George Perry

Summary

Affiliation: University of Texas at San Antonio
Country: USA

Publications

  1. ncbi Leucine-rich repeat kinase 2 colocalizes with alpha-synuclein in Parkinson's disease, but not tau-containing deposits in tauopathies
    George Perry
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Neurodegener Dis 5:222-4. 2008
  2. ncbi 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
  3. ncbi A novel perspective on tau in Alzheimer's disease
    D J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Curr Alzheimer Res 8:639-42. 2011
  4. ncbi Mitochondria and vascular lesions as a central target for the development of Alzheimer's disease and Alzheimer disease-like pathology in transgenic mice
    Gjumrakch Aliev
    Microscopy Research Center, Department of Anatomy, Department of Pathology, Case Western Reserve University, University Hospitals of Cleveland, Cleveland, OH, USA
    Neurol Res 25:665-74. 2003
  5. ncbi 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
  6. ncbi 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
  7. ncbi 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
  8. ncbi 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
  9. ncbi Ribosomal RNA in Alzheimer disease is oxidized by bound redox-active iron
    Kazuhiro Honda
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Biol Chem 280:20978-86. 2005
  10. ncbi 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

Collaborators

Detail Information

Publications121 found, 100 shown here

  1. ncbi Leucine-rich repeat kinase 2 colocalizes with alpha-synuclein in Parkinson's disease, but not tau-containing deposits in tauopathies
    George Perry
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Neurodegener Dis 5:222-4. 2008
    ..Mutations in leucine-rich repeat kinase 2 (LRRK2) are thus far the most frequent genetic cause associated with autosomal dominant and idiopathic Parkinson's disease...
  2. ncbi 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...
  3. ncbi A novel perspective on tau in Alzheimer's disease
    D J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Curr Alzheimer Res 8:639-42. 2011
    ..This concept provides a better understanding of the mechanisms underlying disease pathophysiology and also provides a window for therapeutic intervention...
  4. ncbi Mitochondria and vascular lesions as a central target for the development of Alzheimer's disease and Alzheimer disease-like pathology in transgenic mice
    Gjumrakch Aliev
    Microscopy Research Center, Department of Anatomy, Department of Pathology, Case Western Reserve University, University Hospitals of Cleveland, Cleveland, OH, USA
    Neurol Res 25:665-74. 2003
    ..Our observations first time demonstrate that vascular wall cells, especially their mitochondria, appear to be a central target for oxidative stress induced damage...
  5. ncbi 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...
  6. ncbi 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...
  7. ncbi 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
    ....
  8. ncbi 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...
  9. ncbi Ribosomal RNA in Alzheimer disease is oxidized by bound redox-active iron
    Kazuhiro Honda
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Biol Chem 280:20978-86. 2005
    ....
  10. ncbi 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...
  11. ncbi Autophagocytosis of mitochondria is prominent in Alzheimer disease
    Paula I Moreira
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    J Neuropathol Exp Neurol 66:525-32. 2007
    ..Whether increased autophagocytosis is a consequence of an increased turnover of mitochondria or whether the mitochondria in Alzheimer disease are more susceptible to autophagy remains to be resolved...
  12. ncbi Hydroxynonenal-generated crosslinking fluorophore accumulation in Alzheimer disease reveals a dichotomy of protein turnover
    Xiongwei Zhu
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Free Radic Biol Med 52:699-704. 2012
    ..These findings directly implicate lipid crosslinking peroxidation products as accumulating not in the lesions or the lipofuscin pathways, but instead in a distinct pathway, GVD, that accumulates cytosolic proteins...
  13. ncbi Chronic antioxidant therapy reduces oxidative stress in a mouse model of Alzheimer's disease
    Sandra L Siedlak
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Free Radic Res 43:156-64. 2009
    ....
  14. ncbi Mitochondrial dynamics in Alzheimer's disease: opportunities for future treatment strategies
    David J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Drugs Aging 27:181-92. 2010
    ..e. mitochondrial protection) that has the potential to significantly deter AD progression if adequately developed. Current treatment strategies under investigation are described in this review...
  15. ncbi Metal ions and oxidative protein modification in neurological disease
    Lawrence M Sayre
    Department of Chemistry, Case Western Reserve University, Cleveland, OH 44106, USA
    Ann Ist Super Sanita 41:143-64. 2005
    ....
  16. ncbi Vascular oxidative stress in Alzheimer disease
    Xiongwei Zhu
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurol Sci 257:240-6. 2007
    ..Here, we discuss vascular factors in relation to Alzheimer disease and review hypoperfusion as a potential cause by triggering mitochondrial dysfunction and increased oxidative stress initiating the pathogenic process...
