxidant approaches for the treatment of Alzheimer's disease
    Hyun Pil Lee
    Case Western Reserve University, OH, USA
    Expert Rev Neurother 10:1201-8. 2010
    ..In this article, we discuss the multiple pathogenic mechanisms of oxidative stress in AD and the potential targeting approaches...
  34. ncbi request reprint Antioxidant protection and neurodegenerative disease: the role of amyloid-beta and tau
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, Maryland, USA
    Am J Alzheimers Dis Other Demen 21:126-30. 2006
    ....
  35. pmc Alzheimer disease pathology as a host response
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, Maryland, USA
    J Neuropathol Exp Neurol 67:523-31. 2008
    ..Therefore, renewed efforts aimed at elucidating fundamental age-related processes such as oxidative stress and/or inflammatory mediators are warranted...
  36. ncbi request reprint Neuropathology and treatment of Alzheimer disease: did we lose the forest for the trees?
    Rudy J Castellani
    University of Maryland, Department of Pathology, Baltimore, MD 21201, USA
    Expert Rev Neurother 7:473-85. 2007
    ..An acceptance that lesion-based therapies do not address etiology or rate-limiting pathogenic factors is probably necessary for the best chance of significant advances that have thus far been elusive...
  37. ncbi request reprint Distribution, levels, and activation of MEK1 in Alzheimer's disease
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurochem 86:136-42. 2003
    ..Together, these findings lend further credence to the notion that the ERK pathway is dysregulated in AD and also indicate an active role for this pathway in disease pathogenesis...
  38. ncbi request reprint Oxidative damage and Alzheimer's disease: are antioxidant therapies useful?
    Paula I Moreira
    Institute of Pathology, Case Western Research University, Cleveland, OH 44106, USA
    Drug News Perspect 18:13-9. 2005
    ..However, the results obtained in clinical trials with antioxidants are promising and propel us in the search of new and more effective antioxidant therapies...
  39. ncbi request reprint The role of metabotropic glutamate receptors in Alzheimer's disease
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
    Acta Neurobiol Exp (Wars) 64:89-98. 2004
    ..Thus, we here discuss the possible role of mGluR in the pathogenesis of AD based on the results from other neurodegenerative diseases that may give us clues to solve the mysterious selective neurodegeneration evident in AD...
  40. ncbi request reprint The (un)balance between metabolic and oxidative abnormalities and cellular compensatory responses in Alzheimer disease
    Paula I Moreira
    Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA
    Mech Ageing Dev 127:501-6. 2006
    ..However, in the initial stages of disease development, neurons adapt to the oxidative environment through the development of compensatory responses resulting in a shift of neuronal priority from normal function to basic survival...
  41. ncbi request reprint Differential regulation of glutamate receptors in Alzheimer's disease
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Neurosignals 11:282-92. 2002
    ..Additionally, we assess the potential therapeutic value of glutamate receptors as a target for drug intervention in Alzheimer's disease...
  42. ncbi request reprint P38 activation mediates amyloid-beta cytotoxicity
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
    Neurochem Res 30:791-6. 2005
    ..Taken together, these data suggest that p38 is a key downstream effector of amyloid-beta-induced neuronal death and blocking this pathway may be of therapeutic value...
  43. ncbi request reprint 4-Oxo-2-nonenal is both more neurotoxic and more protein reactive than 4-hydroxy-2-nonenal
    De Lin
    Department of Chemistry, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Chem Res Toxicol 18:1219-31. 2005
    ..The greater neurotoxicity of ONE could reflect in part the different reactivity characteristics of ONE as compared to HNE...
  44. ncbi request reprint Amyloid-beta, BACE, and oxidative stress in Alzheimer's disease, a commentary on "The different aggregation state of beta-amyloid 1-42 mediates different effects on oxidative stress, neurodegeneration and BACE-1 expression"
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA
    Free Radic Biol Med 41:188-9. 2006
  45. ncbi request reprint Presenilin mutation: a deadly first hit in Alzheimer disease. A commentary on "aging sensitizes towards ROS formation and lipid peroxidation in PS1M146L transgenic mice"
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, OH 44106, USA
    Free Radic Biol Med 40:737-9. 2006
  46. pmc Early induction of c-Myc is associated with neuronal cell death
    Hyun Pil Lee
    Department of Pathology, Case Western Reserve University, Cleveland, OH, USA
    Neurosci Lett 505:124-7. 2011
    ....
