Gunnar K Gouras

Summary

Affiliation: Cornell University
Country: USA

Publications

  1. pmc Intraneuronal beta-amyloid accumulation and synapse pathology in Alzheimer's disease
    Gunnar K Gouras
    Department for Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
    Acta Neuropathol 119:523-41. 2010
  2. pmc Immunotherapy for Alzheimer disease
    Gunnar K Gouras
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
    MAbs 1:112-4. 2009
  3. ncbi request reprint Intraneuronal Abeta accumulation and origin of plaques in Alzheimer's disease
    Gunnar K Gouras
    Laboratory of Alzheimer s Disease Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, New York, NY 10021, USA
    Neurobiol Aging 26:1235-44. 2005
  4. pmc Effects of synaptic modulation on beta-amyloid, synaptophysin, and memory performance in Alzheimer's disease transgenic mice
    Davide Tampellini
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10065, USA
    J Neurosci 30:14299-304. 2010
  5. ncbi request reprint Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses
    Claudia G Almeida
    Department of Neurology and Neuroscience, Laboratory of Alzheimer s Disease Neurobiology, Weill Medical College of Cornell University, 525 E 68th Street, NY 10021, USA
    Neurobiol Dis 20:187-98. 2005
  6. ncbi request reprint Oligomerization of Alzheimer's beta-amyloid within processes and synapses of cultured neurons and brain
    Reisuke H Takahashi
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Neurosci 24:3592-9. 2004
  7. pmc Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer's disease
    Magali Dumont
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
    J Alzheimers Dis 27:211-23. 2011
  8. ncbi request reprint Internalized antibodies to the Abeta domain of APP reduce neuronal Abeta and protect against synaptic alterations
    Davide Tampellini
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Biol Chem 282:18895-906. 2007
  9. pmc Co-occurrence of Alzheimer's disease ß-amyloid and τ pathologies at synapses
    Reisuke H Takahashi
    Department of Neurology and Neuroscience, Weill Cornell Medical College, 525 East 68th Street, New York, NY 10065, USA
    Neurobiol Aging 31:1145-52. 2010
  10. ncbi request reprint Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice
    Feng Li
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, New York, NY 10021, USA
    J Neurochem 89:1308-12. 2004