  17. ncbi 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...
  18. ncbi DLP1-dependent mitochondrial fragmentation mediates 1-methyl-4-phenylpyridinium toxicity in neurons: implications for Parkinson's disease
    Xinglong Wang
    Department of Pathology, Case Western Reserve University, 2103 Connell Road, Cleveland, OH 44106, USA
    Aging Cell 10:807-23. 2011
    ..Overall, these findings suggest that DLP1-dependent mitochondrial fragmentation plays a crucial role in mediating MPP(+) -induced mitochondria abnormalities and cellular dysfunction and may represent a novel therapeutic target for PD...
  19. ncbi 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
    ....
  20. ncbi Contribution of redox-active iron and copper to oxidative damage in Alzheimer disease
    Rudy J Castellani
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Ageing Res Rev 3:319-26. 2004
    ....
  21. ncbi 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...
  22. ncbi Alzheimer-specific epitopes of tau represent lipid peroxidation-induced conformations
    Quan Liu
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Free Radic Biol Med 38:746-54. 2005
    ....
  23. ncbi Increased expression of p130 in Alzheimer disease
    Laura A Previll
    Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA
    Neurochem Res 32:639-44. 2007
    ..Our data suggest that, despite its upregulation, the aberrant localization of p130 to the neuronal cytoplasm facilitates neuronal cell cycle re-entry in AD...
  24. ncbi 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...
  25. ncbi Compensatory responses induced by oxidative stress in Alzheimer disease
    Paula I Moreira
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44100, USA
    Biol Res 39:7-13. 2006
    ..These findings suggest that Alzheimer disease is associated with a novel balance in oxidant homeostasis...
  26. ncbi 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...
  27. ncbi Mitochondria DNA deletions in atherosclerotic hypoperfused brain microvessels as a primary target for the development of Alzheimer's disease
    Ali Aliyev
    The Microscopy Research Center, Case Western Reserve University, Cleveland, OH 44106, USA
    J Neurol Sci 229:285-92. 2005
    ..Therefore, selective pharmacological intervention, directed for abolishing the chronic hypoperfusion state, would possibly change the natural course of development of dementing neurodegeneration...
  28. ncbi Is oxidative damage the fundamental pathogenic mechanism of Alzheimer's and other neurodegenerative diseases?
    George Perry
    Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Free Radic Biol Med 33:1475-9. 2002
    ..Although much data remain to be collected, the broad spectrum of changes found in AD are only seen, albeit to a lesser extent, in normal aging with other neurodegenerative diseases showing distinct spectrums of change...
  29. ncbi 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
    ....
  30. ncbi 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
    ....
  31. ncbi 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...
  32. ncbi Oxidative damage in cultured human olfactory neurons from Alzheimer's disease patients
    Hossein A Ghanbari
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Aging Cell 3:41-4. 2004
    ..Primary culture of human olfactory neurons will be useful in understanding the mechanism of oxidative damage in Alzheimer's disease and can even be utilized in developing therapeutic strategies...
  33. ncbi The cell cycle in Alzheimer disease: a unique target for neuropharmacology
    Kate M Webber
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Mech Ageing Dev 126:1019-25. 2005
    ..Therefore, therapeutic interventions targeted toward ameliorating mitotic changes would be predicted to have a profound and positive impact on Alzheimer disease progression...
  34. ncbi 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...
  35. ncbi Oxidative stress: the old enemy in Alzheimer's disease pathophysiology
    Paula I Moreira
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Curr Alzheimer Res 2:403-8. 2005
    ....
  36. ncbi 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
    ....
  37. ncbi 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...
  38. ncbi LRRK2 regulates mitochondrial dynamics and function through direct interaction with DLP1
    Xinglong Wang
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Hum Mol Genet 21:1931-44. 2012
    ..We concluded that LRRK2 regulates mitochondrial dynamics by increasing mitochondrial DLP1 through its direct interaction with DLP1, and LRRK2 kinase activity plays a critical role in this process...
  39. ncbi 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
    ....
  40. ncbi 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...
  41. ncbi Luteinizing hormone modulates cognition and amyloid-beta deposition in Alzheimer APP transgenic mice
    Gemma Casadesus
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Biochim Biophys Acta 1762:447-52. 2006
    ..Since both cognitive loss and amyloid-beta deposition are features of Alzheimer disease, leuprolide acetate treatment may prove to be a useful therapeutic strategy for this disease...