  47. pmc The mitochondrial dynamics of Alzheimer's disease and Parkinson's disease offer important opportunities for therapeutic intervention
    David J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Curr Pharm Des 17:3374-80. 2011
    ..We here discuss the role of mitochondrial dynamics in AD and PD and assess the need for their therapeutic exploitation...
  48. pmc Novel therapeutics for Alzheimer's disease: an update
    David J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Curr Opin Drug Discov Devel 13:235-46. 2010
    ..Current hypotheses for the pathogenesis of AD are discussed in this review, with a particular emphasis on the implications of these hypotheses with respect to treatment strategies and preventive measures...
  49. pmc Widespread distribution of reticulon-3 in various neurodegenerative diseases
    Jonathon E Heath
    Department of Pathology, University of Maryland, Baltimore, Maryland, USA
    Neuropathology 30:574-9. 2010
    ....
  50. pmc Staying connected: synapses in Alzheimer disease
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Am J Pathol 165:1461-4. 2004
  51. pmc Phosphorylated tau: toxic, protective, or none of the above
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, MD, USA
    J Alzheimers Dis 14:377-83. 2008
    ..However, since we also know that phosphorylated tau sequesters redox active heavy metals and protects against oxidative stress, here we suggest that phosphorylated tau serves a protective role against cellular toxicity...
  52. pmc Amyloid-beta vaccination: testing the amyloid hypothesis?: heads we win, tails you lose!
    Hyoung gon Lee
    Department of Pathology, Case Western Reserve University, 2103 Cornell Rd, Cleveland, OH 44106, USA
    Am J Pathol 169:738-9. 2006
  53. pmc BRCA1 may modulate neuronal cell cycle re-entry in Alzheimer disease
    Teresa A Evans
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Int J Med Sci 4:140-5. 2007
    ....
  54. ncbi request reprint Chronological primacy of oxidative stress in Alzheimer disease
    Mark A Smith
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Neurobiol Aging 26:579-80. 2005
  55. pmc Amyloid-beta in Alzheimer's disease: the horse or the cart? Pathogenic or protective?
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Int J Exp Pathol 86:133-8. 2005
    ..Thus, in this review, we discuss the role of amyloid-beta in the pathogenesis of AD and provide an alternative view to the widely accepted dogma...
  56. doi request reprint Cell cycle deregulation in the neurons of Alzheimer's disease
    Calvin Moh
    Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA
    Results Probl Cell Differ 53:565-76. 2011
    ..Once both of these hits are activated, AD can develop and produce senile plaques and neurofibrillary tangles throughout brain tissue. In this review, we propose a mechanism for neuronal cell cycle reentry and the development of AD...
  57. pmc The sirtuin pathway in ageing and Alzheimer disease: mechanistic and therapeutic considerations
    David J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Lancet Neurol 10:275-9. 2011
    ....
  58. pmc Antigen-antibody dissociation in Alzheimer disease: a novel approach to diagnosis
    Katarzyna A Gustaw
    Department of Neurology, Case Western Reserve University, Cleveland, Ohio, USA
    J Neurochem 106:1350-6. 2008
    ....
  59. ncbi request reprint Oxidative imbalance in Alzheimer's disease
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, Cleveland, OH, USA
    Mol Neurobiol 31:205-17. 2005
    ..In this review, we present the evidence for oxidative stress in Alzheimer's disease and its likely sources and consequence in relation to other pathological changes...
  60. ncbi request reprint Sources and mechanisms of cytoplasmic oxidative damage in Alzheimer's disease
    Michael Marlatt
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
    Acta Neurobiol Exp (Wars) 64:81-7. 2004
    ....
  61. pmc The role of E2F1 in the development of hypertrophic cardiomyopathy
    Julie A Wolfram
    Departments of Pathology and 2Medicine, Case Western Reserve University, Cleveland, Ohio, USA
    Int J Clin Exp Pathol 4:521-5. 2011
    ..In conclusion, our data demonstrate that cardiac hypertrophy can be induced in an E2F1-independent fashion and suggest that in contrast to previous reports, targeting E2F1 may not be a good therapeutic approach...
