Research Topics
| C S AtwoodSummaryAffiliation: Case Western Reserve University Country: USA Publications
| Collaborators
|
Detail Information
Publications
Human neurons express type I GnRH receptor and respond to GnRH I by increasing luteinizing hormone expressionAndrea C Wilson
Department of Pathology and Laboratory Medicine, Veterans Administration Hospital, University of Wisconsin, 2500 Overlook Terrace, Madison, Wisconsin 53705, USA
J Endocrinol 191:651-63. 2006..Post-reproductive surges in GnRH I secretion may explain the accumulation of LH in pyramidal neurons of the aged human and rat...- Senile plaque composition and posttranslational modification of amyloid-beta peptide and associated proteinsCraig S Atwood
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
Peptides 23:1343-50. 2002.... - Amyloid-beta: a chameleon walking in two worlds: a review of the trophic and toxic properties of amyloid-betaCraig 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... - Amyloid-beta: a vascular sealant that protects against hemorrhage?Craig S Atwood
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106 USA
J Neurosci Res 70:356. 2002 - Amyloid-beta: redox-metal chelator and antioxidantC S Atwood
Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
J Alzheimers Dis 4:203-14. 2002 - Mitochondrial abnormalities in Alzheimer's diseaseK Hirai
Institute of Pathology, Department of Neurology, Case Western Reserve University, Cleveland, Ohio 44106, USA
J Neurosci 21:3017-23. 2001..The relationship shown here between the site and extent of mitochondrial abnormalities and oxidative damage suggests an intimate and early association between these features in Alzheimer's disease... - Oxidative damage is the earliest event in Alzheimer diseaseA Nunomura
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
J Neuropathol Exp Neurol 60:759-67. 2001..These findings suggest that AD is associated with compensatory changes that reduce damage from reactive oxygen... - Differential activation of neuronal ERK, JNK/SAPK and p38 in Alzheimer disease: the 'two hit' hypothesisX Zhu
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
Mech Ageing Dev 123:39-46. 2001..Therefore, we propose that both 'hits', oxidative stress and mitotic alterations, are necessary for the progression of Alzheimer disease... - Evidence for the role of gonadotropin hormones in the development of Alzheimer diseaseG Casadesus
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
Cell Mol Life Sci 62:293-8. 2005..Given the evidence supporting a pathogenic role for LH in AD, a trial of leuprolide acetate, which suppresses LH release, has been initiated in patients... - Active glycation in neurofibrillary pathology of Alzheimer disease: N(epsilon)-(carboxymethyl) lysine and hexitol-lysineR J Castellani
Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
Free Radic Biol Med 31:175-80. 2001..Our findings support the notion that aldehyde-mediated modifications, together with oxyradical-mediated modifications, are critical pathogenic factors in AD... - Mitotic and gender parallels in Alzheimer disease: therapeutic opportunitiesX Zhu
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
Curr Drug Targets 5:559-63. 2004..As such, agents targeted toward luteinizing hormone or downstream sequelae may be of great therapeutic value in the treatment of Alzheimer disease... - 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... - What is aging? What is its role in Alzheimer's disease? What can we do about it?J Wesson Ashford
Stanford VA Alzheimer Center, Palo Alto, CA 94304 1207, USA
J Alzheimers Dis 7:247-53; discussion 255-62. 2005 - Amyloid-beta-induced toxicity of primary neurons is dependent upon differentiation-associated increases in tau and cyclin-dependent kinase 5 expressionTianbing Liu
Department of Medicine, University of Wisconsin-Madison, Geriatrics, Research, Education and Clinical Center, Wm. S. Middleton Memorial Veterans Hospital, 53705, USA
J Neurochem 88:554-63. 2004..Our results predict that only cells containing appreciable levels of tau are susceptible to Abeta-induced toxicity and may explain why Abeta is more toxic to neurons compared with other cell types... - Copper mediates dityrosine cross-linking of Alzheimer's amyloid-betaCraig S Atwood
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
