T A Bayer

Summary

Affiliation: Saarland University
Country: Germany

Publications

  1. ncbi request reprint Gender dependent APP processing in a transgenic mouse model of Alzheimer's disease
    S Schafer
    Department of Psychiatry, Division of Neurobiology, Saarland University, Homburg Saar, Germany
    J Neural Transm 114:387-94. 2007
  2. ncbi request reprint Involvement of amyloid beta precursor protein (AbetaPP) modulated copper homeostasis in Alzheimer's disease
    Thomas A Bayer
    Universitat des Saarlandes, Klinik fur Psychiatrie, Abteilung für Neurobiologie, D 66421 Homburg, Germany
    J Alzheimers Dis 8:201-6; discussion 209-15. 2005
  3. pmc Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Abeta production in APP23 transgenic mice
    Thomas A Bayer
    Department of Psychiatry, Division of Neurobiology, University of the Saarland Medical Center, D 66421 Homburg, Germany
    Proc Natl Acad Sci U S A 100:14187-92. 2003
  4. ncbi request reprint Intraneuronal Abeta accumulation precedes plaque formation in beta-amyloid precursor protein and presenilin-1 double-transgenic mice
    O Wirths
    Department of Psychiatry, University of Bonn Medical Center, Sigmund-Freud-Strasse 25, 53105, Bonn, Germany
    Neurosci Lett 306:116-20. 2001
  5. ncbi request reprint Alpha-synuclein accumulates in Lewy bodies in Parkinson's disease and dementia with Lewy bodies but not in Alzheimer's disease beta-amyloid plaque cores
    T A Bayer
    Department of Psychiatry, University of Bonn Medical Center, Germany
    Neurosci Lett 266:213-6. 1999
  6. ncbi request reprint Traumatic brain injury: cause or risk of Alzheimer's disease? A review of experimental studies
    J Szczygielski
    Department of Psychiatry, Section Neurobiology, Saarland University, Homburg, Germany
    J Neural Transm 112:1547-64. 2005
  7. ncbi request reprint Reelin in plaques of beta-amyloid precursor protein and presenilin-1 double-transgenic mice
    O Wirths
    Department of Psychiatry, University of Bonn Medical Center, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Neurosci Lett 316:145-8. 2001
  8. ncbi request reprint Key factors in Alzheimer's disease: beta-amyloid precursor protein processing, metabolism and intraneuronal transport
    T A Bayer
    Department of Psychiatry, University of Bonn Medical Center, Germany
    Brain Pathol 11:1-11. 2001
  9. doi request reprint Motor impairment in Alzheimer's disease and transgenic Alzheimer's disease mouse models
    O Wirths
    Division of Molecular Psychiatry, Department of Psychiatry, University of Goettingen, Goettingen, Germany
    Genes Brain Behav 7:1-5. 2008
  10. doi request reprint Review on the APP/PS1KI mouse model: intraneuronal Abeta accumulation triggers axonopathy, neuron loss and working memory impairment
    T A Bayer
    Division of Molecular Psychiatry, Department of Psychiatry, University of Goettingen, Goettingen, Germany
    Genes Brain Behav 7:6-11. 2008

Collaborators

Detail Information

Publications44

  1. ncbi request reprint Gender dependent APP processing in a transgenic mouse model of Alzheimer's disease
    S Schafer
    Department of Psychiatry, Division of Neurobiology, Saarland University, Homburg Saar, Germany
    J Neural Transm 114:387-94. 2007
    ....
  2. ncbi request reprint Involvement of amyloid beta precursor protein (AbetaPP) modulated copper homeostasis in Alzheimer's disease
    Thomas A Bayer
    Universitat des Saarlandes, Klinik fur Psychiatrie, Abteilung für Neurobiologie, D 66421 Homburg, Germany
    J Alzheimers Dis 8:201-6; discussion 209-15. 2005
    ....
  3. pmc Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Abeta production in APP23 transgenic mice
    Thomas A Bayer
    Department of Psychiatry, Division of Neurobiology, University of the Saarland Medical Center, D 66421 Homburg, Germany
    Proc Natl Acad Sci U S A 100:14187-92. 2003
    ..Cu treatment lowered endogenous CNS Abeta before a detectable reduction of amyloid plaques. Thus, APP23 mice reveal APP-induced alterations linked to Cu homeostasis, which can be reversed by addition of dietary Cu...
