Grace E Stutzmann

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Ca2+ signaling in mouse cortical neurons studied by two-photon imaging and photoreleased inositol triphosphate
    Grace E Stutzmann
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697 4550, USA
    J Neurosci 23:758-65. 2003
  2. ncbi request reprint Calcium dysregulation, IP3 signaling, and Alzheimer's disease
    Grace E Stutzmann
    Department of Neurobiology and Behavior, 1146 McGaugh Hall, University of California Irvine, Irvine, CA 92697, USA
    Neuroscientist 11:110-5. 2005
  3. ncbi request reprint Dysregulated IP3 signaling in cortical neurons of knock-in mice expressing an Alzheimer's-linked mutation in presenilin1 results in exaggerated Ca2+ signals and altered membrane excitability
    Grace E Stutzmann
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697 4550, USA
    J Neurosci 24:508-13. 2004
  4. ncbi request reprint Enhanced ryanodine receptor recruitment contributes to Ca2+ disruptions in young, adult, and aged Alzheimer's disease mice
    Grace E Stutzmann
    Department of Neurobiology and Behavior, University of California, Irvine, California 92697 4550, USA
    J Neurosci 26:5180-9. 2006
  5. pmc Calcium signaling and amyloid toxicity in Alzheimer disease
    Angelo Demuro
    Department of Neurobiology and Behavior, University of California, Irvine, California 92697, USA
    J Biol Chem 285:12463-8. 2010
  6. ncbi request reprint Amyloid deposition precedes tangle formation in a triple transgenic model of Alzheimer's disease
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, 1109 Gillespie Neuroscience Research Facility, Irvine, CA 92697 4545, USA
    Neurobiol Aging 24:1063-70. 2003
  7. ncbi request reprint Temporal profile of amyloid-beta (Abeta) oligomerization in an in vivo model of Alzheimer disease. A link between Abeta and tau pathology
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, California 92697 4545, USA
    J Biol Chem 281:1599-604. 2006
  8. pmc A dynamic relationship between intracellular and extracellular pools of Abeta
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, 1109 Gillespie Neuroscience Bldg, Irvine, CA 92697 4545, USA
    Am J Pathol 168:184-94. 2006
  9. ncbi request reprint M1 receptors play a central role in modulating AD-like pathology in transgenic mice
    Antonella Caccamo
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697, USA
    Neuron 49:671-82. 2006
  10. pmc Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, CA 92697, USA
    Proc Natl Acad Sci U S A 102:3046-51. 2005