Collaborators

Detail Information

Publications28

  1. pmc Intraneuronal beta-amyloid accumulation and synapse pathology in Alzheimer's disease
    Gunnar K Gouras
    Department for Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
    Acta Neuropathol 119:523-41. 2010
    ....
  2. pmc Immunotherapy for Alzheimer disease
    Gunnar K Gouras
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
    MAbs 1:112-4. 2009
    ..Several ongoing immunotherapy clinical trials for Alzheimer disease are in progress. The background and ongoing challenges for these immunological approaches for the treatment of Alzheimer disease are discussed...
  3. ncbi request reprint Intraneuronal Abeta accumulation and origin of plaques in Alzheimer's disease
    Gunnar K Gouras
    Laboratory of Alzheimer s Disease Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, New York, NY 10021, USA
    Neurobiol Aging 26:1235-44. 2005
    ..Here we provide a historical overview on the origin of plaques and a discussion on potential biological and therapeutic implications of intraneuronal Abeta accumulation for AD...
  4. pmc Effects of synaptic modulation on beta-amyloid, synaptophysin, and memory performance in Alzheimer's disease transgenic mice
    Davide Tampellini
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10065, USA
    J Neurosci 30:14299-304. 2010
    ..These data support beneficial effects of synaptic activation on Aβ-related synaptic and behavioral impairment in AD...
  5. ncbi request reprint Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses
    Claudia G Almeida
    Department of Neurology and Neuroscience, Laboratory of Alzheimer s Disease Neurobiology, Weill Medical College of Cornell University, 525 E 68th Street, NY 10021, USA
    Neurobiol Dis 20:187-98. 2005
    ....
  6. ncbi request reprint Oligomerization of Alzheimer's beta-amyloid within processes and synapses of cultured neurons and brain
    Reisuke H Takahashi
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Neurosci 24:3592-9. 2004
    ..These Abeta42 oligomer accumulations are associated with pathological alterations within processes and synaptic compartments in Tg2576 mouse and human AD brains...
  7. pmc Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer's disease
    Magali Dumont
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
    J Alzheimers Dis 27:211-23. 2011
    ..Our results show decreased pathology and improved behavior in transgenic AD mice treated with the naturally occurring antioxidant compound CoQ10. CoQ10 is well tolerated in humans and may be promising for therapeutic trials in AD...
  8. ncbi request reprint Internalized antibodies to the Abeta domain of APP reduce neuronal Abeta and protect against synaptic alterations
    Davide Tampellini
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Biol Chem 282:18895-906. 2007
    ..In addition, treatment with Abeta antibodies protects against synaptic alterations that occur in APP mutant neurons...
  9. pmc Co-occurrence of Alzheimer's disease ß-amyloid and τ pathologies at synapses
    Reisuke H Takahashi
    Department of Neurology and Neuroscience, Weill Cornell Medical College, 525 East 68th Street, New York, NY 10065, USA
    Neurobiol Aging 31:1145-52. 2010
    ..We now report that pathological accumulation of Abeta and hyperphosphorylation of tau develop concomitantly within synaptic terminals...
  10. ncbi request reprint Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice
    Feng Li
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, New York, NY 10021, USA
    J Neurochem 89:1308-12. 2004
    ..These results indicate that oxidative stress can promote the pathogenesis of AD and further support the feasibility of antioxidant approaches for AD therapy...
  11. pmc Synaptic activity reduces intraneuronal Abeta, promotes APP transport to synapses, and protects against Abeta-related synaptic alterations
    Davide Tampellini
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10065, USA
    J Neurosci 29:9704-13. 2009
    ....
  12. pmc High-resolution 3D reconstruction reveals intra-synaptic amyloid fibrils
    Estibaliz Capetillo-Zarate
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York, USA
    Am J Pathol 179:2551-8. 2011
    ..Thus, HR-3D volumetric image analysis allows for better visualization of intraneuronal Aβ pathology and provides new insights into plaque formation in AD...
  13. ncbi request reprint Regulation of NMDA receptor trafficking by amyloid-beta
    Eric M Snyder
    Laboratory for Molecular and Cellular Neuroscience, Rockefeller University, 1230 York Avenue, New York, New York 10021, USA
    Nat Neurosci 8:1051-8. 2005
    ..Dephosphorylation of the NMDA receptor subunit NR2B at Tyr1472 correlated with receptor endocytosis. These data indicate a new mechanism by which amyloid-beta can cause synaptic dysfunction and contribute to Alzheimer disease pathology...
  14. pmc Impaired β-amyloid secretion in Alzheimer's disease pathogenesis
    Davide Tampellini
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10065, USA
    J Neurosci 31:15384-90. 2011
    ..This impaired ability to secrete Aβ and reduce intraneuronal Aβ has important implications for the pathogenesis and treatment of AD...
  15. pmc Triterpenoid CDDO-methylamide improves memory and decreases amyloid plaques in a transgenic mouse model of Alzheimer's disease
    Magali Dumont
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, New York 10065, USA
    J Neurochem 109:502-12. 2009
    ..CDDO-MA was provided with chow (800 mg/kg) from 1 to 4 months of age. CDDO-MA significantly improved spatial memory retention and reduced plaque burden, Abeta42 levels, microgliosis, and oxidative stress in Tg19959 mice...
  16. doi request reprint Intraneuronal Aβ accumulation, amyloid plaques, and synapse pathology in Alzheimer's disease
    Estibaliz Capetillo-Zarate
    Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10065, USA
    Neurodegener Dis 10:56-9. 2012
    ..The progression of Aβ accumulation to synapse loss and plaque formation remains incomplete. The objective is to investigate the progression of intraneuronal Aβ accumulation in the brain...
  17. pmc Chaperones increase association of tau protein with microtubules
    Fei Dou
    Fisher Center for Research on Alzheimer s Disease, Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 100:721-6. 2003
    ..Our results suggest that up-regulation of molecular chaperones may suppress formation of neurofibrillary tangles by partitioning tau into a productive folding pathway and thereby preventing tau aggregation...
  18. pmc Degradation of Alzheimer's amyloid fibrils by microglia requires delivery of ClC-7 to lysosomes
    Amitabha Majumdar
    Department of Biochemistry and Weill Cornell Medical College, New York, NY 10065, USA
    Mol Biol Cell 22:1664-76. 2011
    ..Our findings suggest a novel mechanism of lysosomal pH regulation in activated microglia that is required for fAβ degradation...
  19. pmc Intraneuronal Alzheimer abeta42 accumulates in multivesicular bodies and is associated with synaptic pathology
    Reisuke H Takahashi
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    Am J Pathol 161:1869-79. 2002
    ..This accumulation was associated with abnormal synaptic morphology, before beta-amyloid plaque pathology, suggesting that intracellular accumulation of beta-amyloid plays a crucial role in Alzheimer's disease...
  20. ncbi request reprint Beta-amyloid accumulation impairs multivesicular body sorting by inhibiting the ubiquitin-proteasome system
    Claudia G Almeida
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA
    J Neurosci 26:4277-88. 2006
    ..These data suggest a mechanism whereby Abeta accumulation in neurons impairs the MVB sorting pathway via the UPS in AD...
  21. pmc Accumulation of intraneuronal β-amyloid 42 peptides is associated with early changes in microtubule-associated protein 2 in neurites and synapses
    Reisuke H Takahashi
    Department of Anatomic Pathology, Tokyo Medical University, Tokyo, Japan
    PLoS ONE 8:e51965. 2013
    ....
  22. pmc Beta-amyloid modulation of synaptic transmission and plasticity
    Deepa V Venkitaramani
    Child Study Center, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Neurosci 27:11832-7. 2007
  23. ncbi request reprint The Arctic Alzheimer mutation favors intracellular amyloid-beta production by making amyloid precursor protein less available to alpha-secretase
    Charlotte Sahlin
    Department of Public Health and Caring Sciences, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden
    J Neurochem 101:854-62. 2007
    ....
  24. ncbi request reprint Intraneuronal beta-amyloid expression downregulates the Akt survival pathway and blunts the stress response
    Jordi Magrane
    Department of Neurology, Caritas Saint Elizabeth s Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA
    J Neurosci 25:10960-9. 2005
    ..These results suggest that the early dysfunction associated with intraneuronal Abeta accumulation in AD involve the associated impairments of Akt signaling and suppression of the stress response...
  25. ncbi request reprint Conditional inactivation of presenilin 1 prevents amyloid accumulation and temporarily rescues contextual and spatial working memory impairments in amyloid precursor protein transgenic mice
    Carlos A Saura
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 25:6755-64. 2005
    ..These results reveal that in vivo reduction of Abeta via the inactivation of PS1 effectively prevents amyloid-associated neuropathological changes and can, but only temporarily, improve cognitive impairments in APP transgenic mice...
  26. ncbi request reprint Amyloid-beta oligomers are inefficiently measured by enzyme-linked immunosorbent assay
    Charlotte Stenh
    Department of Public Health Geriatrics, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden
    Ann Neurol 58:147-50. 2005
    ..Our findings might be of relevance for many neurodegenerative disorders in which soluble protein aggregates are the main neurotoxic species...

