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Genomes and Genes | Hyoung gon LeeSummaryAffiliation: Case Western Reserve University Country: USA Publications
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The effect of mGluR2 activation on signal transduction pathways and neuronal cell survivalHyoung 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...- Cell cycle re-entry mediated neurodegeneration and its treatment role in the pathogenesis of Alzheimer's diseaseHyoung 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... - The neuronal expression of MYC causes a neurodegenerative phenotype in a novel transgenic mouseHyoung gon Lee
Department of Pathology, Case Western Reserve University, 2103 Cornell Rd, Cleveland, OH 44106, USA
Am J Pathol 174:891-7. 2009.... - Aberrant localization of importin alpha1 in hippocampal neurons in Alzheimer diseaseHyoung 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... - Cell cycle re-entry and mitochondrial defects in myc-mediated hypertrophic cardiomyopathy and heart failureHyoung gon Lee
Department of Pathology, Case Western Reserve University, Cleveland, Ohio, United States of America
PLoS ONE 4:e7172. 2009.... - Signal transduction cascades associated with oxidative stress in Alzheimer's diseaseRobert 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... - Increased p27, an essential component of cell cycle control, in Alzheimer's diseaseOsamu 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... - Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer's diseaseBaiyang 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... - The cell cycle regulator phosphorylated retinoblastoma protein is associated with tau pathology in several tauopathiesJeremy 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... - Chronic oxidative stress causes increased tau phosphorylation in M17 neuroblastoma cellsBo 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... - Oxidative stress and neuronal adaptation in Alzheimer disease: the role of SAPK pathwaysXiongwei Zhu
Institute of Pathology, Case Western Reserve University, Cleveland, OH, USA
Antioxid Redox Signal 5:571-6. 2003.... - Evidence for the progression through S-phase in the ectopic cell cycle re-entry of neurons in Alzheimer diseaseDavid J Bonda
Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
Aging (Albany NY) 1:382-8. 2009.... - 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.... - Reexamining Alzheimer's disease: evidence for a protective role for amyloid-beta protein precursor and amyloid-betaRudy J Castellani
Department of Pathology, University of Maryland, Baltimore, MD 21201, USA
J Alzheimers Dis 18:447-52. 2009.... - Indoleamine 2,3-dioxygenase and 3-hydroxykynurenine modifications are found in the neuropathology of Alzheimer's diseaseDavid J Bonda
Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
Redox Rep 15:161-8. 2010.... - Amyloid-beta in Alzheimer disease: the null versus the alternate hypothesesHyoung 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... - Biomarkers in Alzheimer's disease: past, present and futureKatarzyna 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.... - Neuroprotective properties of Bcl-w in Alzheimer diseaseXiongwei 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... - The role of mitogen-activated protein kinase pathways in Alzheimer's diseaseXiongwei 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... - Distribution, levels, and activation of MEK1 in Alzheimer's diseaseXiongwei 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... - Alzheimer disease pathology as a host responseRudy 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... - Impaired balance of mitochondrial fission and fusion in Alzheimer's diseaseXinglong 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... - Antioxidant approaches for the treatment of Alzheimer's diseaseHyun 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... - 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... - P38 activation mediates amyloid-beta cytotoxicityXiongwei 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... - The mitochondrial dynamics of Alzheimer's disease and Parkinson's disease offer important opportunities for therapeutic interventionDavid 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... - Novel therapeutics for Alzheimer's disease: an updateDavid 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... - Phosphorylated tau: toxic, protective, or none of the aboveRudy 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... - BRCA1 may modulate neuronal cell cycle re-entry in Alzheimer diseaseTeresa A Evans
Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
Int J Med Sci 4:140-5. 2007.... - Widespread distribution of reticulon-3 in various neurodegenerative diseasesJonathon E Heath
Department of Pathology, University of Maryland, Baltimore, Maryland, USA
Neuropathology 30:574-9. 2010.... - Cellular prion protein is essential for oligomeric amyloid-?-induced neuronal cell deathWataru 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 A? oligomer-induced neuronal cell death, the pathology essential to cognitive loss... - Antigen-antibody dissociation in Alzheimer disease: a novel approach to diagnosisKatarzyna A Gustaw
Department of Neurology, Case Western Reserve University, Cleveland, Ohio, USA
J Neurochem 106:1350-6. 2008.... - Oxidative imbalance in Alzheimer's diseaseXiongwei 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... - The sirtuin pathway in ageing and Alzheimer disease: mechanistic and therapeutic considerationsDavid J Bonda
Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
Lancet Neurol 10:275-9. 2011..Ultimately, further analysis into both aspects is necessary if any progress is to be made... - Cell cycle deregulation in the neurons of Alzheimer's diseaseCalvin 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... - Pathological implications of cell cycle re-entry in Alzheimer diseaseDavid 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... - Alzheimer disease, the two-hit hypothesis: an updateXiongwei Zhu
Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA
Biochim Biophys Acta 1772:494-502. 2007.... - The essential role of ERK in 4-oxo-2-nonenal-mediated cytotoxicity in SH-SY5Y human neuroblastoma cellsHyun 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... - CD3 in Lewy pathology: does the abnormal recall of neurodevelopmental processes underlie Parkinson's diseaseRudy J Castellani