Collaborators

Detail Information

Publications21

  1. ncbi request reprint Ca2+ signaling in mouse cortical neurons studied by two-photon imaging and photoreleased inositol triphosphate
    Grace E Stutzmann
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697 4550, USA
    J Neurosci 23:758-65. 2003
    ..Metabotropic signaling via the phosphoinositide pathway thus serves as a powerful and sustained modulator of excitability in cortical neurons and displays complex reciprocal interactions between electrical and chemical signals...
  2. ncbi request reprint Calcium dysregulation, IP3 signaling, and Alzheimer's disease
    Grace E Stutzmann
    Department of Neurobiology and Behavior, 1146 McGaugh Hall, University of California Irvine, Irvine, CA 92697, USA
    Neuroscientist 11:110-5. 2005
    ..The author discusses recent findings in both the physiological functioning of the IP(3)-signaling pathway in neurons and the involvement of ERCa(2+) disruptions in the pathogenesis of AD...
  3. ncbi request reprint Dysregulated IP3 signaling in cortical neurons of knock-in mice expressing an Alzheimer's-linked mutation in presenilin1 results in exaggerated Ca2+ signals and altered membrane excitability
    Grace E Stutzmann
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697 4550, USA
    J Neurosci 24:508-13. 2004
    ..Even in young animals, PS1 mutations have profound effects on neuronal Ca2+ and electrical signaling: cumulatively, these disruptions may contribute to the long-term pathophysiology of AD...
  4. ncbi request reprint Enhanced ryanodine receptor recruitment contributes to Ca2+ disruptions in young, adult, and aged Alzheimer's disease mice
    Grace E Stutzmann
    Department of Neurobiology and Behavior, University of California, Irvine, California 92697 4550, USA
    J Neurosci 26:5180-9. 2006
    ..We conclude that lifelong ER Ca2+ disruptions in AD are related to a modulation of RyR signaling associated with PS1 mutations and represent a discrete "calciumopathy," not merely an acceleration of normal aging...
  5. pmc Calcium signaling and amyloid toxicity in Alzheimer disease
    Angelo Demuro
    Department of Neurobiology and Behavior, University of California, Irvine, California 92697, USA
    J Biol Chem 285:12463-8. 2010
    ..Although no cause or cure is currently known, targeting Ca(2+) dyshomeostasis as an underlying and integral component of AD pathology may result in novel and effective treatments for AD...
  6. ncbi request reprint Amyloid deposition precedes tangle formation in a triple transgenic model of Alzheimer's disease
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, 1109 Gillespie Neuroscience Research Facility, Irvine, CA 92697 4545, USA
    Neurobiol Aging 24:1063-70. 2003
    ....
  7. ncbi request reprint Temporal profile of amyloid-beta (Abeta) oligomerization in an in vivo model of Alzheimer disease. A link between Abeta and tau pathology
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, California 92697 4545, USA
    J Biol Chem 281:1599-604. 2006
    ..Therefore, Abeta oligomers may play a role in the induction of tau pathology, making the interference of Abeta oligomerization a valid therapeutic target...
  8. pmc A dynamic relationship between intracellular and extracellular pools of Abeta
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, 1109 Gillespie Neuroscience Bldg, Irvine, CA 92697 4545, USA
    Am J Pathol 168:184-94. 2006
    ..Taken together, these results provide strong experimental evidence that intraneuronal Abeta may serve as a source for some of the extracellular amyloid deposits...
  9. ncbi request reprint M1 receptors play a central role in modulating AD-like pathology in transgenic mice
    Antonella Caccamo
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697, USA
    Neuron 49:671-82. 2006
    ..Therefore, selective M1 agonists may be efficacious for the treatment of AD...
  10. pmc Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, CA 92697, USA
    Proc Natl Acad Sci U S A 102:3046-51. 2005
    ..Finally, this study highlights the importance of testing compounds designed to ameliorate AD pathology in a model with both neuropathological lesions because of the differential effects it can have on either Abeta or tau...
  11. doi request reprint Blocking Abeta42 accumulation delays the onset and progression of tau pathology via the C terminus of heat shock protein70-interacting protein: a mechanistic link between Abeta and tau pathology
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697, USA
    J Neurosci 28:12163-75. 2008
    ..These data highlight the critical role CHIP plays as a link between Abeta and tau and identify CHIP as a new potential target not only for AD but for other neurodegenerative disorders characterized by tau accumulation...
  12. pmc Age-dependent sexual dimorphism in cognition and stress response in the 3xTg-AD mice
    Lani K Clinton
    Department of Neurobiology and Behavior, 1109 Gillespie Neuroscience Research Facility, University of California, Irvine, Irvine, CA 92697 4545, USA
    Neurobiol Dis 28:76-82. 2007
    ..Thus, the enhanced corticosterone response of the young female mice likely underlies their poorer performance on stressful tasks...
  13. ncbi request reprint Genetically augmenting tau levels does not modulate the onset or progression of Abeta pathology in transgenic mice
    Salvatore Oddo
    Department of Neurobiology and Behavior, Institute for Brain Aging and Dementia, University of California, Irvine, California, USA
    J Neurochem 102:1053-63. 2007
    ....
  14. ncbi request reprint Reduction of soluble Abeta and tau, but not soluble Abeta alone, ameliorates cognitive decline in transgenic mice with plaques and tangles
    Salvatore Oddo
    Departments of Neurobiology and Behavior and Neurology, and Institute for Brain Aging and Dementia, University of California, Irvine, California 92697, USA
    J Biol Chem 281:39413-23. 2006
    ..Notably, reducing soluble Abeta alone did not improve the cognitive phenotype in mice with plaques and NFTs. Our results show that Abeta immunotherapy reduces soluble tau and ameliorates behavioral deficit in old transgenic mice...
  15. pmc Genetically augmenting Abeta42 levels in skeletal muscle exacerbates inclusion body myositis-like pathology and motor deficits in transgenic mice
    Masashi Kitazawa
    Department of Neurobiology and Behavior, 1109 Gillespie Neuroscience Facility, University of California, Irvine, Irvine, CA 92697 4545, USA
    Am J Pathol 168:1986-97. 2006
    ..The data presented here provide experimental evidence that Abeta42 plays a proximal and critical role in the muscle degenerative process...
  16. ncbi request reprint Triple-transgenic model of Alzheimer's disease with plaques and tangles: intracellular Abeta and synaptic dysfunction
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697, USA
    Neuron 39:409-21. 2003
    ....
  17. pmc Lithium reduces tau phosphorylation but not A beta or working memory deficits in a transgenic model with both plaques and tangles
    Antonella Caccamo
    Department of Neurobiology and Behavior, University of California, Irvine, 1109 Gillespie Neuroscience Bldg, Irvine, CA 92697 4545, USA
    Am J Pathol 170:1669-75. 2007
    ..These results, however, suggest that the most efficacious treatment will be combining lithium with other anti-A beta interventions...
  18. ncbi request reprint Genetically altering Abeta distribution from the brain to the vasculature ameliorates tau pathology
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA 92697 4545, USA
    Brain Pathol 19:421-30. 2009
    ..The 3xTg-AD mice expressing the human apoE4 gene were virtually depleted of any somatodendritic tau deposits. These data strongly suggest that the somatodendritic tau accumulation is dependent on the parenchyma Abeta deposits...
  19. ncbi request reprint Age- and region-dependent alterations in Abeta-degrading enzymes: implications for Abeta-induced disorders
    Antonella Caccamo
    Department of Neurobiology and Behavior, University of California, Irvine, 1109 Gillespie Neuroscience Bldg, Irvine, CA 92697 4545, USA
    Neurobiol Aging 26:645-54. 2005
    ..These findings suggest that age- and region-specific changes in the proteolytic clearance of Abeta represent a critical pathogenic mechanism that may account for the susceptibility of particular brain or muscle regions in AD and IBM...
  20. ncbi request reprint M1 agonists as a potential disease-modifying therapy for Alzheimer's disease
    Antonella Caccamo
    Department of Neurobiology, University of California, Irvine, Irvine, CA 92697, USA
    Curr Alzheimer Res 6:112-7. 2009
    ..In this review, we discuss the role of M1 agonists as a potential disease-modifying therapy for Alzheimer's disease...
  21. pmc Loss of muscarinic M1 receptor exacerbates Alzheimer's disease-like pathology and cognitive decline
    Rodrigo Medeiros
    Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, California 92697 4545, USA
    Am J Pathol 179:980-91. 2011
    ....