  4. ncbi request reprint Intraneuronal Abeta accumulation precedes plaque formation in beta-amyloid precursor protein and presenilin-1 double-transgenic mice
    O Wirths
    Department of Psychiatry, University of Bonn Medical Center, Sigmund-Freud-Strasse 25, 53105, Bonn, Germany
    Neurosci Lett 306:116-20. 2001
    ..Interestingly, intraneuronal Abeta staining was no longer detected in the brain of aged double-transgenic mice, which correlates with the typical neuropathology in the brain of chronic AD patients...
  5. ncbi request reprint Alpha-synuclein accumulates in Lewy bodies in Parkinson's disease and dementia with Lewy bodies but not in Alzheimer's disease beta-amyloid plaque cores
    T A Bayer
    Department of Psychiatry, University of Bonn Medical Center, Germany
    Neurosci Lett 266:213-6. 1999
    ..These observations suggest that alpha-synuclein does not contribute to late neurodegenerative processes in AD brains...
  6. ncbi request reprint Traumatic brain injury: cause or risk of Alzheimer's disease? A review of experimental studies
    J Szczygielski
    Department of Psychiatry, Section Neurobiology, Saarland University, Homburg, Germany
    J Neural Transm 112:1547-64. 2005
    ..We further evaluate the connection between traumatic brain insults and subsequent development of dementia and try to differentiate between primary and secondary pathological mechanisms...
  7. ncbi request reprint Reelin in plaques of beta-amyloid precursor protein and presenilin-1 double-transgenic mice
    O Wirths
    Department of Psychiatry, University of Bonn Medical Center, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Neurosci Lett 316:145-8. 2001
    ..This observation gives the first evidence for the association of reelin with amyloid deposits...
  8. ncbi request reprint Key factors in Alzheimer's disease: beta-amyloid precursor protein processing, metabolism and intraneuronal transport
    T A Bayer
    Department of Psychiatry, University of Bonn Medical Center, Germany
    Brain Pathol 11:1-11. 2001
    ..Beta-amyloid precursor protein has a pivotal role in Alzheimer's disease...
  9. doi request reprint Motor impairment in Alzheimer's disease and transgenic Alzheimer's disease mouse models
    O Wirths
    Division of Molecular Psychiatry, Department of Psychiatry, University of Goettingen, Goettingen, Germany
    Genes Brain Behav 7:1-5. 2008
    ..In addition, we summarize the state of knowledge on this phenotype in experimental mouse models, expressing AD-associated genes like tau or amyloid precursor protein...
  10. doi request reprint Review on the APP/PS1KI mouse model: intraneuronal Abeta accumulation triggers axonopathy, neuron loss and working memory impairment
    T A Bayer
    Division of Molecular Psychiatry, Department of Psychiatry, University of Goettingen, Goettingen, Germany
    Genes Brain Behav 7:6-11. 2008
    ..4) Onset of the observed behavioral alterations correlates well with robust axonal degeneration in brain and spinal cord and with abundant hippocampal CA1 neuron loss...
  11. ncbi request reprint Cerebrospinal fluid diagnostic markers correlate with lower plasma copper and ceruloplasmin in patients with Alzheimer's disease
    H Kessler
    Department of Psychiatry and Psychotherapy, Saarland University, Homburg Saar, Germany
    J Neural Transm 113:1763-9. 2006
    ..Although only AD patients were included, the reduced plasma Cu and CB levels in patients with a CSF diagnosis of advanced AD supports previous observations that a mild Cu deficiency might contribute to AD progression...
  12. ncbi request reprint [The role of copper in the pathophysiology of Alzheimer's disease]
    H Kessler
    Klinik fur Psychiatrie und Psychotherapie, Universitatsklinikum des Saarlandes, Homburg Saar
    Nervenarzt 76:581-5. 2005
    ....
  13. ncbi request reprint Evidence for activation of microglia in patients with psychiatric illnesses
    T A Bayer
    Department of Psychiatry, University of Bonn Medical Center, Germany
    Neurosci Lett 271:126-8. 1999
    ..The activation of microglia cells, which represent a major part of the brain immune response, may help to unravel the pathophysiological processes in severe psychiatric illnesses...
  14. ncbi request reprint Disturbed gyrification of the prefrontal region in male schizophrenic patients: A morphometric postmortem study
    K Vogeley
    Department of Psychiatry, Freidrich Wilhelms University of Bonn, Germany
    Am J Psychiatry 157:34-9. 2000
    ..The goal was to test the hypothesis that abnormalities of gyrification are present in the prefrontal region of postmortem brains from schizophrenic patients...
