Salvatore Oddo

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Ibuprofen reduces Abeta, hyperphosphorylated tau and memory deficits in Alzheimer mice
    Ann C McKee
    Department of Neurology, Boston University School of Medicine, Boston, MA, USA
    Brain Res 1207:225-36. 2008
  2. doi request reprint The ubiquitin-proteasome system in Alzheimer's disease
    Salvatore Oddo
    Department of Neurobiology and Behavior University of California, Irvine, CA 92697 4545, USA
    J Cell Mol Med 12:363-73. 2008
  3. 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
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. 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

Collaborators

Detail Information

Publications32

  1. pmc Ibuprofen reduces Abeta, hyperphosphorylated tau and memory deficits in Alzheimer mice
    Ann C McKee
    Department of Neurology, Boston University School of Medicine, Boston, MA, USA
    Brain Res 1207:225-36. 2008
    ..These findings provide further support for intraneuronal Abeta as a cause of cognitive impairment, and suggest that pathological alterations of tau are associated with intraneuronal oligomeric Abeta accumulation...
  2. doi request reprint The ubiquitin-proteasome system in Alzheimer's disease
    Salvatore Oddo
    Department of Neurobiology and Behavior University of California, Irvine, CA 92697 4545, USA
    J Cell Mol Med 12:363-73. 2008
    ..This review summarizes the data supporting an involvement of the UPS in the pathogenesis of AD, focusing on the data showing the relationship between Abeta and tau, the two hallmark lesions of AD, and the UPS...
  3. 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...
  4. 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
    ....
  5. 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...
  6. 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...
  7. 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...
  8. 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...
  9. 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...
  10. 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...
  11. pmc 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...
  12. 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...
  13. 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...
  14. ncbi request reprint Neural stem cells improve memory in an inducible mouse model of neuronal loss
    Tritia R Yamasaki
    Department of Neurobiology and Behavior, University of California, Irvine, Irvine, California 92697, USA
    J Neurosci 27:11925-33. 2007
    ..These results show that stem cells may have therapeutic value in diseases and conditions that result in memory loss...
  15. 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...
  16. ncbi request reprint Enhanced caffeine-induced Ca2+ release in the 3xTg-AD mouse model of Alzheimer's disease
    Ian F Smith
    Department of Neurobiology and Behavior, University of California, Irvine, California 92697 4545, USA
    J Neurochem 94:1711-8. 2005
    ....
  17. ncbi request reprint Intracellular amyloid-beta in Alzheimer's disease
    Frank M LaFerla
    Department of Neurobiology and Behaviour, and Institute for Brain Aging and Dementia, University of California, Irvine, California 92697 4545, USA
    Nat Rev Neurosci 8:499-509. 2007
    ....
  18. 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
    ....
  19. ncbi request reprint Intraneuronal Abeta causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice
    Lauren M Billings
    Department of Neurobiology and Behavior and Center for the Neurobiology of Learning and Memory, University of California, Irvine, Irvine, CA 92697, USA
    Neuron 45:675-88. 2005
    ..Reemergence of the Abeta pathology again leads to cognitive deficits. This study strongly implicates intraneuronal Abeta in the onset of cognitive dysfunction...
  20. ncbi request reprint Alzheimer's disease: Abeta, tau and synaptic dysfunction
    Frank M LaFerla
    Department of Neurobiology and Behavior, University of California, Irvine, CA 92697 4545, USA
    Trends Mol Med 11:170-6. 2005
    ....
  21. ncbi request reprint Abeta immunotherapy leads to clearance of early, but not late, hyperphosphorylated tau aggregates via the proteasome
    Salvatore Oddo
    Institute for Brain Aging and Dementia, University of California, Irvine, Irvine, CA 92697, USA
    Neuron 43:321-32. 2004
    ..These findings indicate that Abeta immunization may be useful for clearing both hallmark lesions of AD, provided that intervention occurs early in the disease course...
  22. ncbi request reprint The role of nicotinic acetylcholine receptors in Alzheimer's disease
    Salvatore Oddo
    Department of Neurobiology and Behavior, University of California, Irvine, 1109 Gillespie Neuroscience Building, Irvine, CA 92697 4545, USA
    J Physiol Paris 99:172-9. 2006