Department of Pathology, University of Maryland, 22 South Greene Street, Baltimore, MD 21201, USA
J Neural Transm 118:23-6. 2011.... - All-trans retinoic acid as a novel therapeutic strategy for Alzheimer's diseaseHyun 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... - Evidence of DNA damage in Alzheimer disease: phosphorylation of histone H2AX in astrocytesNa 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... - Down-regulation of serum gonadotropins is as effective as estrogen replacement at improving menopause-associated cognitive deficitsKathryn 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... - The role of E2F1 in the development of hypertrophic cardiomyopathyJulie 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... - Role of metal dyshomeostasis in Alzheimer's diseaseDavid 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... - Aberrant expression of metabotropic glutamate receptor 2 in the vulnerable neurons of Alzheimer's diseaseHyoung-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... - Early induction of oxidative stress in mouse model of Alzheimer disease with reduced mitochondrial superoxide dismutase activityHyun 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... - Ectopic localization of FOXO3a protein in Lewy bodies in Lewy body dementia and Parkinson's diseaseBo 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... - Early induction of c-Myc is associated with neuronal cell deathHyun Pil Lee
Department of Pathology, Case Western Reserve University, Cleveland, OH, USA
Neurosci Lett 505:124-7. 2011.... - Modulation of hippocampal plasticity and cognitive behavior by short-term blueberry supplementation in aged ratsGemma 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... - Mitogen- and stress-activated protein kinase 1: convergence of the ERK and p38 pathways in Alzheimer's diseaseKate M Webber
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
J Neurosci Res 79:554-60. 2005.... - Antioxidant protection and neurodegenerative disease: the role of amyloid-beta and tauRudy J Castellani
Department of Pathology, University of Maryland, Baltimore, Maryland, USA
Am J Alzheimers Dis Other Demen 21:126-30. 2006.... - 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.... - 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 (Berl) 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... - Chronological primacy of oxidative stress in Alzheimer diseaseMark A Smith
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
Neurobiol Aging 26:579-80. 2005 - Therapeutic potential of c-Myc inhibition in the treatment of hypertrophic cardiomyopathyJulie 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... - Amyloid-beta42 interacts mainly with insoluble prion protein in the Alzheimer brainWen 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 A?42 with huPrP in the AD brain, the pathophysiological relevance of the iPrP/A?42 interaction remains to be established... - The (un)balance between metabolic and oxidative abnormalities and cellular compensatory responses in Alzheimer diseasePaula 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... - Perspectives on the amyloid-beta cascade hypothesisHyoung-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... - Tau modifiers as therapeutic targets for Alzheimer's diseaseQuan 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... - 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 - Neuroendocrinology-based therapy for Alzheimer's diseaseRussell Palm
Department of Neurosciences, Case Western Reserve University, Cleveland, OH
Biofactors 38:123-32. 2012.... - Sources and mechanisms of cytoplasmic oxidative damage in Alzheimer's diseaseMichael Marlatt
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
Acta Neurobiol Exp (Wars) 64:81-7. 2004.... - Amyloid beta: the alternate hypothesisHyoung-Gon Lee
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
Curr Alzheimer Res 3:75-80. 2006.... - 4-Oxo-2-nonenal is both more neurotoxic and more protein reactive than 4-hydroxy-2-nonenalDe 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... - Challenging the amyloid cascade hypothesis: senile plaques and amyloid-beta as protective adaptations to Alzheimer diseaseHyoung-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... - 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... - Staying connected: synapses in Alzheimer diseaseHyoung-Gon Lee
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
Am J Pathol 165:1461-4. 2004 - 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... - Oxidative stress signalling in Alzheimer's diseaseXiongwei 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... - Differential regulation of glutamate receptors in Alzheimer's diseaseHyoung-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... - 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... - 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... - Redox metals and oxidative abnormalities in human prion diseasesRobert 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... - 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 - 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 - The role of metabotropic glutamate receptors in Alzheimer's diseaseHyoung-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... - 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... - Neuronal cell cycle re-entry mediates Alzheimer disease-type changesAndrew 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... - The fallacy of amyloid and cognition in Alzheimer's diseaseHyoung-Gon Lee
Drugs Aging 23:179. 2006 - The cellular prion protein (PrPC) prevents apoptotic neuronal cell death and mitochondrial dysfunction induced by serum deprivationBoe-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.... - Neuropathology of Alzheimer disease: pathognomonic but not pathogenicRudy J Castellani
Department of Pathology (Neuropathology, University of Maryland, Baltimore, MD, USA
Acta Neuropathol (Berl) 111:503-9. 2006.... - Neuropathology in Alzheimer's disease: awaking from a hundred-year-old dreamAkihiko 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... - Current approaches in the treatment of Alzheimer's diseaseReena 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... - Lessons from the AN 1792 Alzheimer vaccine: lest we forgetStephen 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...