  15. ncbi request reprint It all sticks together--the APP-related family of proteins and Alzheimer's disease
    T A Bayer
    Department of Psychiatry, University of Bonn Medical Center, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    Mol Psychiatry 4:524-8. 1999
    ..We hypothesize that the functional loss of members of the APP family contributes to the gradual cognitive decline in Alzheimer's disease patients...
  16. ncbi request reprint Decreased plasma cholesterol levels during aging in transgenic mouse models of Alzheimer's disease
    Oliver Wirths
    Department of Psychiatry, University of the Saarland, 66421 Homburg Saar, Germany
    Exp Gerontol 41:220-4. 2006
    ..Furthermore, statistical analysis revealed a significant negative correlation between plasma cholesterol and brain Abeta42 levels during aging in the mice expressing both APP and PS1...
  17. ncbi request reprint Axonopathy in an APP/PS1 transgenic mouse model of Alzheimer's disease
    Oliver Wirths
    Department of Psychiatry, Division of Neurobiology, Saarland University, Building 90, 66421, Homburg, Saar, Germany
    Acta Neuropathol 111:312-9. 2006
    ..This strengthens the prevailing amyloid hypothesis as a primary trigger of AD-typical pathological alterations...
  18. ncbi request reprint Age-dependent axonal degeneration in an Alzheimer mouse model
    Oliver Wirths
    Department of Psychiatry, Division of Neurobiology, Saarland University, Building 90, D 66421 Homburg Saar, Germany
    Neurobiol Aging 28:1689-99. 2007
    ..We conclude that the intraneuronal accumulation of Abeta-amyloid peptides is followed by axonal degeneration, and thus might be a causative factor for the axonal changes seen in AD...
  19. ncbi request reprint Profile of cholesterol-related sterols in aged amyloid precursor protein transgenic mouse brain
    Dieter Lutjohann
    Department of Clinical Pharmacology, University of Bonn, Sigmund Freud Strasse 25, D 53105 Bonn, Germany
    J Lipid Res 43:1078-85. 2002
    ..Moreover, the levels of the exogenous plant sterols campesterol and sitosterol were significantly elevated in the brains of APP23 animals at age 12 and 18 months. This time point coincides with abundant plaque formation...
  20. ncbi request reprint Copper and clioquinol treatment in young APP transgenic and wild-type mice: effects on life expectancy, body weight, and metal-ion levels
    Stephanie Schafer
    Department of Psychiatry, Division of Neurobiology, Saarland University, Homburg, Germany
    J Mol Med (Berl) 85:405-13. 2007
    ....
  21. ncbi request reprint Deficits in working memory and motor performance in the APP/PS1ki mouse model for Alzheimer's disease
    Oliver Wirths
    Department of Psychiatry, University of Goettingen, Von Siebold Str 5, D 37075 Goettingen, Germany
    Neurobiol Aging 29:891-901. 2008
    ....
  22. doi request reprint New insights into Alzheimer's disease: 'modeling neurodegeneration - causes and consequences'
    Thomas A Bayer
    Genes Brain Behav 7:iv. 2008
  23. ncbi request reprint Impaired Cu/Zn-SOD activity contributes to increased oxidative damage in APP transgenic mice
    Katrin Schuessel
    Department of Pharmacology, Biocentre, J W Goethe University of Frankfurt, Germany
    Neurobiol Dis 18:89-99. 2005
    ..Our results demonstrate that impaired Cu/Zn-SOD activity contributes to oxidative damage in Thy1-APP751(SL) transgenic mice, and these findings are closely linked to increased beta-amyloidogenic cleavage of APP...
  24. doi request reprint Intraneuronal beta-amyloid is a major risk factor--novel evidence from the APP/PS1KI mouse model
    Thomas A Bayer
    Department of Psychiatry, Division of Molecular Psychiatry, University of Goettingen, Goettingen, Germany
    Neurodegener Dis 5:140-2. 2008
    ..These observations support a pivotal role of intraneuronal Abeta accumulation as a principal pathological trigger in AD...
  25. doi request reprint Sortilin-related receptor with A-type repeats (SORLA) affects the amyloid precursor protein-dependent stimulation of ERK signaling and adult neurogenesis
    Michael Rohe
    Max Delbrueck Center for Molecular Medicine, Berlin, Germany
    J Biol Chem 283:14826-34. 2008
    ..Our data document a role for SORLA not only in control of plaque burden but also in APP-dependent neuronal signaling and suggest a molecular explanation for increased neurogenesis observed in some AD patients...