    ..In this review, we consider the role of nicotinic acetylcholine receptors in transgenic models and in AD...
  23. 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
    ....
  24. ncbi request reprint Progesterone and estrogen regulate Alzheimer-like neuropathology in female 3xTg-AD mice
    Jenna C Carroll
    Neuroscience Graduate Program, Davis School of Gerontology, University of Southern California, Los Angeles, California 90089, USA
    J Neurosci 27:13357-65. 2007
    ..These results demonstrate that estrogen and progesterone independently and interactively regulate AD-like neuropathology and suggest that an optimized hormone therapy may be useful in reducing the risk of AD in postmenopausal women...
  25. ncbi request reprint Collapsin response mediator protein-2 hyperphosphorylation is an early event in Alzheimer's disease progression
    Adam R Cole
    Division of Pathology and Neurosciences, University of Dundee, Ninewells Hospital, Dundee, Scotland, UK
    J Neurochem 103:1132-44. 2007
    ..These observations implicate hyperphosphorylation of CRMP2 as an early event in the development of AD and suggest that it can be induced by a severe APP over-expression and/or processing defect...
  26. ncbi request reprint Increased intraneuronal resting [Ca2+] in adult Alzheimer's disease mice
    Jose R Lopez
    Department of Anesthesia, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, USA
    J Neurochem 105:262-71. 2008
    ..These results demonstrate that an elevation in resting [Ca2+](i), contributed by aberrant Ca2+entry and release pathways, should be considered a major component of the abnormal Ca2+ homeostasis associated with AD...
  27. ncbi request reprint Congo red and thioflavin-T analogs detect Abeta oligomers
    Izumi Maezawa
    M I N D Institute and Department of Pathology, University of California Davis, Sacramento, California 95817, USA
    J Neurochem 104:457-68. 2008
    ..We propose that by improving the binding affinity of current ligands, in vivo imaging of AbetaO is feasible by a 'signal subtraction' procedure. This approach may facilitate the identification of individuals with early AD...
  28. ncbi request reprint Enhanced ryanodine-mediated calcium release in mutant PS1-expressing Alzheimer's mouse models
    Grace E Stutzmann
    Department of Neuroscience, Rosalind Franklin University of Medicine and Science, The Chicago Medical School, 3333 Green Bay Road, North Chicago, IL 60064, USA
    Ann N Y Acad Sci 1097:265-77. 2007
    ..Our results highlight the critical roles of RyR-mediated Ca(2+) signaling in both neuronal physiology and pathophysiology, and point to presenilin-linked disruptions in RyR signaling as an important genetic factor in AD...
  29. ncbi request reprint Androgens regulate the development of neuropathology in a triple transgenic mouse model of Alzheimer's disease
    Emily R Rosario
    Neuroscience Graduate Program, University of Southern California, Los Angeles, California 90089, USA
    J Neurosci 26:13384-9. 2006
    ..In addition, our finding that DHT protects against acceleration of AD-like neuropathology predicts that androgen-based hormone therapy may be a useful strategy for the prevention and treatment of AD in aging men...
  30. pmc Caspase-cleavage of tau is an early event in Alzheimer disease tangle pathology
    Robert A Rissman
    Institute for Brain Aging and Dementia, University of California, Irvine 92697, USA
    J Clin Invest 114:121-30. 2004
    ..These results suggest that therapeutics aimed at inhibiting tau caspase-cleavage may prove beneficial not only in preventing NFT formation, but also in slowing cognitive decline...
  31. ncbi request reprint Lipopolysaccharide-induced inflammation exacerbates tau pathology by a cyclin-dependent kinase 5-mediated pathway in a transgenic model of Alzheimer's disease
    Masashi Kitazawa
    Department of Neurobiology and Behavior, University of California Irvine, California 92697 4545, USA
    J Neurosci 25:8843-53. 2005
    ..Therefore, this study clearly demonstrates that microglial activation exacerbates key neuropathological features such as tangle formation...
  32. pmc Inclusion body myositis-like phenotype induced by transgenic overexpression of beta APP in skeletal muscle
    Michael C Sugarman
    Department of Neurobiology and Behavior, University of California, Irvine, CA 92697, USA
    Proc Natl Acad Sci U S A 99:6334-9. 2002
    ..These results are consistent with a pathogenic role for betaAPP mismetabolism in human IBM...

Research Grants3

  1. Molecular Mechanisms of Memory Loss in a Transgenic Model of Alzheimer Disease
    Salvatore Oddo; Fiscal Year: 2007
    ..Combined the proposed aims will help to elucidate the underlying molecular pathways linking A¿ to cognition. The identification of pathways leading to cognitive decline may point to new therapeutic targets. ..