The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Antibodies against beta-amyloid reduce Abeta oligomers, glycogen synthase kinase-3beta activation and tau phosphorylation in vivo and in vitro.
Qiu-Lan Ma; Giselle P Lim; Marni E Harris-White; Fusheng Yang; Surendra S Ambegaokar; Oliver J Ubeda; Charles G Glabe; Bruce Teter; Sally A Frautschy; Greg M Cole (Profiled Author: Cole, Greg M)
Department of Medicine, University of California, Los Angeles, California 91343, USA.
Journal of neuroscience research 2006;83(3):374-84.
Although active and passive immunization against the beta-amyloid peptide (Abeta) of amyloid plaque-bearing transgenic mice markedly reduces amyloid plaque deposition and improves cognition, the mechanisms of neuroprotection and impact on toxic oligomer species are not understood. We demonstrate that compared to control IgG2b, passive immunization with intracerebroventricular (icv) anti-Abeta (1-15) antibody into the AD HuAPPsw (Tg2576) transgenic mouse model reduced specific oligomeric forms of Abeta, including the dodecamers that correlate with cognitive decline. Interestingly, the reduction of soluble Abeta oligomers, but not insoluble Abeta, significantly correlated with reduced tau phosphorylation by glycogen synthase kinase-3beta (GSK-3beta), a major tau kinase implicated previously in mediating Abeta toxicity. A conformationally-directed antibody against amyloid oligomers (larger than tetramer) also reduced Abeta oligomer-induced activation of GSK3beta and protected human neuronal SH-SY5Y cells from Abeta oligomer-induced neurotoxicity, supporting a role for Abeta oligomers in human tau kinase activation. These data suggest that antibodies that are highly specific for toxic oligomer subspecies may reduce toxicity via reduction of GSK-3beta, which could be an important strategy for Alzheimer's disease (AD) therapeutics.
1 Originating Grant
Cole, Gregory M
30 September 2001 - 31 August 2007
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
Total Funding: $ 1,285,000
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
BENNETT, DAVID ALAN
1 July 1998 - 30 June 2014
NATIONAL INSTITUTE ON AGING
Total Funding: $ 8,095,647
1 December 2000 - 31 March 2017
NATIONAL INSTITUTE OF MENTAL HEALTH
Total Funding: $ 3,757,746
Edward Rockenstein; Magdalena Torrance; Anthony Adame; Michael Mante; Pazit Bar-on; John B Rose; Leslie Crews; Eliezer Masliah
Neuroprotective effects of regulators of the glycogen synthase kinase-3beta signaling pathway in a transgenic model of Alzheimer's disease are associated with reduced amyloid precursor protein phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience 2007;27(8):1981-91.
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