Biochemistry 43:560-8. 2004..Given the elevated concentration of Cu in senile plaques, our results suggest that Cu interactions with Abeta could be responsible for causing the covalent cross-linking of Abeta in these structures... - Amyloid-beta: phylogenesis of a chameleonAnatol Kontush
Brain Res Brain Res Rev 46:118-20. 2004 - Trace metal contamination initiates the apparent auto-aggregation, amyloidosis, and oligomerization of Alzheimer's Abeta peptidesXudong Huang
Department of Psychiatry, and Laboratory for Oxidation Biology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA
J Biol Inorg Chem 9:954-60. 2004..These data suggest that protein self-assembly and oligomerization are not spontaneous in this system as previously thought, and that there may be an obligatory role for metal ions in initiating Abeta amyloidosis and oligomerization... - Estrogen bows to a new master: the role of gonadotropins in Alzheimer pathogenesisKate 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... - Novel D-penicillamine carrying nanoparticles for metal chelation therapy in Alzheimer's and other CNS diseasesZhengrong Cui
Department of Pharmaceutical Sciences, Center for Pharmaceutical Science and Technology, College of Pharmacy, University of Kentucky, Lexington, KY 40536-0082, USA
Eur J Pharm Biopharm 59:263-72. 2005..These results indicate that nanoparticles have potential to deliver D-penicillamine to the brain for the prevention of Abeta (1-42) accumulation, as well as to reduce metal ion accumulation in other CNS diseases... - The gonadotropin connection in Alzheimer's diseaseSivan Vadakkadath Meethal
Section of Geriatrics and Gerontology, Department of Medicine, University of Wisconsin-Madison, Veterans Administration Hospital, Madison, 53705, USA
Endocrine 26:317-26. 2005..Clinical trials are underway for the treatment of AD using GnRH analogs and should provide further insights into the gonadotropin connection in AD... - Luteinizing hormone modulates cognition and amyloid-beta deposition in Alzheimer APP transgenic miceGemma 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... 
Antibodies to potato virus Y bind the amyloid beta peptide: immunohistochemical and NMR studiesRobert 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...- 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.... - Reduction of inclusion body pathology in ApoE-deficient mice fed a combination of antioxidantsGerald Veurink
Department of Surgery, University of Western Australia, Perth, Western Australia, Australia
Free Radic Biol Med 34:1070-7. 2003.... - Iron: a pathological mediator of Alzheimer disease?Glenda M Bishop
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
Dev Neurosci 24:184-7. 2002..Continued examination of the complex interactions that occur between iron and amyloid-beta may assist in the elucidation of the mechanisms that underlie the neurodegeneration that leads to dementia in AD... - Ill-fated amyloid-beta vaccineMark A Smith
J Neurosci Res 69:285. 2002 - 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... - Iron homeostasis is maintained in the brain, but not the liver, following mild hypoxiaGlenda 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... - Amyloid-beta: a (life) preserver for the brainMark E Obrenovich
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
Neurobiol Aging 23:1097-9. 2002 - The role of iron and copper in the aetiology of neurodegenerative disorders: therapeutic implicationsGeorge Perry
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
CNS Drugs 16:339-52. 2002..In this article, we examine not only the possible mechanism of disease but also how pharmaceuticals may intervene, from direct and indirect antioxidant therapy to strategies involving gene therapy... - Cerebral hemorrhage and amyloid-betaCraig S Atwood
Science 299:1014; author reply 1014. 2003 - The state versus amyloid-beta: the trial of the most wanted criminal in Alzheimer diseaseCatherine 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?.. - 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... - Metal binding and oxidation of amyloid-beta within isolated senile plaque cores: Raman microscopic evidenceJian Dong
Department of Biochemistry, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, Ohio 44106, USA
