Rudy J Castellani

Summary

Affiliation: University of Maryland
Country: USA

Publications

  1. doi request reprint Compounding artefacts with uncertainty, and an amyloid cascade hypothesis that is 'too big to fail'
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, MD, USA
    J Pathol 224:147-52. 2011
  2. 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
  3. pmc Molecular pathogenesis of Alzheimer's disease: reductionist versus expansionist approaches
    Rudy J Castellani
    University of Maryland, Baltimore, USA
    Int J Mol Sci 10:1386-406. 2009
  4. doi request reprint Pathogenesis and disease-modifying therapy in Alzheimer's disease: the flat line of progress
    Rudy J Castellani
    Division of Neuropathology, University of Maryland School of Medicine, Baltimore, Maryland, USA
    Arch Med Res 43:694-8. 2012
  5. pmc A novel origin for granulovacuolar degeneration in aging and Alzheimer's disease: parallels to stress granules
    Rudy J Castellani
    Deparment of Pathology, University of Maryland, Baltimore, MD 21201, USA
    Lab Invest 91:1777-86. 2011
  6. doi request reprint The role of iron as a mediator of oxidative stress in Alzheimer disease
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, MD, USA
    Biofactors 38:133-8. 2012
  7. pmc Expression of CD74 is increased in neurofibrillary tangles in Alzheimer's disease
    Kathryn J Bryan
    Department of Neurosciences, Case Western Reserve University, Cleveland Ohio, USA
    Mol Neurodegener 3:13. 2008
  8. ncbi request reprint Vascular dementia and Alzheimer's disease: a waning dichotomy
    Rudy J Castellani
    Division of Neuropathology, University of Maryland, Baltimore, USA
    J Alzheimers Dis 12:343-4. 2007
  9. 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
  10. 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