  26. doi request reprint Age-dependent loss of dentate gyrus granule cells in APP/PS1KI mice
    Marie Caroline Cotel
    Division of Molecular Psychiatry and Alzheimer Ph D Graduate School, Department of Psychiatry, University of Goettingen, Von Siebold Strasse 5, Goettingen, Germany
    Brain Res 1222:207-13. 2008
    ..Stereological analysis revealed a strongly significant decrease of GCLs in aged APP/PS1KI mice, compared to age-matched PS1KI control animals (-44%), however, the volume of the GCL was not different...
  27. ncbi request reprint Reductions in cholesterol and synaptic markers in association cortex in mood disorders
    Clare L Beasley
    Center for Complex Disorders, Department of Psychiatry, University of British Columbia, Vancouver, Canada
    Bipolar Disord 7:449-55. 2005
    ..The aim of this study was to quantify sterol levels in the brains of patients with major psychiatric disorders and further to relate these levels to markers of myelin and synapses...
  28. ncbi request reprint Cognitive decline correlates with low plasma concentrations of copper in patients with mild to moderate Alzheimer's disease
    Frank Gerald Pajonk
    Department for Psychiatry, Saarland University, Building 90, 66421 Homburg Saar, Germany
    J Alzheimers Dis 8:23-7. 2005
    ..5% of the patients revealed a significant negative correlation between plasma Cu and ADAS-cog. This finding supports the hypothesis of a mild Cu deficiency in most AD patients...
  29. ncbi request reprint Intraneuronal APP/A beta trafficking and plaque formation in beta-amyloid precursor protein and presenilin-1 transgenic mice
    Oliver Wirths
    Department of Psychiatry, University of Bonn Medical Center, Germany
    Brain Pathol 12:275-86. 2002
    ..This is most likely due to an APP/A beta transport problem and may be a model region to study APP/A beta trafficking as an early pathological event...
  30. ncbi request reprint Alpha-synuclein, Abeta and Alzheimer's disease
    Oliver Wirths
    Department of Psychiatry, Section Neurobiology and European Graduate School of Neuroscience EURON, University of Saarland Medical Center, Building 90, D 66421 Homburg Saar, Germany
    Prog Neuropsychopharmacol Biol Psychiatry 27:103-8. 2003
    ..In this review, we report on recent findings on the physiological and pathological role of alpha-synuclein and try to elucidate its possible contribution to AD pathology...
  31. ncbi request reprint No alterations of hippocampal neuronal number and synaptic bouton number in a transgenic mouse model expressing the beta-cleaved C-terminal APP fragment
    Bart P F Rutten
    Department of Psychiatry and Neuropsychology, University of Maastricht, Maastricht, The Netherlands
    Neurobiol Dis 12:110-20. 2003
    ..These data implicate that expression of beta-CTF per se is not neurotoxic, and that other mechanisms are responsible for the neurotoxic events in Alzheimer's disease brain...
  32. ncbi request reprint Possible mechanisms of APP-mediated oxidative stress in Alzheimer's disease
    Gerd Multhaup
    ZMBH Center for Molecular Biology, University of Heidelberg, Heidelberg, Germany
    Free Radic Biol Med 33:45-51. 2002
    ..APP itself binds Zn(II) and Cu(II) at nanomolar concentrations and an altered APP metabolism or expression level is believed to result in neurotoxic processes...
  33. ncbi request reprint Time sequence of maturation of dystrophic neurites associated with Abeta deposits in APP/PS1 transgenic mice
    Veronique Blanchard
    Neurodegenerative Disease Group, Centre de Recherche de Paris, Aventis Pharma 94403, Vitry sur Seine Cedex, France
    Exp Neurol 184:247-63. 2003
    ..The present study demonstrates that oxidative and mitochondrial stress factors are present at several phases of Abeta pathology progression, confirming the neuronal dysfunction in APP transgenic mice...
  34. pmc Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer's disease
    Christoph Schmitz
    Department of Psychiatry and Neuropsychology, Division of Cellular Neuroscience, University of Maastricht, Maastricht, The Netherlands
    Am J Pathol 164:1495-502. 2004
    ..These findings point to the potential involvement of more than one mechanism in hippocampal neuron loss in this APP/PS-1 double-transgenic mouse model of Alzheimer's disease...