Biochemistry 42:2768-73. 2003..The results also reveal a direct chemical basis for oxidative damage caused by amyloid-beta protein in AD... - A luteinizing hormone receptor intronic variant is significantly associated with decreased risk of Alzheimer's disease in males carrying an apolipoprotein E epsilon4 alleleRyan J Haasl
Section of Geriatrics and Gerontology, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA
BMC Med Genet 9:37. 2008.... - Gonadotropins: a cohesive gender-based etiology of Alzheimer diseaseKate M Webber
Department of Pathology, Case Western Reserve University, Cleveland, OH, USA
Mol Cell Endocrinol 260:271-5. 2007..In this review, we examine how the gonadotropins may play a central and determining role in modulating the susceptibility to, and progression of, Alzheimer disease... - The cell cycle and hormonal fluxes in Alzheimer disease: a novel therapeutic targetKate 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... - Menopause, estrogen, and gonadotropins in Alzheimer's diseaseGemma Casadesus
Department of Neurosciences, Case Western Reserve University, Cleveland, Ohio 44106, USA
Adv Clin Chem 45:139-53. 2008..Moreover, targeting gonadotropins appears to have beneficial actions as a therapeutic regimen... - Luteinizing hormone receptor mediates neuronal pregnenolone production via up-regulation of steroidogenic acute regulatory protein expressionTianbing Liu
Department of Pathology and Laboratory Medicine, University of Wisconsin, Madison, Wisconsin 53705, USA
J Neurochem 100:1329-39. 2007.... - Increased expression of the remodeling- and tumorigenic-associated factor osteopontin in pyramidal neurons of the Alzheimer's disease brainJohn K Wung
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
Curr Alzheimer Res 4:67-72. 2007.... - Predicting the failure of amyloid-beta vaccineMark A Smith
Lancet 359:1864-5. 2002 - fMRI activation during episodic encoding and metacognitive appraisal across the lifespan: risk factors for Alzheimer's diseaseMehul A Trivedi
Geriatric Research Education and Clinical Center, Wm S Middleton Memorial Veterans Hospital, Madison, WI 53705, USA
Neuropsychologia 46:1667-78. 2008..These results suggest that FH and aging are exerting independent effects in both tasks while APOE affected the relationship with age in the hippocampus in one of the two tasks given... 
A multi-hit endocrine model of intrinsic adult-onset asthmaCraig S Atwood
Department of Medicine, University of Wisconsin and Geriatric Research, Education and Clinical Center, Veterans Administration Hospital, 2500 Overlook Terrace, Madison, WI 53705, USA
Ageing Res Rev 7:114-25. 2008..Future therapeutic strategies might therefore target the serotonergic, leptinergic and hypothalamic pathways in regulating cellular cAMP production and bronchoconstriction for the treatment of adult-onset asthma...- Reproductive hormones regulate the selective permeability of the blood-brain barrierAndrea C Wilson
Department of Medicine, University of Wisconsin Madison and Geriatric Research, Education and Clinical Center, Veterans Administration Hospital, 2500 Overlook Terrace, Madison, WI 53705 USA
Biochim Biophys Acta 1782:401-7. 2008..Furthermore, these findings implicate Cx43 in mediating changes in BBB permeability, and serum gonadotropins in the cerebropathophysiology of age-related neurodegenerative diseases such as stroke and Alzheimer's disease... - Effects of simvastatin on cerebrospinal fluid biomarkers and cognition in middle-aged adults at risk for Alzheimer's diseaseCynthia M Carlsson
Department of Medicine, Section of Geriatrics and Gerontology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA
J Alzheimers Dis 13:187-97. 2008..It is unclear if statins modify Abeta metabolism or improve cognition in asymptomatic middle-aged adults at increased risk for AD... - The estrogen myth: potential use of gonadotropin-releasing hormone agonists for the treatment of Alzheimer's diseaseGemma Casadesus
Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
Drugs R D 7:187-93. 2006.... - Antigonadotropins: a novel strategy to halt Alzheimer's disease progressionChristopher W Gregory
Voyager Pharmaceutical Corporation, Raleigh, NC 27615, USA
Curr Pharm Des 12:685-90. 2006.... - Gender differences in Alzheimer disease: the role of luteinizing hormone in disease pathogenesisKate M Webber
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
