Affiliation: Elan Pharmaceuticals
- Cellular source of apolipoprotein E4 determines neuronal susceptibility to excitotoxic injury in transgenic miceManuel Buttini
Gladstone Institute of Neurological Disease, San Francisco, CA 94158 2261, USA
Am J Pathol 177:563-9. 2010..Thus, an imbalance between astrocytic (excitoprotective) and neuronal (neurotoxic) apoE4 expression may increase susceptibility to diverse neurological diseases involving excitotoxic mechanisms...
- Beta-amyloid immunotherapy prevents synaptic degeneration in a mouse model of Alzheimer's diseaseManuel Buttini
Elan Pharmaceuticals, South San Francisco, California 94080, USA
J Neurosci 25:9096-101. 2005....
- Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic MiceLisa McConlogue
Department of Biology, Elan Pharmaceuticals, South San Francisco, California 94080, USA
J Biol Chem 282:26326-34. 2007....
- Modulation of Alzheimer-like synaptic and cholinergic deficits in transgenic mice by human apolipoprotein E depends on isoform, aging, and overexpression of amyloid beta peptides but not on plaque formationManuel Buttini
Gladstone Institute of Neurological Disease, University of California, San Francisco, California 94141 9100, USA
J Neurosci 22:10539-48. 2002..Thus, apoE3, but not apoE4, delays age- and Abeta-dependent synaptic deficits through a plaque-independent mechanism. This difference could contribute to the differential effects of apoE isoforms on the risk and onset of AD...
- Neuron-specific apolipoprotein e4 proteolysis is associated with increased tau phosphorylation in brains of transgenic miceWalter J Brecht
Gladstone Institute of Neurological Disease, San Francisco, California 94141 9100, USA
J Neurosci 24:2527-34. 2004..Neuron-specific proteolytic cleavage of apoE4 is associated with increased phosphorylation of tau and may play a key role in the development of AD-related neuronal deficits...
- Neutralization of soluble, synaptotoxic amyloid β species by antibodies is epitope specificWagner Zago
Janssen Alzheimer Immunotherapy Research and Development, South San Francisco, CA 94080, USA
J Neurosci 32:2696-702. 2012..These results, taken with prior studies, suggest that N-terminal anti-Aβ antibodies effectively interact with both soluble and insoluble forms of Aβ and therefore appear particularly well suited for testing the Aβ hypothesis of AD...
- Mice as models: transgenic approaches and Alzheimer's diseaseDora Games
Elan Pharmaceuticals, 800 Gateway Blvd, South San Francisco, CA 94080, USA
J Alzheimers Dis 9:133-49. 2006..As a result, we may see containment or even the elimination of AD in the near future as a direct consequence of these advances...
- Morphological characterization of Thioflavin-S-positive amyloid plaques in transgenic Alzheimer mice and effect of passive Abeta immunotherapy on their clearanceThierry Bussiere
Elan Pharmaceuticals, South San Francisco, California, USA
Am J Pathol 165:987-95. 2004..Our results show that distinct morphological types of plaques are differentially cleared depending upon the isotype of the antibody...
- BACE1 gene deletion: impact on behavioral function in a model of Alzheimer's diseaseDione Kobayashi
Rinat Neurosciences, 230 East Grand Avenue, South San Francisco, CA 94080, USA
Neurobiol Aging 29:861-73. 2008..These results suggest that while excess Abeta is functionally pathological, BACE1-mediated processing of APP and other substrates play a role in "normal" learning, memory and sensorimotor processes...
- Androgens protect against apolipoprotein E4-induced cognitive deficitsJacob Raber
Gladstone Institute of Neurological Disease and Department of Neurology, University of California, San Francisco, California 94141, USA
J Neurosci 22:5204-9. 2002..Our findings suggest that apoE4 contributes to cognitive decline by reducing AR levels in the brain, and that stimulating AR-dependent pathways can reverse apoE4-induced cognitive deficits...
- Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1Marion S Buckwalter
Neurology and Neurological Sciences, Stanford University, Stanford, California 94305, USA
J Neurosci 26:11437-41. 2006..Likewise, levels of TGF-beta1 or other immune factors in brains of AD patients may influence the response to Abeta(1-42) immunization...
- RAGE potentiates Abeta-induced perturbation of neuronal function in transgenic miceOttavio Arancio
Department of Psychiatry, Physiology and Neuroscience, Dementia Research Center, Nathan Kline Institute, New York University School of Medicine, NY 10032, USA
EMBO J 23:4096-105. 2004..These data indicate that RAGE is a cofactor for Abeta-induced neuronal perturbation in a model of Alzheimer's-type pathology, and suggest its potential as a therapeutic target to ameliorate cellular dysfunction...
- Evaluation of alpha-synuclein immunohistochemical methods used by invited expertsThomas G Beach
Civin Laboratory for Neuropathology, Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA
Acta Neuropathol 116:277-88. 2008..Some methods, however, achieved relatively high sensitivities with optimized formic acid protocols combined with a hydrolytic step. One method was developed that allows high sensitivity with commercially available reagents...