  35. ncbi request reprint Human BACE forms dimers and colocalizes with APP
    Ariane Schmechel
    Freie Universitaet Berlin, Institut fuer Chemie Biochemie, Thielallee 63, Berlin D 14195, Germany
    J Biol Chem 279:39710-7. 2004
    ..Thus, homodimerization of BACE may help the enzyme to acquire specific mechanisms to associate with its substrates to exert catalytic activity...
  36. pmc Age-related loss of synaptophysin immunoreactive presynaptic boutons within the hippocampus of APP751SL, PS1M146L, and APP751SL/PS1M146L transgenic mice
    Bart P F Rutten
    Division Cellular Neuroscience, Department of Psychiatry and Neuropsychology, Maastricht University, P O Box 616, 6200 MD, Maastricht, The Netherlands
    Am J Pathol 167:161-73. 2005
    ..The observation of age-related SIPB loss within SR of PS1M146L mice supports a role of mutant PS1 in neurodegeneration apart from its contribution to alterations in Abeta generation...
  37. ncbi request reprint A modified beta-amyloid hypothesis: intraneuronal accumulation of the beta-amyloid peptide--the first step of a fatal cascade
    Oliver Wirths
    Saarland University, Department of Psychiatry, Division of Neurobiology, 66421 Homburg Saar, Germany
    J Neurochem 91:513-20. 2004
    ..Based on these results, a modified A beta hypothesis is formulated, that integrates biochemical, neuropathological and genetic observations with AD-typical neuron loss and plaque formation...
  38. pmc Massive CA1/2 neuronal loss with intraneuronal and N-terminal truncated Abeta42 accumulation in a novel Alzheimer transgenic model
    Caty Casas
    Department of Central Nervous System Alzheimer Disease, Aventis Pharma Paris Research Center, Vitry sur Seine, France
    Am J Pathol 165:1289-300. 2004
    ..Thus, APP(SL)PS1KI mice further confirm the critical role of intraneuronal Abeta(42) in neuronal loss and provide an excellent tool to investigate therapeutic strategies designed to prevent AD neurodegeneration...
  39. ncbi request reprint Clioquinol mediates copper uptake and counteracts copper efflux activities of the amyloid precursor protein of Alzheimer's disease
    Carina Treiber
    Freie Universitaet Berlin, Institut fuer Chemie Biochemie, Thielallee 63, D 14195 Berlin, Germany
    J Biol Chem 279:51958-64. 2004
    ..These data uncover a novel biological function for APP and APLP2 in copper efflux and provide a new conceptual framework for the formerly diverging theories of copper supplementation and chelation in the treatment of Alzheimer's disease...
  40. pmc Intake of copper has no effect on cognition in patients with mild Alzheimer's disease: a pilot phase 2 clinical trial
    Holger Kessler
    Department of Psychiatry and Psychotherapy, Saarland University Hospital, Homburg Saar, Germany
    J Neural Transm 115:1181-7. 2008
    ..Despite a number of findings supporting the hypothesis of environmental Cu modulating AD, our results demonstrate that oral Cu intake has neither a detrimental nor a promoting effect on the progression of AD...
  41. ncbi request reprint Alzheimer beta-amyloid homodimers facilitate A beta fibrillization and the generation of conformational antibodies
    Ariane Schmechel
    Freie Universitaet Berlin, Institut fuer Chemie Biochemie, Thielallee 63, Berlin D 14195, Germany
    J Biol Chem 278:35317-24. 2003
    ..Based on A beta 42 dimer-specific titers of a polyclonal antiserum we propose that the A beta homodimer represents a nidus for plaque formation and a well defined novel therapeutic target...
  42. ncbi request reprint Altered cholesterol metabolism in APP695-transfected neuroblastoma cells
    Oliver Wirths
    Department of Psychiatry, Section Neurobiology, University of Goettingen, Von Siebold Str 5, D 37075 Goettingen, Germany
    Brain Res 1152:209-14. 2007
    ....
  43. ncbi request reprint Abnormalities of SNARE mechanism proteins in anterior frontal cortex in severe mental illness
    William G Honer
    Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada
    Cereb Cortex 12:349-56. 2002
    ..These abnormalities in the SNARE complex could represent a molecular substrate for abnormalities of neural connectivity in severe mental disorders...
  44. ncbi request reprint Evidence for a copper-binding superfamily of the amyloid precursor protein
    Andreas Simons
    ZMBH Center for Molecular Biology, University of Heidelberg, Im Neuenheimer Feld 282, D 69120 Heidelberg, Germany
    Biochemistry 41:9310-20. 2002
    ..The more recently evolved homologues of human APP appear to take advantage of unique redox properties for yet unknown biological functions...