  62. pmc Early induction of oxidative stress in mouse model of Alzheimer disease with reduced mitochondrial superoxide dismutase activity
    Hyun Pil Lee
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, United States of America
    PLoS ONE 7:e28033. 2012
    ..These results suggest that the early neuronal susceptibility to oxidative stress in the hAPP/Sod2(+/-) mice may contribute to the pathological and behavioral changes seen in this animal model...
  63. pmc CD3 in Lewy pathology: does the abnormal recall of neurodevelopmental processes underlie Parkinson's disease
    Rudy J Castellani
    Department of Pathology, University of Maryland, 22 South Greene Street, Baltimore, MD 21201, USA
    J Neural Transm 118:23-6. 2011
    ....
  64. pmc Pathological implications of cell cycle re-entry in Alzheimer disease
    David J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Expert Rev Mol Med 12:e19. 2010
    ..Moreover, multiple inducers of cell cycle re-entry and their interactions in AD have been proposed. Here, we review the most recent advances in understanding the pathological implications of cell cycle re-entry in AD...
  65. ncbi request reprint Alzheimer disease, the two-hit hypothesis: an update
    Xiongwei Zhu
    Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA
    Biochim Biophys Acta 1772:494-502. 2007
    ....
  66. pmc The essential role of ERK in 4-oxo-2-nonenal-mediated cytotoxicity in SH-SY5Y human neuroblastoma cells
    Hyun Pil Lee
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    J Neurochem 108:1434-41. 2009
    ..Overall, these data strongly suggest that ERK plays an essential role in ONE-mediated cytotoxicity and that ERK is an upstream component of p53-mediated apoptosis...
  67. pmc Evidence of DNA damage in Alzheimer disease: phosphorylation of histone H2AX in astrocytes
    Na Hye Myung
    Department of Pathology, Case Western Reserve, 2103 Cornell Road, Cleveland, OH, 44106, USA
    Age (Dordr) 30:209-15. 2008
    ..These findings further define the role of astrocyte dysfunction in the progression of AD...
  68. pmc Down-regulation of serum gonadotropins is as effective as estrogen replacement at improving menopause-associated cognitive deficits
    Kathryn J Bryan
    Department of Neurosciences, Case Western Reserve University, Cleveland, Ohio, USA
    J Neurochem 112:870-81. 2010
    ..These findings provide a potential novel protective strategy to treat menopause/age-related cognitive decline and/or prevent the development of AD...
  69. pmc All-trans retinoic acid as a novel therapeutic strategy for Alzheimer's disease
    Hyun Pil Lee
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Expert Rev Neurother 9:1615-21. 2009
    ..Here, we review the actions of retinoic acid that indicate that it may have therapeutic properties ideally served for the treatment of neurodegenerative diseases such as Alzheimer's disease...
  70. ncbi request reprint The application of microarray technology to neuropathology: cutting edge tool with clinical diagnostics potential or too much information?
    Andrew McShea
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neuropathol Exp Neurol 65:1031-9. 2006
    ..The progression of this technology will lead to earlier detection of the disease through enhanced understanding of disease onset and progression...
  71. pmc Role of metal dyshomeostasis in Alzheimer's disease
    David J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Metallomics 3:267-70. 2011
    ..We here elaborate on the roles of iron, copper, and zinc in AD and describe the therapeutic implications they present...
  72. doi request reprint Neuroendocrinology-based therapy for Alzheimer's disease
    Russell Palm
    Department of Neurosciences, Case Western Reserve University, Cleveland, OH, USA
    Biofactors 38:123-32. 2012
    ....
  73. pmc Ectopic localization of FOXO3a protein in Lewy bodies in Lewy body dementia and Parkinson's disease
    Bo Su
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Mol Neurodegener 4:32. 2009
    ..In light of the known interaction of FOXO3 and 14-3-3, basic protein-protein interaction between these proteins and alpha-synuclein may be key...
  74. ncbi request reprint Modulation of hippocampal plasticity and cognitive behavior by short-term blueberry supplementation in aged rats
    Gemma Casadesus
    USDA, HNRC on Aging at Tufts University, Boston, MA, USA
    Nutr Neurosci 7:309-16. 2004
    ..Therefore, cognitive improvements afforded by polyphenolic-rich fruits such as blueberries appear, in part, to be mediated by their effects on hippocampal plasticity...