Research Grants12

  1. Regulation of Alzheimer Amyloid by Neurons
    Gunnar Gouras; Fiscal Year: 2003
    ..abstract not available ..
  2. Intraneuronal Abeta accumulation: mechanism of pathogenesis
    Gunnar Gouras; Fiscal Year: 2007
    ..A better understanding of the mechanism whereby beta-amyloid is involved in synaptic dysfunction and Alzheimer's disease pathogenesis may be important for devising more effective treatments for Alzheimer's disease. ..
  3. The Subcellular Neuropathology of Alzheimer's Disease
    Gunnar Gouras; Fiscal Year: 2007
    ....
  4. Intraneuronal Abeta accumulation: mechanism of pathogenesis
    Gunnar K Gouras; Fiscal Year: 2010
    ..A better understanding of the mechanism whereby beta-amyloid is involved in synaptic dysfunction and Alzheimer's disease pathogenesis may be important for devising more effective treatments for Alzheimer's disease. ..
  5. The Subcellular Neuropathology of Alzheimer's Disease
    Gunnar Gouras; Fiscal Year: 2003
    ....
  6. Intraneuronal Abeta accumulation: mechanism of pathogenesis
    Gunnar Gouras; Fiscal Year: 2009
    ..A better understanding of the mechanism whereby beta-amyloid is involved in synaptic dysfunction and Alzheimer's disease pathogenesis may be important for devising more effective treatments for Alzheimer's disease. ..
  7. BIOLOGY OF ALZHEIMER AMYLOID IN NEURONS
    Gunnar Gouras; Fiscal Year: 2007
    ....
  8. The Subcellular Neuropathology of Alzheimer's Disease
    Gunnar Gouras; Fiscal Year: 2006
    ....
  9. The Subcellular Neuropathology of Alzheimer's Disease
    Gunnar Gouras; Fiscal Year: 2005
    ....
  10. The Subcellular Neuropathology of Alzheimer's Disease
    Gunnar Gouras; Fiscal Year: 2004
    ....