  42. ncbi 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...
  43. ncbi Increased autophagic degradation of mitochondria in Alzheimer disease
    Paula I Moreira
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Autophagy 3:614-5. 2007
    ..The study of autophagy in Alzheimer disease could clarify the mechanisms underlying this neurodegenerative disorder and, eventually, help in the development of new therapeutic strategies...
  44. ncbi 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
    ....
  45. ncbi 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...
  46. ncbi Adventiously-bound redox active iron and copper are at the center of oxidative damage in Alzheimer disease
    George Perry
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
    Biometals 16:77-81. 2003
    ....
  47. ncbi A second look into the oxidant mechanisms in Alzheimer's disease
    Paula I Moreira
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
    Curr Neurovasc Res 2:179-84. 2005
    ....
  48. ncbi Estrogen bows to a new master: the role of gonadotropins in Alzheimer pathogenesis
    Kate M Webber
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Rd, Cleveland, OH 44106, USA
    Ann N Y Acad Sci 1052:201-9. 2005
    ..On this basis, we suggest that the results of the WHI Memory Study are not only predictable but also avoidable by therapeutically targeting the gonadotropins instead of the sex steroids...
  49. ncbi 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 (Berl) 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...
  50. ncbi Indices of metabolic dysfunction and oxidative stress
    Gemma Casadesus
    Department of Neuroscience, Case Western Reserve University, Cleveland, OH, USA
    Neurochem Res 32:717-22. 2007
    ..Overall, clarifying cellular and molecular manifestations involved in metabolic alterations may contribute to a better understanding of early Alzheimer disease pathophysiology...
  51. ncbi 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...
  52. ncbi Oxidative stress in Alzheimer disease: a possibility for prevention
    David J Bonda
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Neuropharmacology 59:290-4. 2010
    ..In this review, we elaborate on the dynamic role of oxidative stress in AD and present corresponding treatment strategies that are currently under investigation...
  53. ncbi Iron homeostasis is maintained in the brain, but not the liver, following mild hypoxia
    Glenda M Bishop
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Redox Rep 12:257-66. 2007
    ..Together, these results indicate that there is a tighter regulation of iron metabolism in the brain than the liver, which limits the redistribution of Fe3+ following hypoxia...
  54. ncbi Overexpression of GRK2 in Alzheimer disease and in a chronic hypoperfusion rat model is an early marker of brain mitochondrial lesions
    Mark E Obrenovich
    Department of Pathology, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA
    Neurotox Res 10:43-56. 2006
    ....
  55. ncbi 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...
  56. ncbi Mitochondrial abnormalities and oxidative imbalance in Alzheimer disease
    Xiongwei Zhu
    Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, Ohio 44106, USA
    J Alzheimers Dis 9:147-53. 2006
    ....
  57. ncbi 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...
  58. ncbi Microtubule reduction in Alzheimer's disease and aging is independent of tau filament formation
    Adam D Cash
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Am J Pathol 162:1623-7. 2003
    ..016). These findings suggest that reduction in microtubule assembly is not dependent on tau abnormalities of AD and aging...
  59. ncbi Mitochondrial failures in Alzheimer's disease
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Am J Alzheimers Dis Other Demen 19:345-52. 2004
    ..Future studies comparing the spectrum of mitochondrial damage and the relationship to oxidative stress-induced damage during the aging process or, more importantly, during the maturation of AD pathology are warranted...
  60. ncbi 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
    ....
  61. ncbi 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
    ....
  62. ncbi Elevated expression of a regulator of the G2/M phase of the cell cycle, neuronal CIP-1-associated regulator of cyclin B, in Alzheimer's disease
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    J Neurosci Res 75:698-703. 2004
    ..Therefore, therapeutics targeted toward initiators of the cell cycle are likely to prove of great efficacy for the treatment of AD...
  63. ncbi Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels: implication in the pathogenesis of Alzheimer's disease
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, San Antonio, Texas 78249 1664, USA
    Vasc Health Risk Manag 4:721-30. 2008
    ..Therefore, pharmacological interventions, directed at correcting the chronic hypoperfusion state, may change the natural course of the development of dementing neurodegeneration...
  64. ncbi Alzheimer disease: evidence for a central pathogenic role of iron-mediated reactive oxygen species
    Gemma Casadesus
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Alzheimers Dis 6:165-9. 2004
    ..In this review, we consider the wealth of evidence implicating a central role for metals in Alzheimer disease...
  65. ncbi 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...
