B T Lamb

Summary

Affiliation: Case Western Reserve University
Country: USA

Publications

  1. ncbi The role of nitric oxide in the pathogenesis of brain lesions during the development of Alzheimer's disease
    Dilara Seyidova
    Microscopy Research Center, Institute of Pathology, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA
    In Vivo 18:325-33. 2004
  2. ncbi Altered metabolism of familial Alzheimer's disease-linked amyloid precursor protein variants in yeast artificial chromosome transgenic mice
    B T Lamb
    Department of Genetics, Case Western Reserve University, Cleveland, OH 44106, USA
    Hum Mol Genet 6:1535-41. 1997
  3. ncbi Amyloid production and deposition in mutant amyloid precursor protein and presenilin-1 yeast artificial chromosome transgenic mice
    B T Lamb
    Department of Genetics, Case Western Reserve University, Cleveland, Ohio 44106 4955, USA
    Nat Neurosci 2:695-7. 1999
  4. ncbi Neuropathological characterization of mutant amyloid precursor protein yeast artificial chromosome transgenic mice
    L S Kulnane
    Department of Genetics and Neuroscience, Case Western Reserve University and Center for Human Genetics, Cleveland, Ohio 44106, USA
    Neurobiol Dis 8:982-92. 2001
  5. ncbi Transgenic mouse models of Alzheimer's disease
    B J Hock
    Dept of Genetics, Case Western Reserve University, University Hospitals of Cleveland, 10900 Euclid Avenue, Cleveland, OH 44106-4955, USA
    Trends Genet 17:S7-12. 2001
  6. pmc Abnormal neuronal networks and seizure susceptibility in mice overexpressing the APP intracellular domain
    D L Vogt
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Neurobiol Aging 32:1725-9. 2011
  7. ncbi Rapid and efficient detection of transgene homozygosity by FISH of mouse fibroblasts
    Laura Shapiro Kulnane
    Department of Genetics and Neuroscience, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, Ohio 44106 4955, USA
    Mamm Genome 13:223-6. 2002
  8. pmc Genetic loci modulating amyloid-beta levels in a mouse model of Alzheimer's disease
    Davis Ryman
    Lerner Research Institute, Cleveland Clinic Foundation, Department of Neurosciences, NC3 164, 9500 Euclid Avenue, Cleveland, OH 44195 USA
    Neurobiol Aging 29:1190-8. 2008
  9. ncbi Genetic and environmental modifiers of Alzheimer's disease phenotypes in the mouse
    Davis Ryman
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, NC30, Cleveland, OH 44195, USA
    Curr Alzheimer Res 3:465-73. 2006
  10. ncbi Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration
    Ahmad Salehi
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, California 94305, USA
    Neuron 51:29-42. 2006