Collaborators

Detail Information

Publications58

  1. doi request reprint Compounding artefacts with uncertainty, and an amyloid cascade hypothesis that is 'too big to fail'
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, MD, USA
    J Pathol 224:147-52. 2011
    ..The more the neuroscience community perseverates along these lines in the face of accumulating outcome data to the contrary, the more one is left to wonder whether the hypothesis is too big to fail...
  2. 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...
  3. pmc Molecular pathogenesis of Alzheimer's disease: reductionist versus expansionist approaches
    Rudy J Castellani
    University of Maryland, Baltimore, USA
    Int J Mol Sci 10:1386-406. 2009
    ..An "expansionist" view of the disease, we believe, with oxidative stress as a pleiotropic and upstream process, more aptly describes the relationship between various and numerous molecular alterations and clinical disease...
  4. doi request reprint Pathogenesis and disease-modifying therapy in Alzheimer's disease: the flat line of progress
    Rudy J Castellani
    Division of Neuropathology, University of Maryland School of Medicine, Baltimore, Maryland, USA
    Arch Med Res 43:694-8. 2012
    ..that they are responsible for disease when in fact the reverse is true, and will we genuinely consider a systems biology approach to AD or instead continue on the path of the lesion, which has so far followed a flat line of progress?..
  5. pmc A novel origin for granulovacuolar degeneration in aging and Alzheimer's disease: parallels to stress granules
    Rudy J Castellani
    Deparment of Pathology, University of Maryland, Baltimore, MD 21201, USA
    Lab Invest 91:1777-86. 2011
    ..This proposed origin for GVD as a neuroprotective response, may represent a morphologic checkpoint between cell death and reversible cellular stress that proceeds in the absence of other inclusions...
  6. doi request reprint The role of iron as a mediator of oxidative stress in Alzheimer disease
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, MD, USA
    Biofactors 38:133-8. 2012
    ..In this review, we discuss the role of iron in the progression of AD...
  7. pmc Expression of CD74 is increased in neurofibrillary tangles in Alzheimer's disease
    Kathryn J Bryan
    Department of Neurosciences, Case Western Reserve University, Cleveland Ohio, USA
    Mol Neurodegener 3:13. 2008
    ..This is the first finding to our knowledge that CD74 is increased in neurons of AD cases compared to age-matched control cases...
  8. ncbi request reprint Vascular dementia and Alzheimer's disease: a waning dichotomy
    Rudy J Castellani
    Division of Neuropathology, University of Maryland, Baltimore, USA
    J Alzheimers Dis 12:343-4. 2007
  9. 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...
  10. 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...
  11. 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
    ....
  12. ncbi request reprint The role of novel chitin-like polysaccharides in Alzheimer disease
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, MD 21201, USA
    Neurotox Res 12:269-74. 2007
    ..As such, glucosamine may facilitate the process of amyloidosis, and /or provide neuroprotection in the Alzheimer disease brain...
  13. 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...
  14. 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...
  15. 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...
  16. 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...
  17. pmc 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...
  18. 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
    ....
  19. ncbi request reprint Iron: the Redox-active center of oxidative stress in Alzheimer disease
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, MD, USA
    Neurochem Res 32:1640-5. 2007
    ..In this review, we discuss the role of iron in the progression of AD...
  20. ncbi request reprint 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...
  21. doi request reprint Redox active iron accumulation in aceruloplasminemia
    Luis F Gonzalez-Cuyar
    Department of Pathology, University of Maryland, Baltimore, Maryland 21201, USA
    Neuropathology 28:466-71. 2008
    ..As such, aceruloplasminemia is an excellent model of transition metal-driven oxidative stress and neurodegeneration...
  22. 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
    ....
  23. pmc 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...
  24. 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
    ....
  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 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
    ....
  27. 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
    ....
  28. doi request reprint Activation of the extracellular signal-regulated kinase pathway contributes to the behavioral deficit of fragile x-syndrome
    Xinglong Wang
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    J Neurochem 121:672-9. 2012
    ..These findings suggest that activation of the ERK pathway results in some cardinal cognitive and clinical features in FXS patients and likely have profound translational implications...
  29. pmc Frontiers in Alzheimer's disease therapeutics
    Jeremy G Stone
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Ther Adv Chronic Dis 2:9-23. 2011
    ..In this review, we summarize novel AD therapeutics that are currently being explored, and also mechanisms of action of specific drugs within the context of current knowledge of AD pathologic pathways...
  30. 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...
  31. pmc Paraffin-embedded tissue (PET) blot method: application to Alzheimer disease
    Calvin F Moh
    Department of Pathology, Case Western Reserve University, Cleveland, OH, USA
    J Neurosci Methods 190:244-7. 2010
    ..From this, we conclude that PET can be applied to a variety of conditions with a wide spectrum of pathology...
  32. 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...
  33. pmc Sublethal RNA oxidation as a mechanism for neurodegenerative disease
    Rudy J Castellani
    Department of Pathology, University of Maryland, Baltimore, Maryland, USA
    Int J Mol Sci 9:789-806. 2008
    ....
  34. ncbi request reprint Cerebrotendinous xanthomatosis: case report with evidence of oxidative stress
    Luis F Gonzalez-Cuyar