  66. ncbi 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. ncbi Antioxidant therapy in Alzheimer's disease: theory and practice
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, One UTSA Circle, San Antonio, Texas 78249, USA
    Mini Rev Med Chem 8:1395-406. 2008
    ..Efforts to reduce the pathology associated with ROS via antioxidants therefore offer new hope to patients suffering from this devastative disease...
  68. ncbi The cell cycle and hormonal fluxes in Alzheimer disease: a novel therapeutic target
    Kate M Webber
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106. USA
    Curr Pharm Des 12:691-7. 2006
    ..Therapeutic interventions targeted at gonadotropins, if they are indeed the driving mitogenic force, could both prevent disease in those patients currently asymptomatic or halt, and even reverse, disease in those currently afflicted...
  69. ncbi Increased iron and free radical generation in preclinical Alzheimer disease and mild cognitive impairment
    Mark A Smith
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    J Alzheimers Dis 19:363-72. 2010
    ..Iron deposition at the preclinical stage of AD may be useful as a diagnostic tool, using iron imaging methods, as well as a potential therapeutic target, through metal ion chelators...
  70. ncbi Oxidative stress and neurotoxicity
    Lawrence M Sayre
    Department of Chemistry, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Chem Res Toxicol 21:172-88. 2008
    ..Following a review of oxidative stress involvement in individual disease states, some conclusions are provided as to what further research should hope to accomplish in the field...
  71. ncbi 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...
  72. ncbi The estrogen myth: potential use of gonadotropin-releasing hormone agonists for the treatment of Alzheimer's disease
    Gemma Casadesus
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Drugs R D 7:187-93. 2006
    ....
  73. ncbi Therapeutic options in Alzheimer's disease
    Paula I Moreira
    Case Western Reserve University, Department of Pathology, Cleveland, Ohio 44106, USA
    Expert Rev Neurother 6:897-910. 2006
    ..The possibility that oxidative stress is a primary event in AD indicates that antioxidant-based therapies are perhaps the most promising weapons against this devastating neurodegenerative disorder...
  74. ncbi Amyloid-beta: a chameleon walking in two worlds: a review of the trophic and toxic properties of amyloid-beta
    Craig S Atwood
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Brain Res Brain Res Rev 43:1-16. 2003
    ..ccirf;), leading to enhanced, rather than reduced, neuronal oxidative stress...
  75. ncbi Neuronal mitochondrial amelioration by feeding acetyl-L-carnitine and lipoic acid to aged rats
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, 78249, USA
    J Cell Mol Med 13:320-33. 2009
    ..001) in the hippocampus. These results suggest that feeding ALCAR with LA may ameliorate age-associated mitochondrial ultrastructural decay and are consistent with previous studies showing improved brain function...
  76. ncbi Stem cell niches as clinical targets: the future of anti-ischemic therapy?
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, San Antonio, TX 78249 1664, USA
    Nat Clin Pract Cardiovasc Med 5:590-1. 2008
    ..Further assessment is needed to elucidate the factors involved in migration and differentiation of endothelial cell progenitors in ischemia-damaged tissues...
  77. ncbi Role of mitochondrial dysfunction in Alzheimer's disease
    Rudy Castellani
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurosci Res 70:357-60. 2002
    ..Here we review the causes and consequences of mitochondrial disturbances in Alzheimer's disease as well as how this information might impact on therapeutic approaches to this disease...
  78. ncbi Amyloid-beta, tau alterations and mitochondrial dysfunction in Alzheimer disease: the chickens or the eggs?
    Mark A Smith
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Neurochem Int 40:527-31. 2002
    ..However, this rationale may be misguided since new evidence from our laboratories and others suggest that the lesions not only occur as a by-product of the fundamental disease process but also that they may be protective...
  79. ncbi Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels as a central target for the development of human AD and AD-like pathology in aged transgenic mice
    Gjumrakch Aliev
    Microscopy Research Center, Department of Anatomy, Case Western Reserve University and University Hospitals of Cleveland, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Ann N Y Acad Sci 977:45-64. 2002
    ..Our observations demonstrate that vascular wall cells, especially their mitochondria, appear to be a central target for oxidative stress-induced damage...
  80. ncbi Is Alzheimer's disease a mitochondrial disorder?
    Adam D Cash
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Neuroscientist 8:489-96. 2002
    ..Supporting this, the authors have considerable in vivo and in vitro evidence for mitotic disturbances in AD...
  81. ncbi 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...