  75. pmc Amyloid-beta42 interacts mainly with insoluble prion protein in the Alzheimer brain
    Wen Quan Zou
    Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA
    J Biol Chem 286:15095-105. 2011
    ..Although this work indicated the interaction of Aβ42 with huPrP in the AD brain, the pathophysiological relevance of the iPrP/Aβ42 interaction remains to be established...
  76. pmc Therapeutic potential of c-Myc inhibition in the treatment of hypertrophic cardiomyopathy
    Julie A Wolfram
    Department of Pathology, Case Western Reserve University, Cleveland, OH, USA
    Ther Adv Chronic Dis 2:133-44. 2011
    ..Elucidating the role Myc plays in the development, propagation and perpetuation of cardiomyopathy and heart failure will one day translate into potential therapeutics for cardiomyopathy...
  77. pmc Cellular prion protein and Alzheimer disease: link to oligomeric amyloid-β and neuronal cell death
    Wataru Kudo
    Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA
    Prion 7:114-6. 2013
    ..These findings demonstrate that PrP (C) may be involved in neuropathologic conditions other than conventional prion diseases, i.e., Creutzfeldt-Jakob disease...
  78. ncbi request reprint Amyloid beta: the alternate hypothesis
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Curr Alzheimer Res 3:75-80. 2006
    ....
  79. pmc SRPK2 phosphorylates tau and mediates the cognitive defects in Alzheimer's disease
    Yi Hong
    Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    J Neurosci 32:17262-72. 2012
    ..Therefore, our study suggests SRPK2 may contribute to the formation of hyperphosphorylated tau and the pathogenesis of AD...
  80. ncbi request reprint Oxidative stress signalling in Alzheimer's disease
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Brain Res 1000:32-9. 2004
    ..In this paper, we review the evidence of oxidative stress and compensatory responses that occur in AD with a particular focus on the roles and mechanism of activation of SAPK pathways...
  81. ncbi request reprint Neuropathology of Alzheimer disease: pathognomonic but not pathogenic
    Rudy J Castellani
    Department of Pathology Neuropathology, University of Maryland, Baltimore, MD, USA
    Acta Neuropathol 111:503-9. 2006
    ....
  82. doi request reprint Current approaches in the treatment of Alzheimer's disease
    Reena S Shah
    Department of Neurology, University of Maryland, Baltimore, MD 21201, USA
    Biomed Pharmacother 62:199-207. 2008
    ..Drugs directly targeting amyloid-beta, particularly the amyloid-beta vaccine, continue to be investigated and their forthcoming results are eagerly anticipated...
  83. ncbi request reprint The fallacy of amyloid and cognition in Alzheimer's disease
    Hyoung gon Lee
    Drugs Aging 23:179. 2006
  84. ncbi request reprint The cellular prion protein (PrPC) prevents apoptotic neuronal cell death and mitochondrial dysfunction induced by serum deprivation
    Boe Hyun Kim
    Ilsong Institute of Life Science, Hallym Academy of Sciences, Hallym University, Ilsong Building, Kwanyang dong 1605 4, Dongan Gu, Anyang 431 060, South Korea
    Brain Res Mol Brain Res 124:40-50. 2004
    ....
  85. ncbi request reprint Neuronal cell cycle re-entry mediates Alzheimer disease-type changes
    Andrew McShea
    Department of Biology, CombiMatrix Corp, Mukilteo, WA 98275, USA
    Biochim Biophys Acta 1772:467-72. 2007
    ..As such, our neuronal cell model may be extremely valuable for the development of novel therapeutic strategies...
  86. ncbi request reprint Neuropathology in Alzheimer's disease: awaking from a hundred-year-old dream
    Akihiko Nunomura
    Department of Psychiatry and Neurology, Asahikawa Medical College, Asahikawa 078 8510, Japan
    Sci Aging Knowledge Environ 2006:pe10. 2006
    ..Moreover, if this concept holds true for pathology in other neurodegenerative diseases, we may need to restructure our thinking and undergo a paradigm shift before substantial progress can be made in therapeutic intervention...
  87. ncbi request reprint Lessons from the AN 1792 Alzheimer vaccine: lest we forget
    Stephen R Robinson
    School of Psychology, Psychiatry and Psychological Medicine, Monash University, Clayton, VIC 3800, Australia
    Neurobiol Aging 25:609-15. 2004
    ..The most important lesson to be learned from the AN 1792 trials is that new strategies for treating AD should not be tested on humans until they have been extensively tested on non-murine species...