    Department of Pathology, University of Maryland, Baltimore, Maryland, USA
    Redox Rep 12:119-24. 2007
    ..Further, the involvement of oxidative stress in cerebrotendinous xanthomatosis indicates that combined therapy with chenodeoxycholic acid and antioxidants may improve clinical outcome...
  35. 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...
  36. doi request reprint Cocaine-induced intracerebral hemorrhage in a patient with cerebral amyloid angiopathy
    Marianna Shvartsbeyn
    Department of Pathology, New York University School of Medicine, New York, NY, USA
    J Forensic Sci 55:1389-92. 2010
    ..This is the first reported case of CAA-associated ICH precipitated by cocaine...
  37. ncbi request reprint Cerebral amyloid angiopathy: major contributor or decorative response to Alzheimer's disease pathogenesis
    Rudy J Castellani
    Division of Neuropathology, Michigan State University, B218 Clinical Center, 138 Service Road, East Lansing, MI 48824 1313, USA
    Neurobiol Aging 25:599-602; discussion 603-4. 2004
    ..As such, CAA represents tissue homeostasis, such that an abrupt perturbation of this balance (e.g., amyloid beta immunization) is deleterious...
  38. doi request reprint Bilateral internal carotid absence: a case report of a rare congenital anomaly
    Luis F Gonzalez-Cuyar
    Department of Pathology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    Cardiovasc Pathol 17:113-6. 2008
    ..Secondary to the hemodynamical stress through the collateral circulation, affected patients are at an increased risk of developing subarachnoid hemorrhage and intracranial aneurysms...
  39. ncbi request reprint Malignant glioma progression and nitric oxide
    Dora Lam-Himlin
    Department of Pathology, University of Maryland, 22 South Greene Street, Baltimore, MD 21201, USA
    Neurochem Int 49:764-8. 2006
    ..This review discusses the multifaceted activity of nitric oxide with particular reference to malignant gliomas...
  40. ncbi request reprint Prion disease and Alzheimer's disease: pathogenic overlap
    Rudy J Castellani
    Division of Neuropathology, Michigan State University, B218 Clinical Center, 138 Service Road, East Lansing, Michigan 48824, USA
    Acta Neurobiol Exp (Wars) 64:11-7. 2004
    ....
  41. doi request reprint Granulocytic sarcoma mimicking HSV encephalitis
    Reena S Shah
    Departments of Neurology, University of Maryland, Baltimore, MD 21201, USA
    Neurologist 16:319-21. 2010
    ..Granulocytic sarcomas, or chloromas, are extramedullary collections of immature granulocytes. Central nervous system involvement is rare and of those cases described, most are complications of acute myelogenous leukemia...
  42. doi request reprint Sudden unexpected death in lymphocytic hypophysitis
    Luis F Gonzalez-Cuyar
    Department of Pathology, University of Maryland, Baltimore, MD 21201, USA
    Am J Forensic Med Pathol 30:61-3. 2009
    ....
  43. pmc Sulfonylurea receptor 1 expression in human cerebral infarcts
    Rupal I Mehta
    Department of Pathology, University of Maryland School of Medicine, Baltimore, MD 21201 1595, USA
    J Neuropathol Exp Neurol 72:871-83. 2013
    ..In conjunction with previous studies, these data suggest that Sur1 may be a promising treatment target in patients with acute cerebral infarction. ..
  44. ncbi request reprint 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
    ....
  45. 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...
  46. ncbi request reprint Oxidative stress and neurodegeneration
    Paula I Moreira
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Ann N Y Acad Sci 1043:545-52. 2005
    ..Our findings support the idea that aldehyde-mediated modifications, in concert with oxyradical-mediated modifications, are critical early pathogenic factors in Alzheimer's disease...
  47. pmc 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...
  48. ncbi request reprint Chitin-like polysaccharides in Alzheimer's disease brains
    Rudy J Castellani
    Department of Physiology Human Pathology, Michigan State University, East Lansing, MI, USA
    Curr Alzheimer Res 2:419-23. 2005
    ..Since chitin is a highly insoluble molecule and a substrate for glycan-protein interactions, chitin-like polysaccharides within the brain could facilitate nucleation of amyloid proteins in various amyloidoses including AD...
  49. 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...
  50. ncbi request reprint Involvement of oxidative stress in Alzheimer disease
    Akihiko Nunomura
    Department of Psychiatry and Neurology, Asahikawa Medical College, Asahikawa, Japan
    J Neuropathol Exp Neurol 65:631-41. 2006
    ....
  51. 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...
  52. ncbi request reprint Systemic increase of oxidative nucleic acid damage in Parkinson's disease and multiple system atrophy
    Akio Kikuchi
    Department of Neurology, Tohoku University School of Medicine, Sendai, Japan
    Neurobiol Dis 9:244-8. 2002
    ..Our results also imply that female patients with PD show higher levels of oxidative stress, which may explain the faster progression of this disease in females...
  53. ncbi request reprint Oxidative damage to nucleic acids in human prion disease
    Marin Guentchev
    Institute of Neurology, University of Vienna, Austrian Reference Center for Human Prion Disease ORPE
    Neurobiol Dis 9:275-81. 2002
    ..Further, our data support the hypothesis that loss of the anti-oxidant function of PrP(c) plays a key role in the pathogenesis of these disorders...
  54. ncbi request reprint 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
    ....
  55. ncbi request reprint Oxidative damage in the olfactory system in Alzheimer's disease
    George Perry
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Acta Neuropathol 106:552-6. 2003
    ....
  56. ncbi request reprint 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...
  57. ncbi request reprint Hydroxynonenal adducts indicate a role for lipid peroxidation in neocortical and brainstem Lewy bodies in humans
    Rudy J Castellani
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Neurosci Lett 319:25-8. 2002
    ..These findings not only support prior studies indicating that lipid peroxidation is increased in patients with PD and DLBD but that oxidative damage may play a critical role in Lewy body formation...
  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
    ....