Alzheimer Dis Assoc Disord 19:95-9. 2005..Based on this, we suggest that therapeutic interventions targeted at gonadotropins may both prevent disease in those patients currently asymptomatic or may halt, and even reverse, disease in those currently afflicted... - Dangers of the amyloid-beta vaccinationMark A Smith
Acta Neuropathol 104:110. 2002 - Elevated luteinizing hormone expression colocalizes with neurons vulnerable to Alzheimer's disease pathologyRichard L Bowen
Voyager Pharmaceutical Corporation, Raleigh, North Carolina, USA
J Neurosci Res 70:514-8. 2002..Elevated serum and cortical neuron levels of LH, coupled with the decline in sex steroid production, could play important roles in the pathogenesis of AD... - Estrogen replacement and risk of Alzheimer diseaseMark A Smith
JAMA 289:1100; author reply 1101-2. 2003 - Pennington scientific symposium on mechanisms and retardation of agingCraig S Atwood
Section of Geriatrics and Gerontology, University of Wisconsin Medical School, Madison, WI, USA
Exp Gerontol 38:1217-26. 2003 - Luteinizing hormone, a reproductive regulator that modulates the processing of amyloid-beta precursor protein and amyloid-beta depositionRichard L Bowen
Voyager Pharmaceutical Corporation, Raleigh, NC 27615, USA
J Biol Chem 279:20539-45. 2004..Suppression of the age-related increase in serum gonadotropins using anti-gonadotropin agents may represent a novel therapeutic strategy for AD... - Gonadotropins and Alzheimer's disease: the link between estrogen replacement therapy and neuroprotectionKate M Webber
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106, USA
Acta Neurobiol Exp (Wars) 64:113-8. 2004..Based on this, we suggest that therapeutic interventions targeted at gonadotropins could both prevent disease in those patients currently asymptomatic or halt, and even reverse, disease in those currently afflicted... - Cerebrovascular requirement for sealant, anti-coagulant and remodeling molecules that allow for the maintenance of vascular integrity and blood supplyCraig S Atwood
School of Medicine, University of Wisconsin and William S Middleton Memorial Veterans Administration, GRECC 11G, 2500 Overlook Terrace, Madison, WI 53705, USA
Brain Res Brain Res Rev 43:164-78. 2003..e. immunological responses to Abeta vaccination do not discriminate between physiologically purposive deposits of Abeta (vascular deposits) and pathological deposits of Abeta (senile plaques)... - The role of beta amyloid in Alzheimer's disease: still a cause of everything or the only one who got caught?Giuseppe Verdile
Sir James McCusker Alzheimer s Disease Research Unit, School of Psychiatry and Clinical Neurosciences, University of Western Australia, Hollywood Private Hospital, Monash Avenue, Nedlands, WA 6009, Australia
Pharmacol Res 50:397-409. 2004..This research has led to the development of therapeutic agents, currently in human clinical trials, which target A beta... - Living and dying for sex. A theory of aging based on the modulation of cell cycle signaling by reproductive hormonesRichard L Bowen
Voyager Pharmaceutical Corporation, Raleigh, N C, USA
Gerontology 50:265-90. 2004.... - Beyond estrogen: targeting gonadotropin hormones in the treatment of Alzheimer's diseaseGemma Casadesus
Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
Curr Drug Targets CNS Neurol Disord 3:281-5. 2004..Therefore, the effects of agents that abolish LH, such as leuprolide acetate, which are currently being evaluated in Phase II clinical trials for the treatment of AD, are eagerly anticipated... - Dementia and testosterone levels in menRichard L Bowen
JAMA 293:551; author reply 552. 2005 - Feedback on a feedback loop: the hypothalamic-pituitary-gonadal axisCraig S Atwood
J Alzheimers Dis 7:1-2. 2005 - Dysregulation of the hypothalamic-pituitary-gonadal axis with menopause and andropause promotes neurodegenerative senescenceCraig S Atwood
Section of Geriatrics and Gerontology, Department of Medicine, University of Wisconsin Madison, 53705, USA
J Neuropathol Exp Neurol 64:93-103. 2005..Ideally, supplementation with HPG hormones should mimic closely the serum concentrations of all HPG hormones in reproductive men and cycling women to prevent dyotic signaling and attempted neuron division... - Call for Elan to publish Alzheimer's trial detailsGlenda M Bishop
Nature 416:677. 2002