  82. ncbi 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
  83. ncbi Amyloid-beta-derived diffusible ligands cause impaired axonal transport of mitochondria in neurons
    Xinglong Wang
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Neurodegener Dis 7:56-9. 2010
    ..It is believed that soluble amyloid-beta (Abeta) oligomers are involved in the pathogenesis of AD, yet the underlying mechanisms remain elusive...
  84. ncbi High molecular weight neurofilament proteins are physiological substrates of adduction by the lipid peroxidation product hydroxynonenal
    Takafumi Wataya
    Institute of Pathology and Departments of Physiology and Biophysics, and Chemistry, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Biol Chem 277:4644-8. 2002
    ....
  85. ncbi 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...
  86. ncbi The role of abnormal mitochondrial dynamics in the pathogenesis of Alzheimer's disease
    Xinglong Wang
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurochem 109:153-9. 2009
    ..We propose that abnormal mitochondrial dynamics plays a key role in causing the dysfunction of mitochondria that ultimately damage AD neurons...
  87. ncbi Antibodies to potato virus Y bind the amyloid beta peptide: immunohistochemical and NMR studies
    Robert P Friedland
    Department of Neurology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Biol Chem 283:22550-6. 2008
    ..Immune responses generated from dietary exposure to proteins homologous to Abeta may induce antibodies that could influence the normal physiological processing of the protein and the development or progression of AD...
  88. ncbi Amyloid-beta and tau serve antioxidant functions in the aging and Alzheimer brain
    Mark A Smith
    Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Free Radic Biol Med 33:1194-9. 2002
    ..The notion that amyloid-beta and tau function as protective components brings into serious question the rationale of current therapeutic efforts targeted toward lesion removal...
  89. ncbi c-Jun phosphorylation in Alzheimer disease
    Akanksha Thakur
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurosci Res 85:1668-73. 2007
    ..Overall, this study demonstrated specific alterations in c-Jun phosphorylation and distribution in AD which is not necessarily linked to apoptosis but rather may represent an adaptation process in the face of oxidative stress...
  90. ncbi Treating the lesions, not the disease
    Xiongwei Zhu
    Department of Pathology, Case Western Reserve University, 2103 Cornell Rd, Cleveland, OH 44106, USA
    Am J Pathol 170:1457-9. 2007
  91. ncbi 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
  92. ncbi 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
    ....
  93. ncbi Abnormal mitochondrial dynamics and neurodegenerative diseases
    Bo Su
    Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA
    Biochim Biophys Acta 1802:135-42. 2010
    ..We propose that abnormal mitochondrial dynamics represents a key common pathway that mediates or amplifies mitochondrial dysfunction and neuronal dysfunction during the course of neurodegeneration...
  94. ncbi The state versus amyloid-beta: the trial of the most wanted criminal in Alzheimer disease
    Catherine A Rottkamp
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Peptides 23:1333-41. 2002
    ..Below, we present a brief synopsis of the trial for you, the jury, to decide the verdict. Amyloid-beta: guilty or not-guilty?..
  95. ncbi 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
    ....
  96. ncbi Insights into amyloid-beta-induced mitochondrial dysfunction in Alzheimer disease
    Xinglong Wang
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Free Radic Biol Med 43:1569-73. 2007
    ..Here, we review the role that amyloid-beta plays in mitochondrial structure and function of neurons and the importance of this in the pathogenesis of Alzheimer disease...
  97. ncbi 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
  98. ncbi A metabolic basis for Alzheimer disease
    George Perry
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Neurochem Res 28:1549-52. 2003
    ..Here we present data indicating that metabolic rate, nutrition, and neuronal size are all early indicators of AD. Understanding the cellular and molecular basis for these changes may open a new dimension to understanding AD...
  99. ncbi Insights into cerebrovascular complications and Alzheimer disease through the selective loss of GRK2 regulation
    Mark E Obrenovich
    Department of Pathology, Case Western Reserve University, Cleveland, OH, USA
    J Cell Mol Med 13:853-65. 2009
    ..We synthesize this newer information and attempt to put it into context with GRKs as regulators of diverse physiological cellular functions that could be appropriate targets for future pharmacological intervention...
  100. ncbi Amyloid-beta: a (life) preserver for the brain
    Mark E Obrenovich
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Neurobiol Aging 23:1097-9. 2002
  101. ncbi JKK1, an upstream activator of JNK/SAPK, is activated in Alzheimer's disease
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurochem 85:87-93. 2003
    ..Together, these findings lend further credence to the notion that the JNK/SAPK pathway is dysregulated in AD and also indicate an active role for this pathway in disease pathogenesis...