Collaborators

Detail Information

Publications22

  1. ncbi The role of nitric oxide in the pathogenesis of brain lesions during the development of Alzheimer's disease
    Dilara Seyidova
    Microscopy Research Center, Institute of Pathology, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA
    In Vivo 18:325-33. 2004
    ..We theorize that pharmacological intervention using NO donors and/or NO suppressors should delay or minimize brain lesion development and further progression of brain pathology and dementia...
  2. ncbi Altered metabolism of familial Alzheimer's disease-linked amyloid precursor protein variants in yeast artificial chromosome transgenic mice
    B T Lamb
    Department of Genetics, Case Western Reserve University, Cleveland, OH 44106, USA
    Hum Mol Genet 6:1535-41. 1997
    ....
  3. ncbi Amyloid production and deposition in mutant amyloid precursor protein and presenilin-1 yeast artificial chromosome transgenic mice
    B T Lamb
    Department of Genetics, Case Western Reserve University, Cleveland, Ohio 44106 4955, USA
    Nat Neurosci 2:695-7. 1999
  4. ncbi Neuropathological characterization of mutant amyloid precursor protein yeast artificial chromosome transgenic mice
    L S Kulnane
    Department of Genetics and Neuroscience, Case Western Reserve University and Center for Human Genetics, Cleveland, Ohio 44106, USA
    Neurobiol Dis 8:982-92. 2001
    ..Our results also suggest that APP YAC transgenic mice possess unique pathological attributes when compared to other transgenic mouse models of AD that may reflect the experimental design of each model...
  5. ncbi Transgenic mouse models of Alzheimer's disease
    B J Hock
    Dept of Genetics, Case Western Reserve University, University Hospitals of Cleveland, 10900 Euclid Avenue, Cleveland, OH 44106-4955, USA
    Trends Genet 17:S7-12. 2001
    ..Utilizing both cDNA- and genomic-based approaches, these mouse models for Alzheimer's disease have already provided valuable insights into the pathogenesis of the disease and potential therapeutic interventions...
  6. pmc Abnormal neuronal networks and seizure susceptibility in mice overexpressing the APP intracellular domain
    D L Vogt
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Neurobiol Aging 32:1725-9. 2011
    ..These data suggest that alterations in the levels of AICD contribute to network dysfunction in AD...
  7. ncbi Rapid and efficient detection of transgene homozygosity by FISH of mouse fibroblasts
    Laura Shapiro Kulnane
    Department of Genetics and Neuroscience, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, Ohio 44106 4955, USA
    Mamm Genome 13:223-6. 2002
  8. pmc Genetic loci modulating amyloid-beta levels in a mouse model of Alzheimer's disease
    Davis Ryman
    Lerner Research Institute, Cleveland Clinic Foundation, Department of Neurosciences, NC3 164, 9500 Euclid Avenue, Cleveland, OH 44195 USA
    Neurobiol Aging 29:1190-8. 2008
    ..Our studies have identified three loci on mouse chromosomes 1, 2, and 7 showing significant or suggestive associations with brain Abeta levels, several of which contain regions syntenic to previous reports of linkage in human AD...
  9. ncbi Genetic and environmental modifiers of Alzheimer's disease phenotypes in the mouse
    Davis Ryman
    Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, NC30, Cleveland, OH 44195, USA
    Curr Alzheimer Res 3:465-73. 2006
    ....
  10. ncbi Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration
    Ahmad Salehi
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, California 94305, USA
    Neuron 51:29-42. 2006
    ..Our study thus provides evidence for a pathogenic mechanism for DS in which increased expression of App, in the context of trisomy, causes abnormal transport of NGF and cholinergic neurodegeneration...
  11. ncbi Ectopic cell cycle events link human Alzheimer's disease and amyloid precursor protein transgenic mouse models
    Yan Yang
    Department of Neurology, University Hospitals of Cleveland, Cleveland, Ohio 44106, USA
    J Neurosci 26:775-84. 2006
    ..Finally, the relative timing suggests that neither the activated microglia nor the amyloid plaques themselves are necessary to initiate the pathogenic events in AD...
  12. pmc Altered amyloid-beta metabolism and deposition in genomic-based beta-secretase transgenic mice
    Matthew J Chiocco
    Department of Genetics, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, Ohio 44106, USA
    J Biol Chem 279:52535-42. 2004
    ..Our studies demonstrate, for the first time, that modulation of BACE1 activity may play a significant role in AD pathogenesis in vivo...
  13. ncbi The role of oxidative stress in the pathophysiology of cerebrovascular lesions in Alzheimer's disease
    Gjumrakch Aliev
    Electron Microscopy Center, and Department of Anatomy, Case Western Reserve University, School of Medicine and University Hospital of the Cleveland, OH 44106 4938, USA
    Brain Pathol 12:21-35. 2002
    ..We also consider the opportunities for therapeutic interventions based on the molecular pathways involved with these causal relationships...
  14. ncbi Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels as a central target for the development of human AD and AD-like pathology in aged transgenic mice
    Gjumrakch Aliev
    Microscopy Research Center, Department of Anatomy, Case Western Reserve University and University Hospitals of Cleveland, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Ann N Y Acad Sci 977:45-64. 2002
    ..Our observations demonstrate that vascular wall cells, especially their mitochondria, appear to be a central target for oxidative stress-induced damage...
  15. ncbi Alterations in beta-amyloid production and deposition in brain regions of two transgenic models
    Emily J H Lehman
    Department of Genetics and Neurosciences, Center for Human Genetics, Case Western Reserve University, University Center for Memory and Aging and Ireland Cancer Center, University Hospitals of Cleveland, Cleveland, OH 44106, USA
    Neurobiol Aging 24:645-53. 2003
    ..Our results suggest that AD transgenic models are not equal; their unique characteristics must be considered when studying AD pathogenesis and therapies...
  16. ncbi Mitochondria and vascular lesions as a central target for the development of Alzheimer's disease and Alzheimer disease-like pathology in transgenic mice
    Gjumrakch Aliev
    Microscopy Research Center, Department of Anatomy, Department of Pathology, Case Western Reserve University, University Hospitals of Cleveland, Cleveland, OH, USA
    Neurol Res 25:665-74. 2003
    ..Our observations first time demonstrate that vascular wall cells, especially their mitochondria, appear to be a central target for oxidative stress induced damage...
  17. ncbi Genetic background regulates beta-amyloid precursor protein processing and beta-amyloid deposition in the mouse
    Emily J H Lehman
    Department of Genetics, Case Western Reserve University, and Center for Human Genetics, University Hospitals of Cleveland, OH 44106 4955, USA
    Hum Mol Genet 12:2949-56. 2003
    ....
  18. ncbi Is nitric oxide a key target in the pathogenesis of brain lesions during the development of Alzheimer's disease?
    Ali Aliyev
    Microscopy Research Center, Case Western Reserve University, Cleveland, OH 44106, USA
    Neurol Res 26:547-53. 2004
    ..We speculate that pharmacological intervention using NO donors and/or NO suppressors will be able to delay or minimize the development of brain pathology and further progression of mental retardation...
  19. pmc Spatial and temporal control of age-related APP processing in genomic-based beta-secretase transgenic mice
    Matthew J Chiocco
    Department of Genetics, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH 44106, USA
    Neurobiol Aging 28:75-84. 2007
    ..Furthermore, our studies provide further evidence that BACE1 plays a major role in the regulation of the APP processing pathway, influencing the age-dependent onset of AD pathogenesis...
  20. pmc The Ter mutation in the dead end gene causes germ cell loss and testicular germ cell tumours
    Kirsten K Youngren
    Department of Genetics and
    Nature 435:360-4. 2005
    ..TGCT development in the 129-Ter mouse strain models paediatric TGCT in humans. This work will have important implications for our understanding of the genetic control of TGCT pathogenesis and PGC biology...
  21. ncbi Reductions in beta-amyloid concentrations in vivo by the gamma-secretase inhibitors BMS-289948 and BMS-299897
    Jeffery J Anderson
    SIBIA Neurosciences, Inc, 300 S Coast Blvd, La Jolla, CA 92037, USA
    Biochem Pharmacol 69:689-98. 2005
    ..These compounds may be useful pharmacologically for examining the effects of reductions in beta-amyloid peptides in both animal models and in Alzheimer's disease...
  22. ncbi Independent effects of APOE on cholesterol metabolism and brain Abeta levels in an Alzheimer disease mouse model
    Karen M Mann
    Department of Genetics, Case Western Reserve University, Cleveland, OH 44106, USA
    Hum Mol Genet 13:1959-68. 2004
    ....