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Genomes and Genes | Rudy J CastellaniSummaryAffiliation: University of Maryland Country: USA Publications
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Publications
Pathogenesis and disease-modifying therapy in Alzheimer's disease: the flat line of progressRudy 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?..
A novel origin for granulovacuolar degeneration in aging and Alzheimer's disease: parallels to stress granulesRudy 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...- The role of iron as a mediator of oxidative stress in Alzheimer diseaseRudy 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... - Expression of CD74 is increased in neurofibrillary tangles in Alzheimer's diseaseKathryn 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... 
The role of novel chitin-like polysaccharides in Alzheimer diseaseRudy 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...- 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... - Vascular dementia and Alzheimer's disease: a waning dichotomyRudy J Castellani
Division of Neuropathology, University of Maryland, Baltimore, USA
J Alzheimers Dis 12:343-4. 2007 - 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... - 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.... - 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... - 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.... - 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... - 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... - 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... - 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... - 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.... - DLP1-dependent mitochondrial fragmentation mediates 1-methyl-4-phenylpyridinium toxicity in neurons: implications for Parkinson's diseaseXinglong 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... - Iron: the Redox-active center of oxidative stress in Alzheimer diseaseRudy 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... - Increased expression of p130 in Alzheimer diseaseLaura 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... - Redox active iron accumulation in aceruloplasminemiaLuis 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... - 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.... - Hydroxynonenal-generated crosslinking fluorophore accumulation in Alzheimer disease reveals a dichotomy of protein turnoverXiongwei 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... - 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.... - 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.... - 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.... - 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.... - Activation of the extracellular signal-regulated kinase pathway contributes to the behavioral deficit of fragile x-syndromeXinglong 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... - Frontiers in Alzheimer's disease therapeuticsJeremy 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... - 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... - Paraffin-embedded tissue (PET) blot method: application to Alzheimer diseaseCalvin 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... - 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... - Sublethal RNA oxidation as a mechanism for neurodegenerative diseaseRudy J Castellani
Department of Pathology, University of Maryland, Baltimore, Maryland, USA
Int J Mol Sci 9:789-806. 2008.... - Cerebrotendinous xanthomatosis: case report with evidence of oxidative stressLuis 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... - Molecular Pathogenesis of Alzheimer's Disease: Reductionist versus Expansionist ApproachesRudy J Castellani
Division of Neuropathology, University of Maryland, Baltimore, Maryland, 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... - 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... - Prion disease and Alzheimer's disease: pathogenic overlapRudy 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.... - Cerebral amyloid angiopathy: major contributor or decorative response to Alzheimer's disease pathogenesisRudy 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... - Cocaine-induced intracerebral hemorrhage in a patient with cerebral amyloid angiopathyMarianna 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... - Bilateral internal carotid absence: a case report of a rare congenital anomalyLuis 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... - Malignant glioma progression and nitric oxideDora 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... - Sudden unexpected death in lymphocytic hypophysitisLuis F Gonzalez-Cuyar
Department of Pathology, University of Maryland, Baltimore, MD 21201, USA
Am J Forensic Med Pathol 30:61-3. 2009.... - Granulocytic sarcoma mimicking HSV encephalitisReena 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... - Contribution of redox-active iron and copper to oxidative damage in Alzheimer diseaseRudy J Castellani
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
Ageing Res Rev 3:319-26. 2004.... - 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... - Oxidative stress and neurodegenerationPaula 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... - Involvement of oxidative stress in Alzheimer diseaseAkihiko Nunomura
Department of Psychiatry and Neurology, Asahikawa Medical College, Asahikawa, Japan
J Neuropathol Exp Neurol 65:631-41. 2006.... - Microtubule reduction in Alzheimer's disease and aging is independent of tau filament formationAdam 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... - Chitin-like polysaccharides in Alzheimer's disease brainsRudy 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... - 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... - Adventiously-bound redox active iron and copper are at the center of oxidative damage in Alzheimer diseaseGeorge Perry
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
Biometals 16:77-81. 2003.... - Oxidative damage to nucleic acids in human prion diseaseMarin 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... - Oxidative damage in the olfactory system in Alzheimer's diseaseGeorge Perry
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
Acta Neuropathol 106:552-6. 2003.... - 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 diseaseXiongwei 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... - 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.... - 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... - Hydroxynonenal adducts indicate a role for lipid peroxidation in neocortical and brainstem Lewy bodies in humansRudy 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... - Systemic increase of oxidative nucleic acid damage in Parkinson's disease and multiple system atrophyAkio 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...